Nick Gracey WATerian BSc(Hons) Medical BioChemistry, Birmingham University, Adrenaline LIFE2345.©OM

A Spoon Full Of Honey 'CPR' rubbed inside a mouth ... A fainting COMA needs FUEL to recover from a sudden drop / fall of blood fuel [glucose]

noreply@blogger.com (Nicholas Dynes Gracey) — Sun, 01 Mar 2009 10:32:00 +0000

"How Can We Better Help Prevent People From Fainting ?" [~click]
.
.
.

# CARS run out of FUEL and so do HUMANS [~click]

As seizures have a differential diagnosis, it is common for Patients to be simultaneously investigated for cardiac and endocrine causes. Checking glucose levels, for example, is a mandatory action in the management of seizures as HYPOglycemia may cause seizures, and failure to administer glucose would be harmful to the Patient.

COLLAPSED = FAINTED not DIED

seizures, heart attacks, faints & COMA ['low-fuel-diseases'] are still not being given honey [rapidly absorbed by the gums /mouth / tongue]

let's CHANGE the old 'no fuel' CPR ...
'CPR' should include a spoon full of honey

NOW! NOW!! NOW!!!

MiKLOS-FeHER.com

COLLAPSED = FAINTED not DIED

Robert Manning, from Cratloe, in Ireland was a secondary school pupil. The eldest of three boys, he was full of enthusiasm for life in a quiet, unassuming way. He was 6’3” in height and was supposedly very healthy. He was an avid oarsman and also loved karate and rugby. His friends looked up to him as he could defuse any tricky situation or pass a funny “tongue-in-cheek” comment which people found endearing. In his memory, a friend released a tribute single ‘Re-Unite’ for the Robert Manning Fund, which was donated to CROI (the West of Ireland Cardiology Foundation).

Date of death: August 2002
Age at time of death: 16
Prior symptoms detected: None
Circumstances of death: Robert was playing rugby with his family in the back garden. As he went to retrieve the ball he said “Oh no” and lay down on the grass. His family tried to revive him using CPR but to no avail.
Diagnosed cause of death: Because all of Robert’s organs were undamaged, no cause of death was found, leading to a diagnosis of SADS.

COLLAPSED = FAINTED not DIED

Catherine Keane, from Lisheenfurror, Kilkee, in Ireland, was a Pupil in fifth class at Carrigaholt National School. She enjoyed football, swimming and hurling, but the love of her life was horse-riding. From a family of two children, she was a very hard-working, diligent little girl, who was great company and always eager to please people.
Date of death: November 2003
Age at time of death: 10
Prior symptoms detected: Just over a year prior to her death, Catherine fainted and she was referred to hospital by her doctor who had detected tachycardia. The appropriate tests to detect cardiac condition were not carried out at hospital.
Circumstances of death: Catherine was at her riding school when she slumped on her pony, and despite efforts by her father and riding instructors to administer CPR, she could not be revived.
Diagnosed cause of death: The post-mortem reported that she had a massive brain seizure, but the results of an inquest are still awaited, and family investigations indicate that the cause of death was cardiac.

COLLAPSED = FAINTED not DIED

BUT ... IT IS OTHER THAN CLEAR WHETHER MIKLOS FEHER, ROBERT MANNING & CATHERINE KEANE ... HAD SIMPLY FAINTED FROM

GLUCOSE & KETOSIS FUEL EXHAUSTION
aka HYPOglycemia & HYPOketosis & HYPOxemia [commonly associated with cardiac related seizures] and that, in the apparent [see video / text] absence of a rapid SPOON FULL OF HONEY the questionable CPR procedure 'received' had EXHAUSTED ... MIKLOS FEHER, ROBERT MANNING & CATHERINE KEANE to death ... all for the lack of GLUCOSE EG via a GLUCAGON injection and the questionable medical practice of treating Someone who faints [ie a COMA being a natural safety mechanism of a fuel exhausted body] ...
apparently without providing any treatment for

a lack of GLUCOSE or DEHYDRATION

COLLAPSED = FAINTED not DIED

http://www.DietFitnessFAQ.com/diet-fitness/index_6012.html
http://www.ManchesterEveningNews.co.uk/news/s/1051084_girl_dies_in_school_game
http://Express.Lineone.net/posts/view/45997/Girl-14-dies-of-a-heart-attack-playing-rounders
http://www.NutraIngredients-USA.com/news/ng.asp?n=85729-red-bull-federal-institute-for-risk-assessment-energy-drinks-taurine-caffeine

http://JoyShadow.livejournal.com/13405.html
http://www.SalfordAdvertiser.co.uk/news/s/1051789_parents_mourn_shock_death_of_sporty_teenager
http://www.Telegraph.co.uk/news/uknews/2047319/Teenager-dies-in-school-game-of-rounders.html
http://www.ManchesterEveningnews.co.uk/news/s/1051387_tributes_flood_in_for_olivia
http://www.aipsmedia.com/index.php?page=news&cod=3171&tp=n [Sebastian Faißt]

http://www.TheCormacTrust.cOM/sudden-cardiac-death-ireland
.
.
.

ARMAGH

John McCall, from Collone, near Armagh City, was an A-Level pupil at Armagh Royal School. He hoped to go on to study architecture at Queen’s University, Belfast.
Playing in the flanker position, he was one of the most promising young rugby players in Ireland. On St Patrick’s Day 2004 he captained his school to its first victory in the Ulster Senior Schools’ Cup in 27 years, and he was selected to play for Ireland in the World Under-19 Rugby Cup just over a week later. It was while playing in that competition that John met his tragic death.

Date of death: March 2004
Age at time of death: 18
Prior symptoms detected: None
Circumstances of death: John collapsed and died while playing for the Ireland under-19 team against New Zealand in Durban, South Africa
Diagnosed cause of death: Viral cardiomyopathy
Diagnosed cause of death: The post-mortem report said sudden arrhythmic death; it has since been found that Brughada Syndrome is in the family.

Catherine Hand, from Lurgan, was a sales assistant. She was very physically active, and took a lot of exercise.
Date of death: April 2004
Age at time of death: 20
Prior symptoms detected: Catherine had suffered a blackout and palpitations, but doctors did not seem to suspect a serious cardiac condition.
Circumstances of death: Catherine died in her sleep
Diagnosed cause of death: Cardiac Arrhythmia

Rory McGee, from Dorsey, was employed as an Engineer in FM Systems, Newry.
He was a former pupil of St Colman’s College, Newry College of Further Education and a graduate of University of Ulster Jordanstown. He was married to Sabrina, who gave birth to their baby daughter Gemma, just 8 weeks before his death. He was a founder member of Dorsey Emmet’s GAC in 2000, and worked as club secretary. He received the award for Club Person of the Year in 2002. Rory was a kind and loving person who was liked by everyone.
Date of death: March 2005
Age at time of death: 26
Prior symptoms detected: None
Circumstances of death: Rory died suddenly at home at around 11 pm
Diagnosed cause of death: (Awaiting Coroner’s report)

ANTRIM

Ciara Agnew, from Derriaghy, was a pupil at St Dominic’s High School, Belfast, and was one of five children. She was a normal fun-loving girl, who was full of life and always seemed healthy. She loved playing music and enjoyed swimming and netball at school.
Date of death: February 2002
Age at time of death: 14
Prior symptoms detected: None
Circumstances of death: Ciara was on the bus home from school, laughing and joking, when she collapsed on the seat suddenly and died.
Diagnosed cause of death: “unascertained”, but suspected sudden cardiac death

Nicholas Collins, from Ballinderry, near Lisburn, had just finished his GCSE examinations and started a Media Studies course at Belfast Institute of Further & Higher Education. He was very fit and played basketball for a club in Lisburn.
Date of death: November 1998
Age at time of death: 16
Prior symptoms detected: Seven weeks before he died, Nicholas developed a throat-cold and an irregular temperature, and was taken into hospital. It was then found that he had an endocarditis, possibly due to a viral infection. He got over this, but his condition caused an auto-immune reaction, from which he never improved.
Circumstances of death: Nicholas died in hospital
Diagnosed cause of death: Viral Endocarditis

DERRY

Aaron Lundy, from Portstewart, was a very talented all-round sportsman. He won the Irish Under-15 Championship trophy in golf and was selected to play for Ulster at 16. At 17 he won the Irish Daily Mail Championship and in the same year the British Daily Mail Boys’ Championship in the USA. He was then selected for the Irish national boys’ squad, playing off a scratch handicap. A very fit young man, he also enjoyed participating in basketball, cross-country running and football. Aaron’s father, John, is now the Northern Ireland representative of the CRY group.
Date of death: September 1999
Age at time of death: 19
Prior symptoms detected: Aaron was diagnosed as having Wolff Parkinson White syndrome a couple of years earlier but was told not to worry about it.
Circumstances of death: Aaron died two hours after a football game.
Diagnosed cause of death: Wolff Parkinson White syndrome

Marcella Doherty, from Bellaghy, worked as a hairdresser in her home village, and hoped to expand her business to include a beauty salon in the near future. She loved driving and had an ambition to buy a red Audi A4. She took a lot of exercise in the nine months before her death, and on one night a week before she experienced palpitations she completed 40 lengths of the swimming-pool.
Date of death: September 2005
Age at time of death: 24
Prior symptoms detected: None – a week before her death, Marcella collapsed and was taken to hospital. After some brief tests, she was discharged a short time later. Despite great anxiety over her racing heart and several frantic requests to be seen, she could not get a private appointment with a cardiologist that week.
Circumstances of death: Marcella died with a watch in her hand, taking her own pulse, on a Sunday, as she waited to go to the doctor the following morning to make an appointment to see a cardiologist.
Diagnosed cause of death: Arrhythmogenic Right Ventricular Cardiomyopathy / Dysplasia (ARVC/D)

DOWN

Mary Mooney, from Newry, had just completed Beauty Therapy examinations at Newry Institute of Further & Higher Education, and was about to embark on a course of Aromatherapy. She was naturally fit and liked to take exercise. Her family has set up Mary’s Trust in her memory, to provide life-saving equipment in the local area.
Date of death: February 2003
Age at time of death: 18
Circumstances of death: Mary was found dead in her bed in the morning, with her left hand up in the air, as if she had been trying to reach out. It was four years to the day that her father had died from a heart attack.
Prior symptoms detected: None – she had felt palpitations and shaking during the previous two years, and had lost weight, but no cardiac conditions had been detected.
Diagnosed cause of death: “sudden adult death syndrome”

DONEGAL

Paul Cavanagh, from Moville, was a fisherman, who spent long hours out at sea. He had a big interest in cars. He had also played Gaelic football and soccer for local teams, and golf in his spare time.
Date of death: May 2004
Age at time of death: 20
Prior symptoms detected: None (he had fallen out of his boat bunk-bed five months earlier, but all tests were inconclusive)
Circumstances of death: Paul was found dead in his bed one afternoon
Diagnosed cause of death: officially stated as “epileptic-type seizure, brought on by a chest infection”, but he had no history of epilepsy, and his death showed various characteristics of sudden cardiac death.

FERMANAGH

Richard Martin, from Cabra, near Irvinestown, was a pupil at Portora Royal School, Enniskillen. The youngest of four brothers, he was a model pupil, having got four As in his AS Level examinations, and he hoped to study Medicine at university. He was also an able sportsman, which he showed by earning his place on the school rugby first team within weeks of taking up the game. He was very active in various other activities, including those of the Boys’ Brigade, of which he was a member.
Date of death: November 2004
Age at time of death: 17
Prior symptoms detected: Doctors identified a congenital heart problem and advised Richard to give up rugby, which he did, just before the school team went on tour to Australia.
Circumstances of death: Richard collapsed while playing tennis, and died
Diagnosed cause of death: Wolff Parkinson White syndrome

MONAGHAN

Éamon McElroy, Monaghan, was a mechanic. He was married with three children, and he kept fit regularly.
Date of death: January 2005
Age at time of death: 41
Prior symptoms detected: none
Circumstances of death: Éamon collapsed and died while training.
Diagnosed cause of death: Hypertrophic cardiomyopathy

TYRONE

Lee Turkington, from Dungannon, was a pupil at Dungannon Royal School. Lee enjoyed playing Rugby at school level and enjoyed life. He had been diagnosed with Hypertrophic Cardiomyopathy after his mother, Dorothy, died of the same condition in 1982, at the age of 27. Dorothy also lost a brother in 1958 at age 16. He died while running up a hill, at the family farm in Stewartstown. His diagnosis only came to light when Dorothy died and both post-mortems where looked at. As a result of Dorothy’s death, it was found that several other members of the family had the same condition of Hypertrophic Cardiomyopathy.

Date of death: 1992
Age at time of death: 16
Prior symptoms detected: Lee had been diagnosed with the condition.
Circumstances of death: Lee collapsed and died in the school playground whilst chasing a ball.
Diagnosed cause of death: Hypertrophic Cardiomyopathy

Jonathan Scott, from Dungannon, was a production Manager with Moy Park. A close relative of the family of Lee Turkington, he had the same condition as his deceased relatives. He was engaged to be married and it was five weeks to his wedding when he died. He also had a daughter. He was always on the go and enjoyed life to the full, whether at work or in his family & social life. He competed at Rugby at school level, and enjoyed playing and watching football and was an avid Manchester United Fan.
Date of death: 2002
Age at time of death: 25
Prior symptoms detected: Jonathan had been diagnosed with Hypertrophic Cardiomyopathy and had an Implantable Defibrillator fitted to prevent sudden death.
Circumstances of death: Jonathan died whilst getting his implantable defibrillator replaced.
Diagnosed cause of death: Hypertrophic Cardiomyopathy

Gary Duffin, from Coalisland, was a joiner with a local construction firm. He was one of five children in the family, and he was engaged to be married in the summer. He played hurling for the Naomh Colmcille club, and also had a keen interest in football.
Date of death: March 2005
Age at time of death: 26
Prior symptoms detected: None – he had previously been found to have a racing heart while in hospital, but this was attributed to an accident.
Circumstances of death: He collapsed and died in his new house one evening while doing household chores.
Diagnosed cause of death: Brughada Syndrome

CONNACHT

LEITRIM

Gerard Gallagher, from Kiltyclogher, had just finished his final examinations at the Institute of Technology, Sligo. On the day that he died he had got the news that he had been appointed to a job in Dublin. He played Gaelic football for Glenfarne club, and soccer for Manorhamilton Rangers. He took part in athletics when he was younger, and was always quite fit.
Date of death: July 1999
Age at time of death: 25
Circumstances of death: Gerard collapsed and died during a Gaelic football league game.
Prior symptoms detected: None – but the post-mortem found that he had had a heart attack three weeks previously.
Diagnosed cause of death: A growth on the left ventricle of his heart – which he had had from the time of his birth.

MAYO

Robert Finnerty, from Ballintubber, Claremorris, had recently qualified as a carpenter and had just gone to London to work for the summer. He planned to go to Australia with friends in the autumn, and intended to undergo a course in the use of Automated External Defibrillator on his return. He qualified as a water safety instructor and went on to instruct kids to be lifeguards, He also taught as a swimming instructor with a local swimming club. He was very passionate about water-safety, and had a way with teaching it. It was something he did in his free time. He also played indoor soccer.
Date of death: June 2004
Age at time of death: 22
Prior symptoms detected: None – Robert had complained of chest pains just over six weeks earlier, and went to the doctor, but no cardiac condition was detected.
Circumstances of death: Robert was working on the building-site of an extension to a hospital in London. One morning he felt unwell at work, took a break, and was asked whether he would like some aspirin. He declined, saying that he would be okay, but moments later he collapsed and died. Within minutes efforts were made to revive him, but were unsuccessful.
Diagnosed cause of death: microcardial ischaemia, due to or as a consequence of arrhythmia

ROSCOMMON

Shane Kennedy, from Ballaghadereen, was a student of Information Technology at the National University of Ireland, Galway (formerly U.C.G.). He had just completed his first year on that course. He was a fit, healthy young man, who played golf and soccer occasionally, and won many medals for running in local Community Games when he was younger. He was also a big fan of Liverpool soccer team and loved listening to music.
Date of death: July 1998
Age at time of death: 20
Prior symptoms detected: None
Circumstances of death: Shane was helping to paint a room in his family home, and then went down to the kitchen, where he told his parents he felt dizzy. He sat down, but his head fell forward onto the table, and his father held him. A nurse and doctor were both on the scene within five minutes but they could not revive him.
Diagnosed cause of death: Myocarditis, most probably of viral origin – but no virus was isolated when tissue samples were sent to a virus reference laboratory.

LEINSTER

DUBLIN

Robbie Simpson, from Monkstown, was an Arts undergraduate at University College Dublin. The youngest of three brothers, he was an active, sports-loving young man, who especially enjoyed swimming, cycling and soccer, as well as socialising. Towards the end of his life he remained brave and optimistic in the face of grave illness. His family, his friends in conjunction with the Mater Hospital, has been inspired to inaugurate a trust in his name. The Robert Simpson Trust Fund will promote research into cardiomyopathy and related areas such as sudden cardiac death as well as providing life saving equipment, such as defibrillators for sports campuses / centres and colleges. One of the first AEDs the Trust provided was to Robbie’s former school – St. Andrew’s College, Booterstown. See www.robstrust.com
Date of death: May 2005
Age at time of death: 19
Prior symptoms detected: Robbie was detected as having a dilated (enlarged) heart, and he was the first person in Ireland to be given an artificial external heart-pump (funded by the Irish Transplants Patients Association).
Circumstances of death: Despite the support of his family, and the innovative and expert care of the Mater Misericordiae University Hospital in Dublin, Robbie died in hospital, where he had spent his last 8 weeks.
Diagnosed cause of death: Robbie died from the above condition – dilated cardiomyopathy – which was a genetic condition in his family.

Darius Vasseghi, Dublin, was a student of Electronic Engineering at University College Dublin. Having lived previously in Iran and France, he was a person of diverse cultural influences and was fluent in six languages. He was a champion fencer and was national champion in both countries several times, representing them in many international competitions, including two world championships. On his death he was captain of UCD team and member of the Irish squad. He was also an accomplished clarinet player, a woodwork marquetry master, computer expert and tennis player. Since Darius’ death, his mother, Mary, has been one of the main founders of the Irish Sudden Cardiac Death (in the young) Support Group.
Date of death: 30 May 2005
Age at time of death: 18
Prior symptoms detected: (Only tiredness on effort as a child.)
Circumstances of death: Darius collapsed and died on his bathroom floor one morning
Diagnosed cause of death: Aorta Hypoplasia (narrowing of the aorta) and left ventricular hypertrophy

Conor Martin, from Rialto, was a pupil completing his transition year at De La Salle School, Churchtown. He was an only child. A tall, well-built boy, he played rugby for his school and for the DLSP club, and was rarely ill. He was always smiling and cheerful. He was very interested in all kinds of music, from Luke Kelly to 2Pac. On the night prior to his death he had attended a school graduation ceremony.
Date of death: June 2005
Age at time of death: 16
Prior symptoms detected: None – he had once complained of feeling dizzy, but his family could only think that this was a flu symptom.
Circumstances of death: Conor died in his bedroom at about 10.30 a.m., soon after he had woken.
Diagnosed cause of death: “Sudden Adult Death Syndrome”

Cliona Murphy, from Raheny, worked as a personal assistant with a leading bank in the Irish Financial Services Centre. From an early age she was very sporty, taking part in school hockey, tennis and swimming. At 18 ‘wanderlust’ took her to the USA. She worked in Washington D.C. and California, and lived in New York City for several years. During a year’s stay in New Zealand and Australia her ambition led her to take up competitive sailing, and she excelled, qualifying for the Sydney to Hobart yacht-race in 1992. On her return to Ireland she joined Howth Yacht Club and raced in the Squib class. Cliona’s dream came true when she was invited onto the all-women’s crew in the ‘Around Ireland’ race 1993. She was very popular and a loyal friend to many. The Cardiomyopathy Support Group was founded in her memory.
Date of death: June 1995
Age at time of death: 30
Prior symptoms detected: None
Circumstances of death: Cliona collapsed and died outside of her workplace on a warm afternoon.
Diagnosed cause of death: Hypertrophic Cardiomyopathy

Paul Stewart, Dublin, was the branch manager of a leading jewellery store in the city centre. He had previously worked in the management teams of various retail stores, and quickly gained respect as a competent leader and was equally well respected in his personal life. He was a young man with a passion for life. Having recently got married Paul decided to get in shape! He enjoyed meeting up with friends on a weekly basis to play a game of football. He was a keen supporter of Arsenal and Celtic and loved music. Since Paul’s death, his family and friends have been actively raising funds to purchase defibrillators for sports halls, football clubs, etc.
Date of death: September 2004
Age at time of death: 30
Prior symptoms detected: None
Circumstances of death: Paul collapsed and died suddenly while playing a game of football with friends.
Diagnosed cause of death: No anatomical cause of death established. Death Certificate states Sudden Adult Death Syndrome.

Lisa Murphy, from Ayrfield, worked as a dental nurse. She was the eldest of four children, and had a baby girl Chloe. Lisa was ostensibly healthy and fit and really enjoyed life; she was always making plans for nights out, foreign holidays, etc.
Date of death: January 2004
Age at time of death: 26
Prior symptoms detected: None
Circumstances of death: Lisa was out dancing one night when she fell. She had no pulse and efforts to revive her proved unsuccessful.
Diagnosed cause of death: “No anatomical cause found. Probably Arrhythmia.”

KILKENNY

Hugh Williams, from Gowran, had recently graduated from Dundee University, and was working as an architect in Dublin. The youngest of three children, he liked to keep fit by swimming, working out, playing tag rugby for the Tag Barbarians team and walking (he did a 50-mile hike in Scotland), although he was not involved in serious competitive sport. He and two friends were in the process of buying an old farmhouse in Co. Carlow, to renovate to his completed designs. This house was subsequently purchased and the renovations will be complete by September 2006.
Date of death: June 2005
Age at time of death: 23
Prior symptoms detected: None – he had fainted once three years previously and experienced a dizzy spell two months before he died, but had not reported these to a doctor or to his family.
Circumstances of death: Hugh collapsed and died on the sideline having played for just ten minutes in a tag rugby game.
Diagnosed cause of death: Cardiomyopathy

LAOIS

Brian Bergin, from Ballybrophy, Borris-in-Ossory, worked in construction, doing building and chimney repair work. He was one of a family of seven children, and was married in June 2001, one year prior to his death.
A very fit and competent hurler, he played for the Kilcotton club and was once on the Laois senior county hurling panel. He also played golf.
Date of death: June 2002
Age at time of death: 34
Prior symptoms detected: None
Circumstances of death: Brian was jogging on the local hurling field when he collapsed and died.
Diagnosed cause of death: Hypertrophic cardiomyopathy

LOUTH

Gerard Leddy, from Collon, was a manager of a dairy farm, and was about to travel to England for a change of employment. It is possible that his family has had a possible history of conditions which cause sudden cardiac death.
Date of death: October 1990
Age at time of death: 21
Prior symptoms detected: None
Circumstances of death: Gerard was found lying across his bed in the evening, having gone to bed early.
Diagnosed cause of death: (inconclusive – suspected arrhythmia)

Peter Brennan, from Dunleer, was a farmer and a very accomplished athlete. He won all-Ireland medals with Dunleer AC in Shot-Putt, Discus-Throwing, Hammer-Throwing competitions.
Date of death: July 1985
Age at time of death: 37
Prior symptoms detected: He had felt light pains in his chest, but had not been diagnosed with a heart condition.
Circumstances of death: Peter died suddenly while training with Dunleer AC between 7.30-8.00 p.m.
Diagnosed cause of death: Heart Attack

OFFALY

Cormac Devine, from Shannonbridge, was a pupil at Garbally College, Ballinasloe. He was a talented and very fit sportsman. He was a member of the college’s senior schoolboy rugby squad, played Gaelic football for the Shannonbridge club, and also played golf and badminton. He was well loved by everyone who knew him.
Date of death: January 1998
Age at time of death: 16
Prior symptoms detected: none
Circumstances of death: Cormac collapsed and died during rugby training at school.
Diagnosed cause of death: Hypertrophic Cardiomyopathy

WEXFORD

Noel Quill came from Johnstown, Castlebridge, near Wexford. He was the eldest of a family of four children, and he played Gaelic football for the local Shelmalier club. He had just got his Degree in Business Studies from Waterford Institute of Technology, and he was on the verge of many exciting things when he died. He commenced his first full time job the previous Monday with American company PFPC International in Drinagh, Wexford. He booked a holiday to Florida with a group of friends on Thursday, and bought a car on Friday evening. He was to be groomsman at his uncles wedding on Saturday - the day that he died.
Date of death: 17 July 2004
Age at time of death: 22
Prior symptoms detected: None
Circumstances of death: Noel died in his sleep. On the previous evening he complained of feeling dizzy during a game of Gaelic football for his club and was substituted.
Diagnosed cause of death: Sudden Adult Death Syndrome in the absence of any positive cause.

Nicola Ryan, from Ardross, New Ross, was a pupil at St Mary’s Secondary School, New Ross. The second eldest of four children, she was a fit, healthy, beautiful young girl. She loved to play basketball and to swim, and she had never been seriously ill in her life.
Date of death: June 2002
Age at time of death: 14
Prior symptoms detected: None
Circumstances of death: Nicola died as she lay on the sofa one evening, at approximately 6.40 p.m. She was found by her older sister and all efforts to resuscitate her failed.
Diagnosed cause of death: “Sudden Adult Death Syndrome”

WICKLOW

Darragh Kelly, from Greystones, was a student embarking on a Construction Engineering course at Dundalk Institute of Technology, having returned some months previously from travelling abroad. He was the eldest and only boy of four children in his family. He participated in a wide range of sports – he played soccer for Greystones and later Kilcoole; he excelled in Gaelic football and rugby at St. David’s Secondary School in Greystones, travelling to a schools international rugby tournament in Italy in 1999. He was also proficient at both swimming and sprinting.
Date of death: 1 October 2003
Age at time of death: 21
Prior symptoms detected: None
Circumstances of death: Darragh collapsed and died in his room at about 8.30 in the evening. He was found by a housemate just 20 minutes after he had been speaking to his mother on the phone and told her that he felt a lot better, having followed her advice to stay in bed, take paracetamol and plenty of fluids. He had experienced flu-like symptoms for two days prior to his death; on the day he died he had complained of heart palpitations, but felt a lot better having slept. Darragh was getting dressed and collapsed onto the floor beside his bed.
Diagnosed cause of death: “sudden unexplained death in an adult”

Richie Doyle, from Bray, was a sales rep. and a graduate of Dublin Institute of Technology. He was 6 feet 6 inches tall, and kept very fit – he was a very keen soccer player, he jogged and walked the dog regularly, and he was very careful about what he ate. Since his death his family has raised funds for the purchase and distribution of 14 defibrillators for local sports clubs and secondary schools.
Date of death: April 2005
Age at time of death: 27
Prior symptoms detected: None
Circumstances of death: Richie collapsed and died just after he had finished playing in a soccer match.
Diagnosed cause of death: Probably myocarditis

MUNSTER

CLARE

Kevin Quinn, from Glanworth, was an apprentice plumber. He was a very promising hurler for the Harbour Rovers club, and he also played football. He was always very fit and strong, and rarely sick in any way.
Date of death: August 2004
Age at time of death: 18
Prior symptoms detected: None – he did not have an abnormal heart condition.
Circumstances of death: Kevin collapsed clutching his chest just four minutes into a hurling game in which he was playing, and died then.
Diagnosed cause of death: Commotio cordis – a blow to the chest from the camán (hurling stick) caused sudden cardiac arrest.

Emmet Neville, from Cork City, was a store-manager at the ESB. He was a star in a range of sports. In hurling he captained the Glen Rovers under-21 team; in Gaelic football he captained St. Nicholas’ under-21 team; and in basketball he was a key member of the Neptune club, having won international caps for Ireland at youth level.
He was committed to training and consequently very fit.
Date of death: January 2003
Age at time of death: 21
Prior symptoms detected: None
Circumstances of death: Emmet fell from his bed at 5.00 a.m. and was heard by his sister, who found him dead. He had been making an apparent choking noise and looked as if he had been trying to get up.
Diagnosed cause of death: It was officially reported as “possible epilepsy”, but no inquest was heard, and the family believes that it was a sudden cardiac death, given the circumstances and with the first post-mortem report finding no obvious cause of death on the exterior.

CLARE

Robert Manning, from Cratloe, was a secondary school pupil. The eldest of three boys, he was full of enthusiasm for life in a quiet, unassuming way. He was 6’3” in height and was supposedly very healthy. He was an avid oarsman and also loved karate and rugby. His friends looked up to him as he could defuse any tricky situation or pass a funny “tongue-in-cheek” comment which people found endearing. In his memory, a friend released a tribute single ‘Re-Unite’ for the Robert Manning Fund, which was donated to CROI (the West of Ireland Cardiology Foundation).
Date of death: August 2002
Age at time of death: 16
Prior symptoms detected: None
Circumstances of death: Robert was playing rugby with his family in the back garden. As he went to retrieve the ball he said “Oh no” and lay down on the grass. His family tried to revive him using CPR but to no avail.
Diagnosed cause of death: Because all of Robert’s organs were undamaged, no cause of death was found, leading to a diagnosis of SADS.

Catherine Keane, from Lisheenfurror, Kilkee, was a pupil in fifth class at Carrigaholt National School. She enjoyed football, swimming and hurling, but the love of her life was horse-riding. From a family of two children, she was a very hard-working, diligent little girl, who was great company and always eager to please people.
Date of death: November 2003
Age at time of death: 10
Prior symptoms detected: Just over a year prior to her death, Catherine fainted and she was referred to hospital by her doctor who had detected tachycardia. The appropriate tests to detect cardiac condition were not carried out at hospital.
Circumstances of death: Catherine was at her riding school when she slumped on her pony, and despite efforts by her father and riding instructors to administer CPR, she could not be revived.
Diagnosed cause of death: The post-mortem reported that she had a massive brain seizure, but the results of an inquest are still awaited, and family investigations indicate that the cause of death was cardiac.

KERRY

Miriam O’Sullivan, from Firies, worked as a marketing manager in the Gleneagle Hotel in Killarney. The youngest of three children, she was engaged to be married in June 2004. She was very active generally and apparently very fit; at the time she died she was taking swimming lessons and building a house. She was also very helpful and wise beyond her years.
Date of death: November 2003
Age at time of death: 26
Prior symptoms detected: She used to feel palpitations occasionally during exertion, and in August 2003 she went for a minor operation to burn off tissue that was blocking the flow of blood. At a check-up three months later she was given an all-clear.
Circumstances of death: Miriam felt dizzy at work and immediately fell sideways. She was caught by a colleague and a call for help was made. Ambulance personnel and a doctor were there immediately but efforts to revive her were unsuccessful.
Diagnosed cause of death: Viral infection of the heart

LIMERICK

Jamie Curtin, from Limerick City, worked with horses. He was a very laid-back person, who although not athletic, was apparently healthy and had never spent time in hospital since birth. He loved horses and motorbikes, and was just ten days short of his 16th birthday when he died.
Date of death: December 2004
Age at time of death: 15
Prior symptoms: None
Circumstances of death: Jamie collapsed while doing light work in the stables, tending horses. His friend thought he had fainted, and brought him to the hospital where Jamie was pronounced dead.
Diagnosed cause of death: “SADS”

Ross Cooney, from Limerick, was a first-year Business Studies student at the University of Limerick. Ross was an only son, with one younger sister. He was a young man of many talents: he was a skilful debater, a qualified lifeguard, and a holder of a Chief Scout Award, and standing 6’4” tall he was a promising athlete. He is equally remembered as a lovable character, with a bright and bubbly personality and a high regard for others. Ross’s life was cut short while representing his university at the National Basketball Arena in Tallaght, in an intervarsities tournament. He died suddenly on court when the team had just started a match.
Date of death: November 1999
Age at time of death: 18
Prior symptoms detected: none
Diagnosed cause of death: Sudden Adult Death Syndrome (unexplained).

WATERFORD

Kieran Clancy, from Ballysaggart, Lios Mór, was a self-employed carpenter by trade and also a part-time farmer. He was married to Úna. He is described by his family as “the picture of health and as strong a man as you could ever meet”. He was a committed member of the Ballysaggart GAA club and played for the club hurling team at full-back, the position in which he played on the night he died.
Date of death: April 2003
Age at time of death: 31
Prior symptoms detected: None
Circumstances of death: Kieran felt a pain during a hurling game and had to go off the field. He had died by the time he got to hospital.
Diagnosed cause of death: Kieran died due to what was described as a ‘congenitally weak aorta’. Despite his apparent strength and sturdy physique, the aorta, which was tissue-like in structure, was simply not sturdy enough and unravelled to ultimately result in Kieran’s demise.

http://www.TheCormacTrust.cOM/sudden-cardiac-death-ireland

SWEET RELIEF ... SWEET DREAMS

REFERENCES ...

'non-diabetic adults are more affected by HYPOglycemia than people
with type 1 diabetes'
www.ncbi.nlm.nih.gov/pubmed/18709352

__________________________

'potential role of defibrillator associated stresses in distress
induced cardiac death'
www.ncbi.nlm.nih.gov/pubmed/18827773

__________________________

'fibrillation cured by glucose/dextrose'
www.NicholasDynesGracey.blogspot.cOM/2008/06/fibrillation.html

__________________________

Anaesth Intensive Care. 2000 Dec;28(6):698-700.Links

Ventricular arrhythmias associated with HYPOglycemia.

Chelliah YR.

Department of Anaesthesiology, Tan Tock Seng Hospital, Jalan Tan Tock
Seng, Singapore.

HYPOglycemia commonly manifests as increased sympathetic discharge or
as neuroglycopenia in the awake patient. This case may represent an
example of the effect of HYPOglycemia on the heart giving rise to
ventricular tachycardia, which promptly resolved at the time of
correction of HYPOglycemia.

www.ncbi.nlm.nih.gov/pubmed/11153301

_________________________

Afr J Med Med Sci. 2008 Jun;37(2):161-3.

HYPOglycemia as a possible cause of transient ischaemic attack in a
Patient with multiple vascular risk factors.

Okeahialam BN.

Department of Medicine, Jos University Teaching Hospital, Jos, Plateau
State, Nigeria. basokeam@yahoo.com

An elderly, fibrillating, diabetic hypertensive Patient in heart
failure is at risk of stroke from all her cardiovascular morbidities.
When such a Patient presents with stroke, it is usually difficult to
squarely incriminate one. Consequently, precious time is lost while
care Givers conduct expensive investigations to make a definitive
diagnosis. This case report is on one such Patient, in whom
HYPOglycemia was a plausible cause. Treatment resulted in dramatic
recovery. Had neurological complication of drug induced HYPOglycemia
not been suspected, the hemiplegia might have become permanent; and
any of her risk factors given as a rational explanation. Therefore
when a Diabetic on treatment presents with stroke, care givers should
perform immediate blood glucose test to exclude HYPOglycemia; not
withstanding the existence of other risk factors.

www.ncbi.nlm.nih.gov/pubmed/18939400

_________________________

Eur Heart J. 2008 Jan;29(2):166-76. Epub 2007 Dec 21. Links
Comment in: Eur Heart J. 2008 Aug;29(16):2058; author reply 2058-9.
Eur Heart J. 2008 Jan;29(2):141-3.

The impact of glucose lowering treatment on long-term prognosis in
patients with type 2 diabetes and myocardial infarction: a report from
the DIGAMI 2 trial.

Mellbin LG, Malmberg K, Norhammar A, Wedel H, Rydén L; DIGAMI 2 Investigators.

Cardiology Unit, Department of Medicine, Karolinska Institutet,
Stockholm, Sweden.

AIMS: To explore the impact of glucose lowering treatment on prognosis
in diabetic Patients with myocardial infarction. METHODS AND RESULTS:
1181 type 2 diabetic Patients (mean age 68 years; 67% males)
discharged after myocardial infarction were followed (median of 2.1
years). At discharge, 436 Patients (37%) had oral glucose lowering
agents whereof 268 sulphonylureas and 200 metformin, while 690
Patients (58%) were on insulin. The impact of treatment was analysed
by an updated Cox proportional hazards regression model, correcting
for confounders. Cardiovascular mortality was not influenced by
metformin [Hazard ratio (HR) 0.93, 95% CI 0.60-1.43; P = 0.73],
sulphonylureas (HR 1.15, 95% CI 0.80-1.64; P = 0.45), or insulin (HR
1.05, 95% CI 0.75-1.46; P = 0.77). The risk for non-fatal myocardial
infarction and stroke increased significantly in patients on insulin
(HR 1.73, 95% CI 1.26-2.37; P = 0.0007), whereas this risk was lower
among those on metformin (HR 0.63, CI 0.42-0.95; P = 0.03) and
unchanged with sulphonylureas (HR 0.81, 95% CI 0.57-1.14; P = 0.23).
This finding remained analysing only patients with newly instituted
insulin and those randomly allocated to newly instituted insulin.
CONCLUSION: Controlling for confounders including glycemic control,
there was no significant difference in mortality between
sulphonylureas, metformin, and insulin. In this post hoc analysis, the
risk of non-fatal myocardial infarction and stroke increased
significantly by insulin treatment while metformin was protective. It
is emphasized that this observation is done in an epidemiological
analysis and should encourage to further confirmation in randomized
trials.

www.ncbi.nlm.nih.gov/pubmed/18156614

_________________________

Europace. 2008 Nov 6. [Epub ahead of print]

Endurance sport practice as a risk factor for atrial fibrillation and
atrial flutter.

Mont L, Elosua R, Brugada J.

1Thorax Institute, Hospital Clínic, University of Barcelona, Institut
d'Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Villarroel 170,
Barcelona 08036, Catalonia, Spain.

Although the benefits of regular exercise in controlling
cardiovascular risk factors have been extensively proven, little is
known about the long-term cardiovascular effects of regular and
extreme endurance sport practice, such as jogging, cycling, rowing,
swimming, etc. Recent data from a small series suggest a relationship
between regular, long-term endurance sport practice and atrial
fibrillation (AF) and flutter. Reported case control studies included
less than 300 athletes, with mean age between 40 and 50. Most series
recruited only male patients, or more than 70% males, who had been
involved in intense training for many years. Endurance sport practice
increases between 2 and 10 times the probability of suffering AF,
after adjusting for other risk factors. The possible mechanisms
explaining the association remain speculative. Atrial ectopic beats,
inflammatory changes, and atrial size have been suggested. Some of the
published studies found that atrial size was larger in athletes than
in controls, and this was a predictor for AF. It has also been shown
that the left atrium may be enlarged in as many as 20% of competitive
athletes. Other proposed mechanisms are increased vagal tone and
bradycardia, affecting the atrial refractory period; however, this may
facilitate rather than cause the arrhythmia. In summary, recent data
suggest an association between endurance sport practice and atrial
fibrillation and flutter. The underlying mechanism explaining this
association is unclear, although structural atrial changes (dilatation
and fibrosis) are probably present. Larger longitudinal studies and
mechanistic studies are needed to further characterize the association
to clarify whether a threshold limit for the intensity and duration of
physical activity may prevent AF, without limiting the cardiovascular
benefits of exercise.

www.ncbi.nlm.nih.gov/pubmed/18988654

_________________________

JEMS. 2002 Nov;27(11):54-60.

"... Key role of glucose in 'coma cocktails' ... Using science to
dispel myths & improve patient care ..."

Bledsoe BE. bbledsoe@earthlink.net

"... EMS (emergency medical services) has evolved to a point where any
EMS provider should be able to reasonably determine the most likely
cause of coma, or, in a worst-case scenario, narrow the cause to but a
few possibilities. Certainly, patients with bona fide HYPOglycemia
should receive IV glucose. Because the consequences of prolonged
HYPOglycemia are severe, if there's a doubt about whether HYPOglycemia
is present, then glucose should be empirically administered ..."

www.ncbi.nlm.nih.gov/pubmed/12483195

_________________________

Anaesth Intensive Care. 2000 Dec;28(6):698-700.Links

Ventricular arrhythmias associated with HYPOglycemia.

Chelliah YR.

Department of Anaesthesiology, Tan Tock Seng Hospital, Jalan Tan Tock
Seng, Singapore.

HYPOglycemia commonly manifests as increased sympathetic discharge or
as neuroglycopenia in the awake patient. This case may represent an
example of the effect of HYPOglycemia on the heart giving rise to
ventricular tachycardia, which promptly resolved at the time of
correction of HYPOglycemia.

www.ncbi.nlm.nih.gov/pubmed/11153301

_________________________

J Assoc Physicians India. 1992 Oct;40(10):701.Links

Ventricular fibrillation with HYPOglycemia.

Sharma SN.

Cardiologist Institute of Aerospace Medicine, IAF Bangalore.

www.ncbi.nlm.nih.gov/pubmed/1307366

_________________________

Am J Med Sci. 1975 May-Jun;269(3):403-8.

'... HYPOglycemia induced ventricular tachycardia abolished by glucose
infusion ...'

Miley GB, Binnick SA, Block PJ.

We report the first case of adenocarcinoma of the stomach associated
with severe HYPOglycemia. Accompanying the profound HYPOglycemia, as
low as 5 mg per cent by the orthotoluidine method, were multiple
episodes of ventricular tachycardia which were abolished by glucose
infusion. Following surgical excision of a hemorrhagic portion of the
tumor, normoglycemia levels were achieved and ventricular irritability
was no longer present. The possible mechanisms of HYPOglycemia in
extrapancreatic tumors are discussed as well as a mechanism for
HYPOglycemic-induced ventricular tachycardia. It is postulated that
hemorrhage of a necrotic tumor may release large amounts of an
insulin-like substance and cause HYPOglycemic coma.

www.ncbi.nlm.nih.gov/pubmed/1155497

_________________________

Eur J Emerg Med. 2003 Dec;10(4):331-3. Links

Bradycardia related to HYPOglycemia.

Navarro-Gutiérrez S, González-Martínez F, Fernández-Pérez MT,
García-Moreno MT, Ballester-Vidal MR, Pulido-Morillo FJ.

Department of Emergency Medicine, Hospital Virgen de la Luz, Cuenca,
Spain. sergionavarrog@hotmail.com

Alterations in blood glucose levels are known to be involved in
electrocardiogram changes. Various types of arrhythmias have been
reported. We present here the case of an 81-year-old woman presenting
with transient atrial fibrillation while being treated for
hypoglycaemia with dextrose infusion, and finally developing a sinus
rhythm. The presence of alterations in glucose blood levels should
always be considered as a potential cause of transient atrial
fibrillation.

www.ncbi.nlm.nih.gov/pubmed/14676515

_________________________

EG page 77 of 86 ... if
plasma blood glucose sub 5.5mmol/l can contribute to
'fainting/seizure/coma', as suggested by the FMCSA, then why the lack
of attention to seeing that levels above 5.5mmol/l are maintained in
'emergency situations' associated with 'fainting/seizure/coma'?
.
www.FMCSA.dot.gov/documents/diabetesrpt.pdf
.
Plasma blood glucose = sub 100mg/dL = sub 5.5mmol/l = potential loss
of 'self-control' aka NO safe 'DRIVING' of your car / vehicle =
potential negative physiological consequences upon the Human body
including "... myocardial and cerebral ischaemia and occasionally
infarction
..." ...
.
www.ncbi.nlm.nih.gov/pubmed/18461635
.
www.en.wikipedia.org/wiki/Differential_diagnosis

_________________________

TSG = Transient Supernormal Glycemia ... Why ZERO symptoms following 100% blockage occlusion of coronary artery [0:32 to 0:55 mins] ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Thu, 10 Jul 2008 16:28:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

Ann Med. 2008 May 16:1-7. [Epub ahead of print]

Acute HYPERglycemia [TRANSIENT SUPERNORMAL GLYCEMIA (TSG)] induces a HEALTHY IMMUNE response in young HUMANS withOUT ... 'GM-INSULIN-TREATED diabetes' ...

Gordin D, Forsblom C, Ronnback M, Parkkonen M, Waden J, Hietala K, Groop PH.

Folkhalsan Institute of Genetics, Folkhalsan Research Center, Biomedicum Helsinki, Finland.

Background. Patients with GM INSULIN TREATED [GIT] diabetes are at a substantially increased risk of cardiovascular disease FOR SOME SPECIFIC REASON ...

Stress-induced HYPERglycemia, in turn, ALLEGEDLY APPEARS TO SHOW AN ALLEGED worsenING OF the prognosis of Patients suffering from an acute myocardial infarction [AKA FUEL-ANEMIA STARVATION OF HEART MUSCLE] ?

However, the mechanisms behind these APPARENT findings are ALLEGEDLY incompletely known.

Aim. To investigate whether markers of chronic [MONOTONOUS] inflammation, and oxidative stress respond to acute [SHORT TERM] HYPERglycemia in patients with GM INSULIN TREATED [GIT] diabetes.

Methods. The plasma glucose concentration was rapidly raised from 5 mmol/L [90MG/DL] to 15 mmol/L [270MG/DL] in 35 Males ...

22 Men with GM INSULIN TREATED [GIT] diabetes ...
and
13 age-matched non-Diabetic Volunteers ... and maintained AS TRANSIENT SUPERNORMAL GLYCEMIA [TSG] for 2 HOURS.

All Participants were young non-Smokers without any signs of diabetic or other complications.

Markers of chronic [MONOTONOUS] inflammation, and oxidative stress were analysed in serum/plasma samples drawn at base-line and after 120 min of HYPERglycemia.

Results. Compared to NORMOglycemia, acute HYPERglycemia increased the interleukin (IL)-6 concentrations by 39% in Patients with GM INSULIN TREATED [GIT] diabetes (P<0.01)

During HYPERglycemia the PROFOUNDLY BENEFICIAL superoxide dismutase [SOD] concentration was increased by ...

17% in the HUMAN Volunteers (P<0.01)

5% in the Patients with GM INSULIN TREATED [GIT] diabetes (P=NS)

The increase in tumour necrosis factor (TNF)- was larger in Patients with GM INSULIN TREATED [GIT] diabetes than in non-Diabetic volunteers (35% versus -10%, P<0.05).

Conclusions... This study shows that acute HYPERglycemia induces a HEALTHY IMMUNE response in HEALTHY HUMANS FREE FROM A GM INSULIN TREATMENT [GIT] ... THAT IS ALLEGEDLY FOR DiabetIC HEALTH PURPOSES.

Keywords: Acute HYPERglycemia; cardiovascular disease; inflammation; macrovascular disease; oxidative stress; GM INSULIN TREATMENT [GIT] diabetes

http://www.InformaWorld.cOM/smpp/content~db=all~content=a793151240

Acute hyperglycemia disturbs cardiac repolarization in Type 1 diabetes. [Diabet Med. 2008]
Acute hyperglycemia rapidly increases arterial stiffness in young patients with type 1 diabetes. [Diabetologia. 2007]
Effect of acute hyperglycemia on selected plasma and urinary cytokine antagonists in Type 1 diabetes mellitus. [Diabetologia. 2003]
The effects of insulin and short-term hyperglycemia on myocardial blood flow in young men with uncomplicated Type I diabetes. [Diabetologia. 2002]
Effects of S21403 (mitiglinide) on postprandial generation of oxidative stress and inflammation in type 2 diabetic patients. [Diabetologia. 2005]
» See all Related Articles...

History of wound care AND HYPERGLYCEMIA LIKE HEALING VIA HONEY [AND SUGAR WORKS JUST AS WELL] ...

The history of wound care spans from prehistory to modern medicine. As wounds naturally heal by themselves, regardless of whether recovery from the scar or recovery from lost body tissue was a possibility, hunter-gatherers would have noticed several factors and certain herbal remedies would speed up or assist the process, especially if it was grievous. In ancient history, this was followed by the realisation of the necessity of hygiene and the halting of bleeding, where wound dressing techniques and surgery developed. Eventually the germ theory of disease also assisted in improving wound care.

Ancient medical practice

The treatment of acute and chronic wounds is an ancient area of specialization in medical practice, with a long and eventful clinical history that traces its origins to ancient Egypt and Greece. The Papyrus of Ebers, circa 1500 BC, details the use of lint, animal grease, and honey as topical treatments for wounds. The lint provided a fibrous base that promoted wound site closure, the animal grease provided a barrier to environmental pathogens, and the honey served as an antibiotic agent. The Egyptians believed that closing a wound preserved the soul and prevented the exposure of the spirit to "infernal beings," as was noted in the Berlin papyrus. The Greeks, who had a similar perspective on the importance of wound closure, were the first to differentiate between acute and chronic wounds, calling them "fresh" and "non-healing", respectively. Galen of Pergamum, a Greek surgeon who served Roman gladiators circa 120-201 A.D., made many contributions to the field of wound care. The most important was the acknowledgment of the importance of maintaining wound-site moisture to ensure successful closure of the wound. There were limited advances that continued throughout the Middle Ages and the Renaissance, but the most profound advances, both technological and clinical, came with the development of microbiology and cellular pathology in the 19th century.

Honey [AKA CONCENTRATED HYDRATED LIQUID SUGAR] ...

Honey’s antibacterial properties help promote healing infected wounds.^[1] Honey used as an topical ointment.

19th century

The first advances in wound care in this era began with the work of Ignaz Philipp Semmelweis, a Hungarian obstetrician who developed sterile surgical procedures, and Louis Pasteur, a French scientist known as the "father of microbiology" for his germ theory of disease. Semmelweis's work was furthered by an English surgeon, Joseph Lister, who began treating his surgical gauze with carbolic acid, known today as phenol, and subsequently dropped his surgical team's mortality rate by 45%. Building on the success of Lister's pretreated surgical gauze, Robert Wood Johnson, co-founder of Johnson & Johnson, began producing gauze and wound dressings treated with iodine. These innovations in wound-site dressings marked the first major steps forward in the field since the advances of the Egyptians and Greeks centuries earlier. The next advances would arise from the development of polymer synthetics for wound dressings and the "rediscovery" of moist wound-site care protocols in the mid 20th century.

Wound-site dressing

1950s onward

With advancements in material and tissue sciences, the field of wound-site dressings increased considerably. The ability to bolster wound-site re-epithelialization has been improved as well as improving their clinical efficacy. With the advent of fibrous synthetics of nylon, polyethylene, polypropylene, and polyvinyls in the 1950s, researchers and doctors in the field of wound care are able to significantly accelerate the natural wound healing process. Following the research and articles of George Winter and Howard Maibach in the 1960s, testing the efficacy of synthetic "wet" polymer wound dressings, the 1970s and 1980s represented the dawn of modern wound care treatment. In the 1990s, improvements in composite and hybrid polymers expanded the number of available materials for wound dressings. These improvements, coupled with the developments in tissue engineering, have given rise to a new class of wound dressings called "living skin equivalents." Often cited as a misnomer because they lack key components of whole living skin, "living skin equivalents" represent the future of wound dressings and possess the potential to serve as cellular platforms for the release of growth factors essential for proper wound healing. Other new developments have been focusing on handling patients concerns. Affected individuals often report pain as dominant in their lives^[2] and the pain associated with chronic wounds should be handled as one of the main management priorities. Symptomatic treatment of pain as part of patient centered concerns must go hand-in-hand with treating the underlying etiology or cause of the wound.

References

^ Peter Charles Molan (2001). "Honey as a topical antibacterial agent for treatment of infected wounds". Nurs Times 49 (7-8): 96.
^ Krasner, D. 1998. Painful venous ulcers: themes and stories about living with the pain and suffering. Journal of Wound, Ostomy, and Continence Nursing, Volume 25, Issue 3, Pages 158-168. Accessed January 1, 2007.

Sources

Ovington, L. G. (2002). "The evolution of wound management: ancient origins and advances of the past 20 years." Home Healthcare Nurse. 20, p 652-656.
Sipos, P., Gyory, H., Hagymasi, K., Ondrejka, P., and Blazovics, A. (2004). "Special wound healing methods used in ancient Egypt and the mythological background." World Journal of Surgery. 28, 211-216

External links

Long-chain fatty acids (LCFA) are the major
oxidation fuel of the healthy heart in vivo and in vitro,
while carbohydrates, especially lactate and glucose,
provide the remaining energy source (Neely et al. 1969,
Simonsen and Kjekshus 1978, Stanley et al. 1997).
However, heart metabolism can rapidly adapt to changes
in fuel-type availability. For example, the heart shifts to
preferential utilization of glucose when the arterial
concentration of free fatty acids falls below 0.3 mmol/l
(Nuutila et al. 1994).
A few studies analyzed the role of fuel-type
utilized by vascular tissues. It has been reported that
endothelial cells can use both glucose and fatty acids as
fuel-type substrate, and that they utilize triglycerides as
alternative fuel during glucose deprivation aka Relative-HYPOglycemai-distress (Culic et al.1999).

SOD = SuperOxide Dismutase

noreply@blogger.com (Nicholas Dynes Gracey) — Wed, 09 Jul 2008 14:15:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

Am J Hypertens. 2008 Jun;21(6):708-14. Epub 2008 Apr 10. Links

Hepatic effects of a fructose diet in the stroke-prone spontaneously HYPERtensive rat.

Brosnan MJ, Carkner RD.

Center for Metabolic Disease, Ordway Research Institute, Albany, New York, USA.

jbrosnan@ordwayresearch.org

BACKGROUND: Feeding stroke-prone spontaneously hypertensive rats (SHRSP) a diet rich in fructose results in a profound glucose intolerance not observed in the normotensive Wistar Kyoto (WKY) strain.

The aim of this study was to investigate the role of the liver in the underlying mechanisms in the SHRSP.

METHODS: SHRSP and WKY rats were fed either 60% fructose or regular chow for 2 weeks with blood pressure being measured using tail-cuff plethysmography and radiotelemetry.

Intraperitoneal glucose tolerance tests were performed and livers harvested for analysis of expression of inflammatory mediators and antioxidant proteins by western blotting and quantitative reverse transcriptase-PCR.

The serum triglyceride content and fatty acid profiles were also measured.

RESULTS: Feeding SHRSP and WKY on 60% fructose for 2 weeks resulted in glucose intolerance with no increases in levels of blood pressure.

Serum triglycerides were increased in both strains of fructose-fed rats with the highest levels being observed in the SHRSP.

The serum fatty acid profiles were changed with large increases in the amounts of oleic acid (18.1) and reductions in linoleic acid (18.2).

Levels of expression of c-jun N-terminal kinase/stress activated protein kinase (JNK/SAPK), and nuclear factor kappaB (NF-kappaB) were shown to be unchanged between the livers of the chow and fructose-fed groups.

In contrast, protein levels of the three isoforms of superoxide dismutase (SOD) were upregulated in liver of SHRSP fed on fructose while only manganese SOD (MnSOD) was upregulated in fructose-fed WKY rats.

CONCLUSIONS: These results demonstrate that the major contribution of the liver in the early pathogenesis of metabolic syndrome may be an increased secretion of triglyceride containing altered proportions of fatty acid pools.

Feeding rats a diet rich in fructose does not affect hepatic expression of inflammatory pathways and the increased hepatic SOD expression may constitute an early protective mechanism.

Feeding stroke-prone spontaneously hypertensive rats (SHRSP) a diet rich in fructose results in a profound glucose intolerance associated with increased hepatic SOD expression that is apparently profoundly protective.

Skeletal muscle of stroke-prone spontaneously hypertensive rats exhibits reduced insulin-stimulated glucose transport and elevated levels of caveolin and flotillin. [Diabetes. 2001]
The protective role of Kangen-karyu against fructose-induced metabolic syndrome in a rat model. [J Pharm Pharmacol. 2007]
Increased reactive oxygen species in rostral ventrolateral medulla contribute to neural mechanisms of hypertension in stroke-prone spontaneously hypertensive rats. [Circulation. 2004]
Cardiopulmonary responses of Wistar Kyoto, spontaneously hypertensive, and stroke-prone spontaneously hypertensive rats to particulate matter (PM) exposure. [J Toxicol Environ Health A. 2007]
Genetic determinants of metabolic syndrome components in the stroke-prone spontaneously hypertensive rat. [J Hypertens. 2005]
» See all Related Articles...

SuperOxide Dismutase

Structure of the monomeric unit of human superoxide dismutase 2

superoxide dismutase 1, soluble
Identifiers
Symbol	SOD1
Alt. Symbols	ALS, ALS1
Entrez	6647
HUGO	11179
OMIM	147450
RefSeq	NM_000454
UniProt	P00441
Other data
EC number	1.15.1.1
Locus	Chr. 21 q22.1

superoxide dismutase 2, mitochondrial
Identifiers
Symbol	SOD2
Entrez	6648
HUGO	11180
OMIM	147460
RefSeq	NM_000636
UniProt	P04179
Other data
EC number	1.15.1.1
Locus	Chr. 6 q25

superoxide dismutase 3, extracellular
Identifiers
Symbol	SOD3
Entrez	6649
HUGO	11181
OMIM	185490
RefSeq	NM_003102
UniProt	P08294
Other data
EC number	1.15.1.1
Locus	Chr. 4 pter-q21

The enzyme SuperOxide Dismutase (SOD, EC 1.15.1.1), catalyzes the dismutation of superoxide into oxygen and hydrogen peroxide. As such, it is an important antioxidant defense in nearly all cells exposed to oxygen. One of the exceedingly rare exceptions is Lactobacillus plantarum and related lactobacilli, which use a different mechanism.

Reaction

The SOD-catalysed dismutation of superoxide may be written with the following half-reactions :

M⁽ⁿ⁺¹⁾⁺ − SOD + O₂⁻ → Mⁿ⁺ − SOD + O₂
Mⁿ⁺ − SOD + O₂⁻ + 2H⁺ → M⁽ⁿ⁺¹⁾⁺ − SOD + H₂O₂.

where M = Cu (n=1) ; Mn (n=2) ; Fe (n=2) ; Ni (n=2).

In this reaction the oxidation state of the metal cation oscillates between n and n+1.

Types

General

SOD was discovered by Irwin Fridovich and Joe McCord, which prior were known as several metalloproteins with unknown function (for example, CuZnSOD was known as erythrocuprein). Several common forms of SOD exist: they are proteins cofactored with copper and zinc, or manganese, iron, or nickel.

Brewer (1967) identifed superoxide dismutase as an indophenol oxidase by protein analysis of starch gels using the phenazine-tetrazolium technique. Brewer detected this enzyme in several human tissues an indophenol oxidase A(IPO-A). After that Brewer observed an electrophoretic variant of IPO-A, which he called 'Morenci,' in 3 generations of a family with presumed male-to-male transmission. Using a RT-PCR analysis Brewer has identified 5 splice variants of SOD1. The variants were expressed in brain, a region involved in amyotrophic lateral sclerosis.

The cytosols of virtually all eukaryotic cells contain an SOD enzyme with copper and zinc (Cu-Zn-SOD). (For example, Cu-Zn-SOD available commercially is normally purified from the bovine erythrocytes: PDB 1SXA, EC 1.15.1.1). The Cu-Zn enzyme is a homodimer of molecular weight 32,500. The two subunits are joined primarily by hydrophobic and electrostatic interactions. The ligands of copper and zinc are histidine side chains.
Chicken liver (and nearly all other) mitochondria, and many bacteria (such as E. coli) contain a form with manganese (Mn-SOD). (For example, the Mn-SOD found in a human mitochondrion: PDB 1N0J, EC 1.15.1.1). The ligands of the manganese ions are 3 histidine side chains, an aspartate side chain and a water molecule or hydroxy ligand depending on the Mn oxidation state (respectively II and III).
E. coli and many other bacteria also contain a form of the enzyme with iron (Fe-SOD); some bacteria contain Fe-SOD, others Mn-SOD, and some contain both. (For the E. coli Fe-SOD: PDB 1ISA, EC 1.15.1.1). Fe-SOD can be found in the plastids of plants. The active sites of Mn and Fe superoxide dismutases contain the same type of amino acid side chains.

Structure of the active site of human superoxide dismutase 2

In higher plants, SOD isozymes have been localized in different cell compartments. Mn-SOD is present in mitochondria and peroxisomes. Fe-SOD has been found mainly in chloroplasts but has also been detected in peroxisomes, and CuZn-SOD has been localized in cytosol, chloroplasts, peroxisomes and

apoplast.^[1], ^[2]

Human

In humans, three forms of superoxide dismutase are present. SOD1 is located in the cytoplasm, SOD2 in the mitochondria and SOD3 is extracellular. The first is a dimer (consists of two units), while the others are tetramers (four subunits). SOD1 and SOD3 contain copper and zinc, while SOD2 has manganese in its reactive centre. The genes are located on chromosomes 21, 6 and 4, respectively (21q22.1, 6q25.3 and 4p15.3-p15.1).

A microtiter plate assay for SOD is available.^[3]

Biochemistry

Simply-stated, SOD outcompetes damaging reactions of superoxide, thus protecting the cell from superoxide toxicity. The reaction of superoxide with non-radicals is spin forbidden. In biological systems, this means its main reactions are with itself (dismutation) or with another biological radical such as nitric oxide (NO). The superoxide anion radical (O₂^-) spontaneously dismutes to O₂ and hydrogen peroxide (H₂O₂) quite rapidly (~10⁵ M^-1 s^-1 at pH 7). SOD is biologically necessary because superoxide reacts even faster with certain targets such as NO radical, which makes peroxynitrite. Similarly, the dismutation rate is second order with respect to initial superoxide concentration. Thus, the half-life of superoxide, although very short at high concentrations (e.g. 0.05 seconds at 0.1mM) is actually quite long at low concentrations (e.g. 14 hours at 0.1 nM). In contrast, the reaction of superoxide with SOD is first order with respect to superoxide concentration. Moreover, superoxide dismutase has the fastest turnover number (reaction rate with its substrate) of any known enzyme (~10⁹ M^-1 s^-1)^{[citation needed]}, this reaction being only limited by the frequency of collision between itself and superoxide. That is, the reaction rate is "diffusion limited".

Physiology

Superoxide is one of the main reactive oxygen species in the cell and as such, SOD serves a key antioxidant role. The physiological importance of SODs is illustrated by the severe pathologies evident in mice genetically engineered to lack these enzymes. Mice lacking SOD2 die several days after birth, amidst massive oxidative stress.^[4] Mice lacking SOD1 develop a wide range of pathologies, including hepatocellular carcinoma,^[5] an acceleration of age-related muscle mass loss,^[6] an earlier incidence of cataracts and a reduced lifespan. Mice lacking SOD3 do not show any obvious defects and exhibit a normal lifespan

Role in disease

Mutations in the first SOD enzyme (SOD1) have been linked to familial amyotrophic lateral sclerosis (ALS, a form of motor neuron disease). The other two types have not been linked to any human diseases, however, in mice inactivation of SOD2 causes perinatal lethality^[4] and inactivation of SOD1 causes hepatocellular carcinoma.^[5] Mutations in SOD1 can cause familial ALS, by a mechanism that is presently not understood, but not due to loss of enzymatic activity or a decrease in the conformational stability of the SOD1 protein. Overexpression of SOD1 has been linked to Down's syndrome.^[7] The veterinary antiinflammatory drug "Orgotein" is purified bovine liver superoxide dismutase.

Delivery systems

Superoxide dismutase is effective as a nutritional supplement when bound to the polymeric films of wheat matrix gliadin (a delivery method also known as glisodin). Gliadin is an ideal carrier because it protects SOD from stomach acid and enzymes found in the digestive system which break down its molecular structure. This has been established in a variety of animal studies and human clinical trials, in which SOD's generally high antioxidant capacity is kept intact under a variety of conditions.

Cosmetic uses

SOD is used in cosmetic products to reduce free radical damage to skin, for example to reduce fibrosis following radiation for breast cancer. Studies of this kind must be regarded as tentative however, as there were not adequate controls in the study including a lack of randomization, double-blinding or placebo.^[8] Superoxide dismutase is known to reverse fibrosis, perhaps through reversion of myofibroblasts back to fibroblasts.^[9]

References

^ Corpas FJ, Barroso JB, del Río LA. (2001). "Peroxisomes as a source of reactive oxygen species and nitric oxide signal molecules in plant cells.". Trends Plant Sci. 6 (4): 145–50..
^ Corpas FJ et al. (2006). "The expression of different superoxide dismutase forms is cell-type dependent in olive (Olea europaea L.) leaves.". Plant Cell Physio. 47 (7): 984–94.
^ A.V. Peskin, C.C. Winterbourn (2000). "A microtiter plate assay for superoxide dismutase using a water-soluble tetrazolium salt (WST-1)". Clinica Chimica Acta 293: 157–166. doi:10.1016/S0009-8981(99)00246-6.
^ ^a ^b Li, et al., Y. (1995). "Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase.". Nat. Genet. 11: 376–381. doi:10.1038/ng1295-376.
^ ^a ^b Elchuri, et al., S. (2005). "CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in life.". Oncogene 24: 367–380. doi:10.1038/sj.onc.1208207.
^ Muller, et al., F. L. (2006). "Absence of CuZn superoxide dismutase leads to elevated oxidative stress and acceleration of age-dependent skeletal muscle atrophy.". Free Radic. Biol. Med 40: 1993–2004. doi:10.1016/j.freeradbiomed.2006.01.036.
^ Groner, Y. et al. (1994). "Cell damage by excess CuZnSOD and Down's syndrome.". Biomed Pharmacother. 48: 231–40. doi:10.1016/0753-3322(94)90138-4. PMID 7999984.
^ Campana, F. (2004). "Topical superoxide dismutase reduces post-irradiation breast cancer fibrosis" (available free). J. Cell. Mol. Med. 8 (1): 109–116. doi:10.1111/j.1582-4934.2004.tb00265.x. PMID 15090266.
^ Vozenin-Brotons MC; Sivan V, Gault N, Renard C, Geffrotin C, Delanian S, Lefaix JL, Martin M (January 1, 2001). "Antifibrotic action of Cu/Zn SOD is mediated by TGF-beta1 repression and phenotypic reversion of myofibroblasts". Free Radic Biol Med 30 (1): 30–42. Elsevier. doi:10.1016/S0891-5849(00)00431-7. PMID 11134893.

External links

Online 'Mendelian Inheritance in Man' (OMIM) 105400 (ALS)
The ALS Online Database
A short but substantive overview of SOD and its literature.
Damage-Based Theories of Aging Includes a discussion of the roles of SOD1 and SOD2 in aging.
Physicians' Comm. For Responsible Med.
SOD and Oxidative Stress Pathway Image
Historical information on SOD research"The evolution of Free Radical Biology & Medicine: A 20-year history" and "Free Radical Biology & Medicine The last 20 years: The most highly cited papers"
JM McCord discusses the discovery of SOD

v • d • e Other oxidoreductases (EC 1.15-1.18)

1.15 - Acting on superoxide as acceptor	Superoxide dismutase

1.16 - Oxidizing metal ions	Ceruloplasmin

1.17 - Acting on CH or CH2 groups	Xanthine oxidase - Ribonucleotide reductase - 4-hydroxy-3-methylbut-2-enyl diphosphate reductase

1.18 - Acting on iron-sulfur proteins as donors	Nitrogenase

v • d • e

Anti-inflammatory and antirheumatic products (M01)

TSG-type1-CURE

noreply@blogger.com (Nicholas Dynes Gracey) — Tue, 08 Jul 2008 12:24:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

J Endocrinol. 2002 Aug;174(2):225-31. Links: Mechanisms involved in the beta-cell mass increase induced by chronic sucrose feeding to normal rats.

Del Zotto H, Gómez Dumm CL, Drago S, Fortino A, Luna GC, Gagliardino JJ.

CENEXA, Centre of Experimental and Applied Endocrinology (UNLP-CONICET), University of La Plata School of Medicine, La Plata, Argentina.; The aim of the present study was to clarify the mechanisms by which a sucrose-rich diet (SRD) produces an
increase in the pancreatic beta-cell mass in the rat.; Normal Wistar rats were fed for 30 weeks either an SRD (SRD rats; 63% wt/wt), or the same diet but with starch instead of sucrose in the same proportion (CD rats).; We studied body weight, serum glucose and triacylglycerol levels, endocrine tissue and beta-cell mass, beta-cell replication rate (proliferating cell nuclear antigen; PCNA), islet neogenesis (cytokeratin immunostaining) and beta-cell apoptosis (propidium iodide).; Body weight (g) recorded in the SRD rats was significantly (P<0.05); Both serum glucose and triacylglycerol levels (mmol/l) were also significantly higher (P<0.05); The number of pancreatic islets per unit area increased significantly (P<0.05)>; A significant increment (2.6 times) in the mass of endocrine tissue was detected in SRD animals, mainly due to an increase in the beta-cell mass (P=0.0025).

The islet cell replication rate, measured as the percentage of PCNA-labelled beta cells increased 6.8 times in SRD rats (P<0.03).

The number of apoptotic cells in the endocrine pancreas decreased significantly (three times) in the SRD animals (P=0.03).

The cytokeratin-positive area did not show significant differences between CD and SRD rats.

The increase of beta-cell mass induced by SRD was accomplished by an enhanced replication of beta cells together with a decrease in the rate of beta-cell apoptosis, without any evident participation of islet neogenesis.

This pancreatic reaction was unable to maintain serum glucose levels of these rats at the level measured in CD animals.; A significant increment (2.6 times) in the mass of endocrine tissue was detected in SRD animals, mainly due to an increase in the beta-cell mass (P=0.0025).; The islet cell replication rate, measured as the percentage of PCNA-labelled beta cells increased 6.8 times in SRD rats (P<0.03).; The number of apoptotic cells in the endocrine pancreas decreased significantly (three times) in the SRD animals (P=0.03).; The cytokeratin-positive area did not show significant differences between CD and SRD rats.; The increase of beta-cell mass induced by SRD was accomplished by an enhanced replication of beta cells together with a decrease in the rate of beta-cell apoptosis, without any evident participation of islet neogenesis.; This pancreatic reaction was unable to maintain serum glucose levels of these rats at the level measured in CD animals.

Islet neogenesis: an apparent key component of long-term pancreas adaptation to increased insulin demand. [J Endocrinol. 2004]
Changes induced by sucrose administration upon the morphology and function of pancreatic islets in the normal hamster. [Diabetes Metab Res Rev. 1999]
Possible relationship between changes in islet neogenesis and islet neogenesis-associated protein-positive cell mass induced by sucrose administration to normal hamsters. [J Endocrinol. 2000]
A low protein diet alters the balance of islet cell replication and apoptosis in the fetal and neonatal rat and is associated with a reduced pancreatic expression of insulin-like growth factor-II. [Endocrinology. 1999]
Multiphasic metabolic changes in the heart of rats fed a sucrose-rich diet. [Horm Metab Res. 1994]
» See all Related Articles...

Patient Drug Information

Glucagon (GlucaGen Diagnostic Kit®) Glucagon is a hormone produced in the pancreas. Glucagon is used to raise very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs.
» read more ...

http://joe.endocrinology-journals.org/cgi/content/abstract/174/2/225

Beta cells (beta-cells, β-cells) are a type of cell in the pancreas in areas called the islets of Langerhans. They make up 65-80% of the cells in the islets.

Function

Beta cells make and release insulin, a hormone that controls the level of glucose in the blood. There is a baseline level of insulin maintained by the pancreas, but it can respond quickly to spikes in blood glucose by releasing stored insulin while simultaneously producing more. The response time is fairly quick, taking approximately 10 minutes.

Apart from insulin, beta cells release C-peptide, a byproduct of insulin production, into the bloodstream in equimolar quantities. C-peptide helps to prevent neuropathy, and other symptoms of diabetes related to vascular deterioration^[1]. Measuring the levels of C-peptide can give a practitioner an idea of the viable beta cell mass.^[2]

β-cells also produce amylin,^[3] also known as IAPP, islet amyloid polypeptide. Amylin functions as part of the endocrine pancreas and contributes to glycemic control. Amylin's metabolic function is now somewhat well characterized as an inhibitor of the appearance of nutrient [especially glucose] in the plasma. It thus functions as a synergistic partner to insulin. Whereas insulin regulates long term food intake, increased amylin decreases food intake in the short term.

Pathology

Diabetes mellitus type 1 is caused by the destruction or dysfunction of insulin-producing beta cells by the cells of the immune system.

In Diabetes mellitus type 2, by contrast, beta cells decline gradually over time, and insulin resistance plays at least as large a role in the disease ^[4]^[5]

Insulinoma is a rare tumor (usually benign) derived from beta cells. It results in recurrent and prolonged attacks of hypoglycemia.

Research

Much research is being done in the field of beta-cell physiology and pathology. One major research topic is its effects on diabetes. Many researchers are trying to find ways to use these beta-cells to help control or prevent diabetes. A major topic is the replication of adult beta-cells and the application of these to diabetes. The Larry L. Hillblom Islet Research Center at UCLA^[6] is a leading research center in the field, within the Diabetes and Endocrinology Research Center^[7], directed by Dr. Peter Butler. ^[8]

A team science effort also exists, known as the Beta Cell Biology Consortium (BCBC).^[9] The BCBC is responsible for facilitating interdisciplinary approaches that will advance the understanding of pancreatic islet development and function. The long-term goal of the BCBC is to develop a cell-based therapy for insulin delivery.

In a study presented on June 8, 2008 at the American Diabetes Association’s 68th Scientific Sessions, a team showed that mice lacking insulin receptors in their beta cells had problems in the processing of insulin leading to excess, unprocessed levels of the hormone. Unprocessed insulin is unable to properly control glucose levels in the body. High circulating levels of unprocessed insulin and insulin resistance, a condition in which normal amounts of insulin are inadequate to produce a normal insulin response, are both known to be early indicators of type 2 diabetes.^[10]

References

^ Y. Ido, A. Vindigni, K. Chang, L. Stramm, R. Chance, W. F. Heath, R. D. DiMarchi, E. Di Cera, J. R. Williamson. 1997. Prevention of Vascular and Neural Dysfunction in Diabetic Rats by C-Peptide. Science, Vol. 277. no. 5325, pp. 563 - 566.
^ Hoogwerf B, Goetz F (1983). "Urinary C-peptide: a simple measure of integrated insulin production with emphasis on the effects of body size, diet, and corticosteroids". J Clin Endocrinol Metab 56 (1): 60–7. PMID 6336620.
^ Moore C, Cooper G (1991). "Co-secretion of amylin and insulin from cultured islet beta-cells: modulation by nutrient secretagogues, islet hormones and hypoglycemic agents". Biochem Biophys Res Commun 179 (1): 1–9. doi:10.1016/0006-291X(91)91325-7. PMID 1679326.
^ "U.K. prospective diabetes study 16. Overview of 6 years' therapy of type II diabetes: a progressive disease. U.K. Prospective Diabetes Study Group" (1995). Diabetes 44 (11): 1249–58. doi:10.2337/diabetes.44.11.1249. PMID 7589820.
^ Rudenski A, Matthews D, Levy J, Turner R (1991). "Understanding "insulin resistance": both glucose resistance and insulin resistance are required to model human diabetes". Metabolism 40 (9): 908–17. doi:10.1016/0026-0495(91)90065-5. PMID 1895955.
^ The Larry L. Hillblom Islet Research Center
^ The DERC Homepage has moved
^ Faculty
^ Beta Cell Biology Consortium
^ Newswise: Beta Cell Defect Linked to Type 2 Diabetes Retrieved on June 8, 2008.

External links

MeSH Pancreatic+beta+cells

v • d • e Endocrine system > Pancreas – Islets of Langerhans

A/B	alpha cell (glucagon) • beta cell (insulin)

Other	delta cell (somatostatin) • PP cell (pancreatic polypeptide) • epsilon cell (ghrelin)

Type3 diabetes

noreply@blogger.com (Nicholas Dynes Gracey) — Sat, 28 Jun 2008 22:09:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.
Adiposity, HYPERinsulinemia, diabetes and Alzheime...[Eur J Pharmacol. 2008] - PubMed Result

Eur J Pharmacol. 2008 May 6;585(1):119-29. Epub 2008 Mar 4. Links

Adiposity, HYPERinsulinemia, diabetes and Alzheimer's disease: an epidemiological perspective.

Luchsinger JA.

Taub Institute for Research of Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA. jal94@columbia.edu

The objective of this manuscript is to provide a comprehensive review of the epidemiologic evidence linking the continuum of adiposity, HYPERinsulinemia, and diabetes with Alzheimer's disease.

The mechanisms for these associations ALLEGEDLY remain to be elucidated, but may include direct actions from insulin, advanced products of glycosilation, cerebrovascular disease, and products of adipose tissue metabolism.

Elevated adiposity in middle age is related to a higher risk of Alzheimer's disease.

The evidence relating adiposity in old age to Alzheimer's disease is conflicting.

Several studies have shown that HYPERinsulinemia [AKA POTENTIAL TRANSIENT RELATIVE HYPO-GLYCEMIA DISTRESS], a consequence of higher adiposity and insulin resistance, is also related to a higher risk of Alzheimer's disease.

HYPERinsulinemia is a risk factor for diabetes, and numerous studies have shown a relation of diabetes with higher Alzheimer's disease risk.

Most studies fail the take into account the continuum linking these risk factors which may result in underestimation of their importance in Alzheimer's disease.

The implication of these associations is that a large proportion of the world population may be at increased risk of Alzheimer's disease given the trends for increasing prevalence of overweight, obesity, HYPERinsulinemia [RELATIVE HYPO-GLYCEMIA DISTRESS AKA FUEL-ANEMIA] and diabetes.

However, if proven causal, these associations also present a unique opportunity for prevention and treatment of Alzheimer's disease.

PMID: 18384771

Adiposity and Alzheimer's disease. [Curr Alzheimer Res. 2007]
Cardiovascular risk factors and Alzheimer's disease. [Curr Atheroscler Rep. 2004]
Diabetes, Alzheimer's disease and apolipoprotein genotype. [Exp Gerontol. 2003]
The epidemiology of adiposity and dementia. [Curr Alzheimer Res. 2007]
The role of insulin resistance in the pathogenesis of Alzheimer's disease: implications for treatment. [CNS Drugs. 2003]
» See all Related Articles...

Curr Alzheimer Res. 2007 Apr;4(2):127-34. Links

Adiposity and Alzheimer's disease.

Luchsinger JA, Mayeux R.

Taub Institute for Research of Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA. jal94@columbia.edu

The objective of this manuscript is to provide a comprehensive review of the relation between adiposity and Alzheimer's disease (AD), its potential mechanisms, and issues in its study.

Adiposity represents the body fat tissue content.

When the degree of adiposity increases it can be defined as being overweight or obese by measures such as the body mass index. Being overweight or obese is a cause of HYPERinsulinemia and diabetes, both of which are risk factors for AD.

However, the epidemiologic evidence linking the degree of adiposity and AD is conflicting.

Traditional adiposity measures such as body mass index have decreased validity in the Elderly.

Increased adiposity in early or middle adult life leads to HYPERinsulinemia [AKA POTENTIAL TRANSIENT RELATIVE HYPO-GLYCEMIA DISTRESS] which may lead to diabetes later in life.

Thus, the timing of ascertainment of adiposity and its related factors is critical in understanding how it might fit into the pathogenesis of AD.

We believe that the most plausible mechanism relating adiposity to AD is HYPERinsulinemia [AKA POTENTIAL TRANSIENT RELATIVE HYPO-GLYCEMIA DISTRESS], but it is unclear whether specific products of adipose tissue also have a role.

Being overweight or obese is increasing in Children and Adults, thus understanding the association between adiposity, HYPERinsulinemia [AKA POTENTIAL TRANSIENT RELATIVE HYPO-GLYCEMIA DISTRESS] and AD has important Public health implications.

PMID: 17430235

Adiposity, HYPERinsulinemia, diabetes and Alzheimer's disease: an epidemiological perspective. [Eur J Pharmacol. 2008]
The epidemiology of adiposity and dementia. [Curr Alzheimer Res. 2007]
Early adiposity rebound: review of papers linking this to subsequent obesity in children and adults. [Curr Opin Clin Nutr Metab Care. 2005]
Body mass index in midlife and risk of Alzheimer disease and vascular dementia. [Curr Alzheimer Res. 2007]
Elevated serum C-reactive protein concentration in Bosnian patients with probable Alzheimer's disease. [J Alzheimers Dis. 2007]
» See all Related Articles...

Gluca-gone

noreply@blogger.com (Nicholas Dynes Gracey) — Fri, 27 Jun 2008 09:13:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.
Effect of near physiologic insulin therapy on HYPO...[Horm Res. 2001] - PubMed Result

Horm Res. 2001;56(5-6):151-8. Links

Effect of near physiologic insulin therapy on HYPOglycemia counter-regulation in type-1 diabetes.

Bischof MG, Bernroider E, Ludwig C, Kurzemann S, Kletter K, Waldhäusl W, Roden M.

Division of Endocrinology and Metabolism, Department of Internal Medicine III, University of Vienna Medical School, Vienna, Austria.

OBJECTIVES: The aim of this study was to examine hormonal counter-regulation during insulin-induced HYPOglycemia in type-1 Diabetic patients during long-term near normo-glycemic insulin therapy and intensive clinical care.

METHODS: Type-1 Diabetic 'Patients' (age 35.3 +/- 2 years, body mass index 22.8 +/- 1 kg x m(-2), mean diabetes duration 13.6 (11-17 years), mean HbA1c during the last year 6.6 +/- 0.1%); and

non-Diabetic 'Subjects' were studied

during (0-120 min) and

after (120-240 min) HYPOglycemia (54.9 mg/dl = 3.05 mmol/l)

HYPERinsulinemic (approximately 330 pmol/l) clamp tests.

RESULTS: During HYPOglycemia peak plasma concentrations of

glucagon (199 +/- 16 vs. 155 +/- 11 ng/l) p less than 0.05,

adrenaline (4,514 +/- 644 vs. 1,676 +/- 513 pmol/l) p less than 0.001,

noradrenaline (2.21 +/- 0.14 vs. 1.35 +/- 0.19 nmol/l) p' 0.01

cortisol (532 +/- 44 vs. 334 +/- 61 nmol/l) ...

... were healthily higher in the non-Diabetic 'Patients'.

Plasma lactate did not change from baseline values (0.51 +/- 0.06 mmol/l) in Diabetic but doubled in the non-Diabetic 'Subjects' (1.13 +/- 0.111 mmol/l) p less than 0.001 vs Control,

During the postHYPOglycemic recovery period plasma concentrations of free fatty acids were higher in Diabetic Patients at 240 min (1.34 +/- 0.12 vs. 2.01 +/- 0.23 mmol/l) p less than 0.05 ...

CONCLUSION: Despite long-term near physiologic insulin substitution and the low incidence of HYPOglycemia, hormonal HYPOglycemia counter-regulation was impaired in type-1 Diabetic Patients after a diabetes duration of more than 10 years.

OR: ... insulin therapy and intensive clinical care down-regulates both proinsulin producing beta-cells AND proglucagon producing alpha-cells ... so that's why glucagon's going ?

PMID: 11910200

Patient Drug Information

Glucagon (GlucaGen Diagnostic Kit®) Glucagon is a hormone produced as proglucagon in the body including the alpha-cells of the pancreas. Glucagon is used to raise very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs.

» read more ...

Exp Clin Endocrinol Diabetes. 2008 May;116(5):255-61. Links

Effect of experimentally induced HYPOglycemia and different insulin levels on feelings of hunger in type 1 Diabetic Patients.

Hermanns N, Plate M, Kulzer B, Fischer B, Linn T, Bretzel R, Haak T.

1Research institute of the Diabetes Academy Mergentheim, Germany.

INTRODUCTION: This study investigates the impacts of experimentally induced HYPOglycemia and different insulin infusion rates on feelings of hunger.

METHODS: Blood glucose and insulin levels were manipulated by HYPERinsulinemic glucose clamp technique.

Participants were 16 Patients with type 1 diabetes (age 36.2+/-11.7 yrs, diabetes duration 9.0+/-6.3 yrs, HbA1c 8.2+/-2.0%).

One group (n=8) received moderate, constant insulin infusion (0.8 muU/kg/min), whereas the insulin infusion was transiently supernormally

doubled in the other group (1.6 muU/kg/min).

Blood glucose was lowered stepwise from alleged 'normal' glycemia (100.8 mg/dl = 5.6 mmol/l) to alleged 'moderate' HYPOglycemia (45mg/dl = 2.5 mmol/l).

RESULTS: As expected, there was a significant effect of HYPOglycemia on feelings of hunger (F (3, 42)=41.7, p<0.01).

But during moderate insulin infusion, feelings of hunger were significantly alarmingly more intense than during transiently supernormal insulin infusion (F (1, 14)=7.2, p=0.02).

CONCLUSION: Peripheral insulin levels seem to be associated with the intensity of feelings of hunger.

OR: ... eating too OFTEN induces, HYPOglycemia associated intense hunger, via moderate constant insulin and/or proinsulin levels in Diabetics & non-Diabetics ... so eat less OFTEN ... because one meal a day or less apparently helps to prevent HYPOglycemia associated intense hunger.

PMID: 18484559

Knight Bill

noreply@blogger.com (Nicholas Dynes Gracey) — Thu, 26 Jun 2008 01:08:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

Euthanasia

Pressure for legalised euthanasia in Britain in recent years has steadily increased.

The word euthanasia comes from the Greek eu and thanatos, which together mean 'good death.' Euthanasia, sometimes called 'mercy killing,' is defined as the intentional killing of a patient either by act or omission, supposedly in the person's own interest. Voluntary euthanasia is killing the person at the person's request. Involuntary euthanasia is killing the person without his request, and possibly against his will. Nonvoluntary euthanasia is killing a person unable to make such a request, such as a young child or a sufferer from dementia.

In Holland for some years, whilst euthanasia was illegal, the Dutch authorities agreed doctors would not be prosecuted for performing euthanasia provided guidelines were observed. These stated that euthanasia was to be for people who were terminally ill, in irrelievable pain, after repeated requests, with the consent of two doctors, and reported to the authorities.

A Dutch Government report in 1991, however, said that active euthanasia was performed on 1,000 patients in 1990 without an explicit request from the patient, and intentional lethal doses of morphine-like drugs were given to 4,941 patients without the patient's knowledge. A report in 1996 said in 1995 euthanasia was performed on 900 patients without an explicit request from the patient, intentional lethal overdoses were given to 1,889 without the patient's knowledge and medical treatment was withheld from 3,644 with the aim of hastening death. Many doctors had performed euthanasia without seeking a second doctor's opinion. In 1990 only 18 per cent of cases and in 1995 only 41 per cent of cases were reported to the authorities.

Dr Herbert Hendin, an American physician who authored a 1997 report following a visit by doctors to research euthanasia in Holland, said virtually every guideline had either failed to protect patients, been modified or been violated, and euthanasia, originally intended for the exceptional case, had become an accepted way of dealing with serious or terminal illness. The Dutch Parliament's lower house finally legalised euthanasia in Holland in 2000. Approval by Parliament's upper house was granted in April, 2001.

A Dutch TV programme in 2003 claimed doctors were now performing euthanasia on thousands of patients without bothering to report it, as required by law, because they considered reporting it too time-consuming. The programme claimed that to avoid the legal procedure, doctors were giving lethal does of morphine under the pretext of pain management, or rendering patients unconscious with sedatives and allowing them to die of dehydration and starvation. Researchers in Holland who surveyed 5,600 doctors and interviewed 500 doctors in 2003 said almost half the cases in Holland went unreported because doctors wanted to avoid the hassle involved and were concerned that regulations might have been breached.

Since legislation, euthanasia has been performed in Holland on people who were not terminally ill, and on children. It is now to be extended to include involuntary euthanasia of infants.

Euthanasia was legalised in Australia's Northern Territory in 1996, but the legislation was later repealed by the federal government. Euthanasia was legalised in Belgium in 2002. The Belgian Medical Journal later reported that several times more cases of euthanasia were being carried out than were being officially recorded.

Assisted suicide is legal in the state of Oregon, but not in other states in the USA.

In Britain, euthanasia and doctor-assisted suicide are illegal.

In 1993 the House of Lords upheld decisions by the High Court and the Appeal Court that feeding by tube constituted medical treatment, and food and water could therefore be withheld from Tony Bland, a young man brain injured in the Hillsborough football stadium disaster, thus effectively starving him to death 'in his own best interests.' Tony Bland was not on a life-support machine, was not in pain, and fed and cared for could have lived for an indefinite period, but doctors said he was in 'persistent vegetative state' and his condition would not improve. This was the first time in history English courts sanctioned the death of an innocent man who was not already dying. Court permission was later given for food and water to be withdrawn from other brain-damaged patients, not all of them in 'persistent vegetative state.'

In 1994 a select committee appointed by the Government to consider euthanasia recommended the law should not be changed.

In 1997 the Government redefined euthanasia for the first time. It had always been understood that euthanasia was an act of commission or an act of omission causing the death of a patient. In 1997, however, the Government published a green paper describing euthanasia as 'a deliberate intervention with the express aim of ending life,' with no mention of killing by omission, allowing the Government to claim since 1997 that withdrawing food and water from patients is not euthanasia. The 1997 green paper suggested legalising the withdrawal of food and water from patients, and suggested making advance directives ('living wills') legally binding. (Living wills are documents that can be signed by people in advance stating they do not want treatment in the event of their becoming incapacitated. They are supported by organisations advocating euthanasia. They are opposed by pro-lifers for a variety of reasons; many consider their use introduces euthanasia by the back door.) Some pro-lifers claimed that politicians, while saying they were opposed to euthanasia, were leaving loopholes so that euthanasia could be introduced by the back door.

In January, 1999 the Times reported that the deaths of at least 50 patients were being investigated at hospitals around Britain. It said seven separate inquiries were under way into claims that doctors had withheld intravenous drips from dehydrated patients, often while they were under sedation, leaving the patients to die of thirst.

In June, 1999 the British Medical Association issued new guidelines to doctors saying doctors could withdraw treatment, including food and water, from seriously ill patients if they considered it in the patient's best interest. The guidelines say there should be no need to apply for the courts' permission. Relatives' wishes should be taken into account, but the doctors' decision should be final, unless relatives could persuade the courts otherwise.The General Medical Council also issued guidelines to doctors.

In 2000 the Medical Treatment (Prevention of Euthanasia) Bill, a private member's bill which would have made it illegal for a doctor intentionally to cause the death of a patient either by deliberate act or by omission, by withholding medication or food and water, failed in the House of Commons after the Government declined to support it.

In 2000, Scottish legislation allowed for 'welfare attorneys' who would be able to take decisions on behalf of patients unable to take decisions for themselves, including the withdrawal from the patient of food and fluids by tube.

In 2002 the British Government issued new guidance on treatment for patients who are mentally incapacitated and unable to take decisions for themselves. It said living wills must be complied with.

Two Private Member's Bills came before Parliament in 2003. Baroness Knight's Patient's Protection Bill would have made it illegal to withhold sustenance for the purpose of hastening or causing the death of a patient. Baroness Knight said hospital patients were being deliberately starved to death, which was in contravention of the Human Rights Act, which said that no one should be deprived of life intentionally. Lord Joffe's bill would have legalised assisted suicide, allowing terminally ill adults to request medical help to die. Neither bill became law.

Towards the end of 2003, however, it was decided a new House of Lords select committee should be appointed to consider assisted suicide. The Lords liaison committee said some 10 years had elapsed since the last committee's report, new legislation had been introduced in other countries, and there had been opinion polls in this country which needed to be taken into account. The committee was unable to agree on whether a change in the law was necessary, but said the issue should be the subject of early parliamentary debate.

Meanwhile, the Mental Capacity Bill was forced through Parliament by the Government. The Mental Capacity Act, as it became, requires doctors to observe living wills, which could require medical treatment, including food and water, to be withdrawn. The act also allows power of attorney to be granted by patients to a friend or relative, which means that if the patient became unable to take decisions for himself, the person with power of attorney could order doctors to withdraw treatment, including food and water, even though the person with power of attorney might stand to benefit from the patient's will. Critics of the bill complained that while living wills which requested food and water be withdrawn when patients became incapacitated would be legally binding, living wills requesting that food and water continued to be given would not.

In 2005 the Government said publicly for the first time that a decision on whether or not to withdraw food and water from a sick patient could be affected by considerations of cost in keeping him alive. During a court hearing in the Leslie Burke case, the Government claimed that 'a general right for an individual patient to require life-prolonging medical treatment has very serious implications for the functioning of the NHS. It may. . .lead to inefficient and unfairly skewed use of resources within the NHS.'

Leslie Burke, who had a degenerative brain condition, had petitioned the courts for the right to be given food and water when he was no longer able to speak for himself. The High Court agreed he should be kept alive unless his condition became 'intolerable.' The General Medical Council and the Government appealed the decision. The Appeal Court upheld the appeal, deciding that a patient could not demand treatment which the doctor considered averse to the patient's clinical needs. The European Court of Human Rights agreed. It said it would be 'burdensome' if doctors had to apply to the High Court every time they wished to end a life by withdrawing food and water.

When euthanasia was debated in the House of Lords, peers were divided on the issue. In the autumn of 2005, Lord Joffe introduced a revised bill proposing legalisation of doctor-assisted suicide. Supporters of the bill made it clear that it was intended as a first step to legalised euthanasia.

The bill came up for its second reading in the Lords in May, 2006, with a remarkable result. A sizeable number of peers were still in favour - but one peer, Lord Carlile, proposed an amendment delaying further progress on the bill for six months, which would effectively kill the bill for lack of parliamentary time. When the amendment went to the vote, it passed by 148 votes to 100. It was the first time for eight years a Private Member's Bill in the House of Lords had been defeated at that stage in its progress.

Although Dignity in Dying - the former Voluntary Euthanasia Society - claimed a majority of the public was in favour of the bill, disability groups and doctors had serious reservations. A poll of the Royal College of Physicians showed 73 per cent against the bill; 91 per cent of doctors involved in geriatric care and 95 per cent of doctors involved in palliative care were opposed to a change in the law.

Members of the House of Lords were bombarded with letters and e-mails, the majority of them against the bill. It is believed the letters received by peers had an important effect on the result.

Although there is evidence of patients being starved or dehydrated to death, officially euthanasia and assisted suicide remain illegal in Britain. It is expected that there may be further attempts to legalise assisted suicide.

Concerned agencies have pointed out that as the number of old people increases and there are increasing demands on NHS funds, so pressure to help the old and seriously ill to an early death can be expected to increase. An estimated two-thirds of NHS beds are occupied by people over 65 years old. The number of people over 85 has doubled in 15 years. There are now over a million men and women between 85 and 89 and 330,000 over 90. In the next 50 years, these numbers are expected to triple.

Whilst pain in cases of terminal illness was once a real fear, tremendous strides in palliative care have been made in the past 30 years. Experts in pain relief now say patients in pain, including terminally ill patients, can be helped in 100 per cent of cases. Pain can be controlled perfectly acceptably in 95 per cent of cases. In many of the remaining five per cent pain can be helped by reducing movement which causes the pain. In the remaining very few cases, pain can be controlled by sedation.

Dr Robert Twycross, an internationally known expert on pain relief, says there is now no need for anyone to die in pain. In a booklet A pain-free death? published by the Medical Education Trust, he says tests at a major cancer centre showed complete relief from pain in 86 per cent of cases, adequate relief ('not what you'd call pain - I can forget it now') in 11 per cent of cases, and poor pain relief in only three per cent. In those three per cent, patients could be sedated so they slept without pain until death intervened. Dr Twycross quotes the World Health Organisation as saying that now a practical alternative to death in pain exists, there should be concentrated efforts to implement programmes of palliative hospice care rather than yielding to pressure for legal euthanasia.

Britain is fortunate in having one of the finest hospice services in the world (supported largely by voluntary funds) to care for terminally ill patients. In the year 2000, there were 3,152 beds in UK hospices. Each year about 250,000 UK patients benefit from hospice care, and 30,000 people die in hospice care. But more palliative care and better training in palliative care for doctors are still needed.

It is ironic, says the All-Party Parliamentary Group on Dying Well, that 30 or 40 years ago, when palliative care and the hospice movement were in their infancy and little could be done to remove the suffering of terminal illness, there was no serious mention of assisted suicide or euthanasia, while today, when such suffering can be dealt with and terminally ill people can die peacefully of natural causes, we are seeing a spate of bills seeking to legalise such killing.

Arguments for and against

In view of the continuing debate on the question of euthanasia, it is useful to be familiar with the arguments for and against. Proponents of euthanasia say a person's life is his own, and he should have a right to die when he wants to. Opponents point out that a 'right to die' for him would presumably mean 'an obligation to kill' for somebody else, and might eventually come to be regarded as a 'duty to die' for the old and sick. A doctor's job is to care and heal, not to kill.

Proponents of euthanasia say there would be strict safeguards if euthanasia were legalised. Opponents say it would be impossible to ensure adequate safeguards, and quote the situation in Holland as an example.

The Bible teaches that man, unlike the rest of the animal kingdom, is made in God's image and likeness (Gen 1:26, 27). It forbids the taking of innocent human life (Gen 9:6; Ex 20:13). For the Christian, the most important consideration will be You shall not murder (Ex 20:13).

Other questions to be considered:

Once it were decided that life did not have absolute value and some people's lives were not worth living, where would it stop? (The 'slippery slope' argument is a valid one. Permitting abortion for a few women led to abortion on demand. In Holland, voluntary euthanasia has led to involuntary euthanasia.)

What effect would the practice of euthanasia have on the medical profession?

What would be the effect on relationships between the medical profession and patients?

What would be the effect on the rest of society?

How would a euthanasia law affect respect for life in the community?

Could more be done to obviate people's feeling the need for euthanasia - providing more care for sick and elderly, visiting the old and lonely in private homes, hospital wards and old people's homes, providing more volunteers in hospices, letting people know they are precious, loved and cared for?

Literature you may find helpful

Cameron, Nigel M. de S. (1990). Death without Dignity: Euthanasia in perspective. Rutherford House Books, Edinburgh.

Euthanasia, a booklet of articles reprinted from the Journal of the Christian Medical Fellowship. Christian Medical Fellowship, London.

Keown, John (1997). Euthanasia Examined: Ethical, clinical and legal perspectives. Cambridge University Press, Cambridge.

Ling, John R. (2001). Responding to the Culture of Death. Day One Publications, Epsom.

Schaeffer, Francis A. and Koop, C. Everett (1980). Whatever Happened to the Human Race? Marshall, Morgan and Scott, London.

Baroness Knight of Collingtree: My Lords, I am very happy to support this amendment put down by the noble Baroness, for whom all of us, already, have a great admiration. I confess that I am feeling a sense of déjà vu as the debates on this Bill continue. Every time we put down an amendment to remedy what we believe is a dangerous implication in the Bill—that it creates a

17 Mar 2005 : Column 1444

serious risk in some of its aspects—we are told soothingly and convincingly "not to worry—that protection is in the Bill already".

Whether we are trying to ensure that suicide by advance decision does not happen, or we are trying to help those with conscientious objections by making it certain in law that their rights would be protected, or whatever protective measures we seek to make, the answer is the same. We are told, "There is no need for this amendment. The Bill will not allow any diminution of patients' rights or the rights of those who care for them". Yet we can never be certain that that is correct because it is never on the face of the Bill.

I have an unhappy feeling that the same anodyne dose will be offered to this amendment. As I have said, I have no wish to endanger the Bill by speaking at length. But if we do not speak now, when can we? Those of us who see and feel the dangers ahead have a clear duty to seek to shield patients from the pain that we have already seen many suffer.

When I introduced my Patient's Protection Bill, I did so because I had such a wealth of shocking evidence that sick people in NHS hospitals were being deliberately denied food and liquids and were dying because of it. Sometimes the food and liquids were deliberately put out of the patient's reach. I am not making those stories up: there is ample evidence for them.

The Government blocked the Bill but a Government Minister, the noble Lord, Lord Filkin, who was responsible for the Bill, assured me when I sat on the Select Committee which studied it, that the matter would be addressed in this Bill. Therefore, in earlier debates, I have not unnaturally sought to be sure that it provides the safeguards which really are so desperately needed. But, yet again, the soothing syrup which so effectively clogs the wheels of action is offered in large spoons.

We are told, "There is no need for this amendment. Such treatments as withholding food and liquids, putting them out of the patient's reach or failing to make the patient comfortable by moistening his dry mouth are already covered by good medical practice. No hospital would act in this way".

If all that is true, why, under these present rulings, which have been referred to so specifically and so frequently, have we so much evidence from patients, their relatives, MPs and public figures who have seen it for themselves, as well evidence from television programmes, newspaper reports and even doctors and nurses? Why does it go on if it is already illegal? That seems a perfectly fair question. When Nelson said, "I see no ships", his motive was brave and noble. But when the BMA pretends that those things do not happen, I fear that I cannot ascribe to it—although I admire that profession greatly—the same noble intentions.

I am getting quite used to being told that amendments are unnecessary. The only reason that this one is in that category is either a belief that all evidence is illusory or that we can afford to turn our backs and close our eyes on people who are suffering. Years ago I would have accepted without question

17 Mar 2005 : Column 1445

that doctors would always do everything possible to help their patients, to keep them alive if possible, and to keep them comfortable. I still admire doctors, but that old belief has gone. I do not believe it any more: how can I, with all the evidence against it?

I understand that newly-trained doctors do not now affirm the Hippocratic oath, which put the patient's care as a priority. They no longer sign automatically that the duties of a doctor mean also taking on the content of that oath. Whatever unwritten laws there may be in the medical profession's rule book, in the name of patients we must face the facts of evidence and try to get this amendment in the Bill.

Julia Quenzler, a famous court artist at the BBC, witnessed her mother being sentenced to an agonising death by thirst as a result of doctors depriving her of water. She said that her mother would give a firm nod when asked whether she wanted a drink of water, but the water never came. She states:

"My mother was not seriously ill when she walked into hospital. In fact she was a relatively healthy woman with a relatively common problem. Six days later she was on her deathbed".

She went on to state that she did not know what more she could have done, apart from abseiling off the hospital roof, to bring attention to her mother's needs. She said that she,

"literally begged [the doctors] with my hands pressed in supplication. I don't know why these doctors did what they did. In the absence of any plausible explanation, I can only conclude that they considered my mother an expendable nuisance".

The examples I give are all cases that have come to my notice since my Patient's Protection Bill failed to become law. A nurse, Pat Tyler, said in respect of her mother:

"She must have died thirsty . . . she must have been dreaming of cups of tea, of rivers of water. They should not have taken the water away from her".

But they did.

Nurses at Kingsway Hospital in Derby have claimed also that their patients were dying of thirst and that they were not given water or drips. I have added all those cases to my large pile on the subject since the last time we debated this issue.

It is undeniable that whatever rules may govern medical procedure, they are not sufficient to stop the cruel things which are going on. Do we want to stop them? I hope that we do. Do we accept that it is wrong? I hope that we do. If so, the remedy is now in our hands to take action. Agreeing the amendment would make it clearly law that patients must not be treated in the way in which they have been treated in the past, and the amendment in the name of the noble Baroness, Lady Chapman, is the answer.

Of course, we recognise that in some cases providing food and liquid might harm the patient. Peers will observe that the amendment does not disallow the stopping of nutrition where that danger exists. The noble Baroness has been very careful about that. We

17 Mar 2005 : Column 1446

cannot fail to agree the amendment if we want patients to receive the very first necessity, which is usually for comfort and well-being, but always for life.

Finally, I must express the profound hope that the other regular formula against amendments—that is, that they will wreck the Bill—will not be made in this regard. This amendment will not wreck the Bill. It will save the lives of many patients.

Lord Alton of Liverpool: My Lords, I support the amendment standing in the name of my noble friend. I also pay tribute to the noble Baroness, Lady Knight, who has just resumed her seat. She previously put before your Lordships' House her Patient's Protection Bill and has assiduously pursued this issue, believing, as she does, that we need to give every possible protection in the Bill to vulnerable people. I know that all parts of this House are not so far apart in wanting to achieve that objective.

However, as my noble friend and the noble Baroness, Lady Knight, have said, the issue is how we go about it. In supporting the amendment, I simply return to a subject that I and others raised during the passage of the Bill that the noble Baroness put forward, and an issue that I also raised at Second Reading and in Committee.

The amendment flows from our discussion last Tuesday. If the loophole that was identified by Professor John Finnis, Professor of Law at Oxford University, and Archbishop Peter Smith of Cardiff had been closed, I doubt that the movers of these amendments would feel the need to pursue the argument further.

During our earlier debates, considerable doubt arose about whether we should believe lawyers such as Professor Finnis or the noble Lords, Lord Carlile of Berriew and Lord Brennan, also distinguished lawyers. As the noble Baroness has just asked, should we trust the many assurances we have been given or should we look for provisions in the Bill. I have always erred on the side of the latter approach, which is why I welcome Clause 58 as a first step in addressing the issues identified today in these amendments by my noble friend.

Curiously, during the 36 hours that have elapsed since we last considered the Bill on Report, an issue has arisen that should inform today's debate about the confidence we place in assurances, and on the importance of writing things in the Bill. In 1990 in another place, I challenged a proposal to permit eugenic abortions up to birth on unborn babies with a disability. I said that it was a discriminatory provision, which is the thrust of the argument put forward today by my noble friend Lady Chapman and which lies at the heart of these amendments. I said that it was also a discriminatory provision that would lead to perfection tests governing our right to life.

In 1990 I circulated a legal opinion drawn up for me by two eminent Oxford lawyers, Professor John Finnis—much cited in our debates two days ago—and Professor John Keown, now professor of law at Cambridge University. Professor Finnis said that if the law was changed in the way proposed in 1990, it would lead to abortions on the grounds of conditions such as cleft

17 Mar 2005 : Column 1447

palate or hare lip. At the time he was ridiculed and castigated. One Member of Parliament, Mr Frank Doran, accused him of "pure scaremongering", while the present Solicitor-General, Harriet Harman, said that both Professor Keown and Professor Finnis should be reported to the Bar Council and to the Law Society.

No doubt Ms Harman will have followed carefully yesterday's decision by the Crown Prosecution Service to take no action in a case raised by a brave young Anglican curate from the Chester diocese, Joanna Jepson. She challenged the abortion of a baby, under the terms of the 1990 law, who had a disability. The baby's life was ended at seven months' gestation. The grounds for the abortion, as correctly anticipated by Professor Finnis in 1990, were that the baby had a cleft palate. The Crown Prosecution Service has now upheld the decision to end the life of a baby of seven months' gestation merely because of a very minor disability.

Was Professor Finnis scaremongering, or did the professor of law at Oxford University have a stronger grasp of the law than the present Solicitor-General, who wanted him brought before the Bar Council and the Law Society for accurately analysing the ramifications of a law that had been laid before Parliament and which was supported by many leading political figures with a great knowledge of the law, even such as the present Prime Minister himself?

In the context of the amendment before us, this case reveals two things. First, that we now routinely practise eugenics in Britain and that, as my noble friend Lady Chapman has just reminded us, the provisions in this Bill could further put the lives of disabled people at risk. Secondly, it puts into sharp relief the things that have been said by Professor Finnis about the need to close a loophole in Clause 58. One noble Baroness said to me yesterday that she had not appreciated that it was Professor Finnis who worked with the Government in drafting Clause 58, and that if anyone should understand its shortcomings, it would be he.

For the sake of the record, and in advance of the extensive debates on Lords amendments that may take place in another place, it is important to put on the record the united view of Professor Finnis and the Archbishop of Cardiff, Peter Smith. However, I see that the noble Lord, Lord Carter, wishes to speak. I shall return to that in a moment, after happily giving way to the noble Lord.

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Lord Carter: My Lords, I rise just to remind the noble Lord that the Joint Committee that I chaired on the draft Bill recommended that there should be a clause in the Bill along the lines of Clause 58 which, strictly speaking in law, is not necessary. It is a declaratory clause and was brought forward, as I say, as a result of the recommendation made by the Joint Committee.

Lord Alton of Liverpool: My Lords, I am grateful to the noble Lord, Lord Carter, for reminding us of that. He will also confirm that throughout the consideration period Professor Finnis had extensive discussions with the department and ensured that this provision was

17 Mar 2005 : Column 1448

placed in the Bill. But it is also important to recognise his view that this provision does not go quite far enough.

I recognise also that the gap between us is one which still could be closed between now and Third Reading. That is why I am offering these thoughts in a constructive way. I want to see a resolution of this issue and I want the Bill, which contains much that is good, to proceed to the statute book.

I remind noble Lords of what the Archbishop of Cardiff said in a letter to the Labour Member of Parliament, Mr Jim Dobbin, earlier this month. The Archbishop wrote:

"Professor Finnis and I believe that a further amendment is still needed to ensure that the Bill confers no authority on expressly suicidal advance decisions. We therefore strongly support efforts of Members of both Houses who are seeking to introduce an amendment to exclude decisions from being given validity or authority by a Bill where they have a purpose of bringing about death or are motivated by a desire of doing so. I very much hope the government will reconsider its opposition to inserting such an amendment, which we firmly believe can be made without affecting the jurisdiction of the courts affirmed in the Bland case".

That point was just made once again by my noble friend Lady Chapman in introducing these amendments.

It is well known that the main promoter of advance decisions is the Voluntary Euthanasia Society. The society has been ominously and curiously quiet about the Bill, knowing how it can be exploited. I know that the Government might now regret it, but it is a fact that the VES advised the Government on the preparation of an earlier consultation document, Making Decisions, which paved the way for this Bill. Is it any wonder, in the light of that and in the light of previous experience, that we now have our suspicions about where the Bill might lead?

My noble friend's amendment and her speech remind us that a great many people outside this House who are following our proceedings fear being inappropriately denied nutrition and hydration, the very basics of life itself. And in the light of the eugenic abortion at seven months' gestation of a baby with a cleft palate, please let no one accuse my noble friend, myself, or Professor Finnis of "pure scaremongering", or threaten us with the Bar Council or some other professional body. This House may dismiss their fears as ill-founded, but I should like to stress a point I have made before in your Lordships' House. We are not legislating for some Utopia where decision makers will always have the best interests of incapacitated persons at heart.

During the 1990 debate, the noble and learned Lord, Lord Brightman, said that, "it would be unthinkable" for a doctor who was carrying out a termination to preserve the mother's life or health to gratuitously terminate the life of the child:

"A doctor does not need an Act of Parliament to teach him that elementary duty".—[Official Report, 18/10/90; col. 1065.]

But sadly, as the noble Baroness Lady Knight, has just said, what was once unthinkable can rapidly become normative if we do not put the necessary safeguards in our legislation. What was once a heinous crime can rapidly become standard medical procedure. It is not enough to leave it to good intentions and, yes, it is

17 Mar 2005 : Column 1449

sometimes the role of Parliament to legislate not just to spell out duties, but also to protect the weak and the vulnerable.

Some individuals, perhaps not many, will seek to use this piece of legislation to end prematurely the lives of those who lack mental capacity. Denial of nutrition and hydration is one of the ways in which this could be done.

Many people's fears were compounded when we learnt that the Secretary of State for Health has argued in his submission to the Court of Appeal in the Burke case that resource considerations need to be brought to bear on the decision on whether artificial nutrition and hydration should be provided. My noble friend Lord Maginnis of Drumglass has been pursuing this point in Questions put to the Minister, the noble Baroness, Lady Ashton of Upholland.

This amendment does not oblige medical professionals to do everything to keep alive patients who are clearly dying and for whom the provision of nutrition and hydration would have no benefit or would be harmful, futile or burdensome. On Tuesday, I listened with great interest to the moving speech of the noble Lord, Lord Carter. He told us that,

"we are all entitled to follow the dictates of our conscience, but not perhaps by attempting to impose them on others through legislation".—[Official Report, 15/3/05; col. 1289.]

Neither this amendment nor the amendments debated in your Lordships' House on Tuesday are an attempt to impose anything on anyone. Rather, they represent an attempt to improve the legislation. They do not necessarily represent perfection, and we are all open to further dialogue and discussion with the Government between now and Third Reading to get this right. These amendments represent an attempt to ensure that the Bill cannot be used as a vehicle for intentional killing. I believe that that is an objective shared by everyone in the House who has contributed to the debates held in the course of these proceedings.

On Tuesday the Minister helpfully answered the seven questions posed by the noble Lord, Lord Carlile. I shall end with just two further questions. First, will the Minister tell us quite explicitly today, in answer to a question raised with her last Tuesday by the right reverend Prelate the Bishop of Oxford and myself, whether Clause 58 covers advance directives? Secondly, do the Government support the legalisation of euthanasia or physician-assisted suicide? They are two, straightforward questions that need to be recorded in our debates. They are different questions from those that have been asked so far. We have received the Government's assurance that the Bill does not legalise euthanasia or physician-assisted suicide, but suspicions will linger for so long as the Government fail to commit themselves to opposing any attempts in Parliament to legalise either euthanasia or assisted suicide.

Many of us would like to see the Bill enacted, but its fate is now in the hands of the Government. Unless the fears raised by my noble friend Lady Chapman are properly addressed between now and Third Reading, the Government will—I know and they know—be in

17 Mar 2005 : Column 1450

deep trouble with their own supporters as well as the Opposition Members in another place. I hope that, between now and Third Reading, they will seize the initiative and re-engage with Professor Finnis and others to seek a mature political resolution of these complex issues. I support the amendment.

Baroness Oppenheim-Barnes: My Lords, I shall intervene briefly following the excellent case made by my noble friend Lady Knight and others. I have just one question for the Minister. If the Bill already covers these points, and these things cannot possibly happen, is there any reason why a relative or close friend, visiting a patient who is unable to communicate in any way, can be prevented from demanding, on behalf of their close relative, that he should be given nutrition and hydration?

Baroness Masham of Ilton: My Lords, I have put my name to the amendments. It was mistakenly omitted from Amendment No. 9A. Many people feel that the Bill is still not clear enough in safeguarding at-risk and vulnerable people as regards food and fluid.

What Ministers and Members of both Houses think should happen may not be what is happening in some busy hospitals and nursing homes. Some disturbing cases have just arisen in a nursing home in Yorkshire. The Minister will no doubt say that the amendments are not necessary, but many people feel that they will help clarify what has become, and what may become, a grey muddle on the ground.

Doctor Anthony Cole, a consultant paediatrician and magistrate whom I know, has said:

"We hold most strongly that death by dehydration is unacceptable, inhumane and leads to a slow and painful death".

I hope that the Minister will accept the amendments, thereby helping many people who are concerned about what is happening and what may happen in the future.

Baroness Murphy: My Lords, I oppose the amendments, but I recognise the cases that the noble Baroness, Lady Knight, has mentioned. Cases of bad care come across my desk every day. Amid the many hundreds of thousands of treatments that are given every year, such cases undoubtedly exist. I would be the first to say that we needed better professional practice than to allow people to remain in that sort of distress.

I shall address what I believe is a false premise about artificial nutrition and hydration. Before doing so, I turn to the priority that we have all given to the autonomy of the individual in making decisions about their future treatment and care in advance directives.

We are all strongly supportive of the idea in the Bill that you should be able to make a decision when you have capacity about whether you wish to accept specific treatments when you lack it. Artificial nutrition and hydration are invasive medical treatments that fall clearly into the categories of treatment that would be included if an individual said that they wished to refuse life-saving interventions. They involve the insertion of a

17 Mar 2005 : Column 1451

nasogastric tube, which is not pleasant at all, or the intravenous infusions of artificial nutriments and chemicals. The paraphernalia restrict movement, and the process requires extensive monitoring. It is uncomfortable and very often distressing.

Only yesterday, I saw new guidance from the National Patient Safety Agency about the serious problems involved in maintaining nasogastric tubes. It is not like eating and drinking. The person who is fed through a nasogastric tube does not have a sensation that he has had a meal. It is not a good meal where you sit down with your friends and have a glass of wine and what I suppose these days would be ciabatta sandwich, panini or whatever. It is not like that at all. You are receiving artificial nutriments which often give you very unpleasant diarrhoea and so on.

How often have I witnessed uncomprehending, distressed older people tugging out the tubes and drips in an attempt to be free of the discomfort? On general medical wards, tubes are all too often left in, when someone would really be better not having them.

The whole procedure is burdensome. While the burdens are generally acceptable to people during a temporary acute illness or during a period after an operation from which one is hoping to recover, they are rarely justified as a long-term form of care when someone is approaching the end of life during a fatal illness. I recognise that the noble Lord, Lord Alton, addressed that issue.

If the individual is at home, the question never arises. If they are being cared for by family, tubes and drips are not put in. The possibility arises only when somebody goes into hospital and receives unnecessary interventions. Having written a letter to express my wish that, in the event of my becoming incapacitated, I do not wish to have life-saving treatments, I have assumed that my statement includes those burdensome treatments. Supporting the amendments would mean that my wishes and most other advance directives could be disregarded and overturned.

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Baroness Knight of Collingtree: My Lords—

Baroness Murphy: My Lords, I have nearly finished. Comfort is all. The many patients with dementia for whom I have cared often have two serious physical problems at the very end of life. The first is their skin care and the comfortable disposition of their body; and the second is oral care and the hydration of the mouth. Above all, those require good, basic nursing care. It is possible to maintain somebody's hydration without all the artificial, intravenous paraphernalia. When we are near to death, we all crave the right touch more than the right food. It is the individual who has the right to decide in advance, and we should do nothing to undermine that right, as the amendments would.

Baroness Knight of Collingtree: My Lords, the noble Baroness has spoken only about artificially conveyed food and liquid, but the amendment does not refer merely to that. It refers to simple feeding and the fact that, so often, food is too far away, yet none of that has

17 Mar 2005 : Column 1452

been addressed by the noble Baroness. Some of us have a great deal of evidence of patients not being fed ordinarily, let alone with tubes. Would the noble Baroness speak for just one second about that?

Baroness Murphy: My Lords, I agree with the noble Baroness completely, but basic care is in the Bill. The way we must address the best interests of the patients is by proving good clinical practice. I believe that there are safeguards in the Bill. Clause 58, for example, would satisfactorily address the concerns of the noble Baroness. We must tackle the problems that the noble Baroness is raising very vigorously, but this Bill is not the place to do it in this way.

Lord Walton of Detchant: My Lords, I must make absolutely clear, despite the great sincerity and force with which the proposers of the amendment have put forward their case, my reasons for deciding, after very careful thought and consideration, that I cannot support it.

I say to the noble Baroness, Lady Knight, that the Hippocratic oath is no longer sworn by doctors and medical students, and the reason is quite clear: it is totally out of date. It includes all kinds of curious suggestions, such as, "I will not cut persons labouring under the stone", and a whole lot of other things that are totally inappropriate to modern medical practice. But all medical students are taught that their primary concern as doctors is to have a duty of care to their patients, which involves the responsibility, particularly with terminal illness, to offer what many people refer to as "tender loving care", including everything that falls within that category.

As I said on Tuesday, the Select Committee on Medical Ethics, which I chaired, made one or two things absolutely clear and explicit. First, the competent patient, after full explanation of all the potential consequences, has an absolute right to refuse medical treatment even if that will ultimately end in death. That is not suicide or an intending of death but a refusal to accept treatment which the individual accepts as having no benefit or adding nothing to their individual well being. If for that reason a competent patient refuses artificial nutrition and hydration, so be it—that is their own responsibility.

The problem is more difficult with the incompetent patient. I must confess that I would not wish to see the withdrawal of food and fluid from an incompetent patient without exceptional reasons, which are very important. I can say to the noble Baroness, Lady Knight, that if a doctor can be shown not to have fulfilled that duty of care by giving appropriate clinical care to a patient, particularly towards the end of life, that doctor could be reported to the General Medical Council, which would have the absolute right to consider whether under its own guidance the doctor had demonstrated such neglect or disregard of personal responsibilities to the patient as to raise an issue of serious professional misconduct. That is in the GMC's rules; it is something that I remember drafting many years ago.

The defect in the amendment is that it would overturn the decision of the Law Lords in the Appellate Committee in the case of Tony Bland. The

17 Mar 2005 : Column 1453

reason for that is quite simple: Tony Bland and many other patients like him were in a permanent vegetative state, which meant that the cerebral cortex was dead. He and other patients in a similar situation had no awareness of the position which they were in or of their surroundings, and no reflex responsibility indicating that they were in any sense conscious. Tony Bland and other patients in a permanent vegetative state were still able to breathe and their hearts were still beating, but they were unable to swallow, and they were fed by a feeding tube and given food and fluid in that way.

In a patient who is totally unaware of his or her surroundings and who has no function in the cerebral cortex, one cannot then claim that to give feeding by a tube would do harm or impose a burden on that individual. The Law Lords' decision was that the maintenance of artificial hydration and feeding in the case of Tony Bland was not in his best interests. That, I think, is the guidance that we must use; and that is why I am firmly of the opinion that to pass this amendment would have the effect of overturning the decision on Tony Bland and would raise an enormous number of very difficult and anxious cases.

I shall say one thing to my noble friend Lord Alton, whose absolute sincerity in contributing to these debates is unassailable, I am sure. That is, that I have signed an advance directive that simply says that if I become incompetent and am in a terminal illness, I would not wish to have life-sustaining treatment of a particular kind. That falls in line with the treatment-limiting decisions which we hallowed in the House of Lords report from the Select Committee on Medical Ethics, which was accepted by this House. For the advance directive to instruct doctors to withhold certain treatment in an incompetent patient in a terminal illness is not assisted suicide; it is a treatment-limiting decision which is entirely valid under the present law. To impose this amendment would make that extremely difficult. I am afraid that I must tell my noble friend Lord Alton that I find no loophole in the Bill and that any further attempt to delay its passage would be very harmful to the many excellent provisions that exist within it.

Lord Carter: My Lords, I wish to address myself to the phrase in Amendment No. 9A relating to the withdrawal of life-sustaining treatment. A lot of what I was going to say has just been said by the noble Lord, Lord Walton of Detchant, and I need not say any more about the Bland judgment except to quote from a it a crucial sentence by Lord Keith of Kinkel. He referred to the state of Tony Bland's brain and so on, and went on to say:

"The undisputed consensus of eminent medical opinion is that there is no prospect whatever that Anthony Bland will ever make any recovery from his present condition, but that there is every likelihood that he will maintain his present state of existence for many years to come, provided that the medical care which he is now receiving is continued".

17 Mar 2005 : Column 1454

If the medical care could keep him alive for many years to come, it clearly was not harmful or burdensome, and this amendment would mean that the Bland judgment would be overturned.

Lord Alton of Liverpool: My Lords, on that point, I am grateful to the noble Lord, Lord Carter, but does he recall that I raised at an earlier stage of our proceedings the case of Andrew Devine, who also entered a persistent vegetative state, on the same day as Tony Bland. He was a constituent of mine then, when I represented a constituency in Liverpool. The noble Lord will recall that it was at the Hillsborough Liverpool game that these terrible events occurred. Five years later Andrew Devine recovered; he is still alive today and has been fed subsequently. Therefore, the predictive nature of the decisions that have been made cannot always be accurate. Also, it is not the intention of the movers of this amendment to overturn that.

Lord Carter: My Lords, that intervention is extremely helpful, because it goes to the heart of the debate. I do not believe that the noble Lord, Lord Alton, believes that those who care for people who are in a persistent vegetative state should have the power to seek the court's approval for the ending of artificial nutrition and hydration so that their life can come to an end. That is a clear division of opinion, and I entirely respect the noble Lord's sincerity. There are those who believe, entirely sincerely, that the beginning and end of life belongs to the Creator and not to us—and I understand those who feel like that. But I do not believe that they should attempt to impose that opinion on the rest of society through legislation.

To move away from the case of Anthony Bland, there are cases of patients in intensive care who are on life support. If they are on life support, they are completely sedated. The treatment that they receive is not harmful or burdensome. Indeed, the only consolation for the relatives in those situations is that the patient feels nothing. To a use a non-medical term, they are completely paralysed. Such treatment is not harmful or burdensome. There are cases in which the attempt at resuscitation can be successful in preserving life but can lead to irreparable brain damage. Those who care for such people—the relatives and doctors—face an agonising decision regarding the withdrawal of life-sustaining treatment.

Amendment No. 9A, which mentions life-sustaining treatment, would prevent a decision being taken to withhold such treatment. I understand and respect those who as a matter of conscience would not wish to make such a decision, but I do not agree that such a right should be removed from those who might wish to exercise it.

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Lord Lester of Herne Hill: My Lords, I promise not to bore the House by repeating the summary that I attempted to make on Tuesday of the legal and ethical principles reflected in the Bland decision, but I would like briefly to deal with one or two matters that have arisen today on the amendments.

17 Mar 2005 : Column 1455

I should say at the outset that I am perfectly sure that it is not the intention of either the noble Lord, Lord Alton of Liverpool, or the noble Baroness, Lady Knight, to wreck this important Bill, but I have no doubt that the effect of these amendments would be to torpedo the Bill, for the following reason. As the noble Lord, Lord Walton of Detchant, emphasised, there are no loopholes in this Bill. These amendments would overturn not only the Bland decision but all the legal and ethical principles contained in it and would in my view breach the human rights in the convention.

I am perfectly sure, although I am no longer on the Joint Committee on Human Rights, that if these amendments were to be referred to that committee and a legal opinion obtained—which, of course, it is too late now to do—that it too would come to the considered view that these amendments were incompatible with, for example, Article 8 of the convention guaranteeing personal autonomy and Article 3 on dignity, and so on. As I say, however, I will not bore the House with that.

I should like to do a couple of things that I hope will be useful in this debate. The first is to remind the House of the safeguards that have been built into the Bill by the Government with our consent, which it seems to me are extremely important in giving the context.

The first point is that the Bill makes it quite clear that decisions to be taken about any treatment for someone who lacks capacity, whether or not it is life sustaining, must be determined by whether it would be in that person's best interests to receive the treatment. That is Clause 4.

Then, the Bill has been amended to make it clear that when someone is making a determination about whether life-sustaining treatment would be in someone's best interests, they cannot be motivated by a desire to cause the person's death. That is in Clause 4(5). That makes it clear that personal value judgments or a desire that someone should die for whatever reason have no part to play in determining what is in someone's best interests. That amendment ensures that artificial nutrition, for example, is not withheld inappropriately as a result of any value judgments by the decision maker.

Then, in addition to that, Clause 25(6) provides that, in addition to requiring advance decisions that refuse life-sustaining treatment which must be made in writing and witnessed, it is made clear that an advance decision is not applicable to life-sustaining treatment unless it includes a statement that it is to apply to the treatment even if the person's life is at risk. That is Clause 25(5). That makes it clearer than the previous provisions. It requires anyone making an advance decision to refuse life-sustaining treatment not only to specify that they wish to refuse particular life-sustaining treatment, but also to specify that they wish that refusal to apply even if it risks death.

Those safeguards, together with the guidance which I understand will be included in a code of practice, will provide a completely balanced and workable framework to protect the sanctity of life and the patient's interests and, if I may say so, the ethical good practices of the medical profession.

17 Mar 2005 : Column 1456

Clause 26(2) provides that where the doctor is in any doubt about the validity and applicability of an advance decision, she or he can provide treatment according to the person's best interests safe from liability.

I have wearied the House with that because it is important to get the framework right.

In order that the House understands the clash of principle which underlines these amendments, I want to go back, as the noble Lords, Lord Carter and Lord Walton, have done, very briefly to one passage in Bland. I only wish that it were possible to summarise some of these principles. They deal, I think quite clearly, with a different philosophy—a complete different philosophy—from that of the movers of this amendment. For those who want to look it up, it is the 1993 Appeal Cases. The particular passage I am looking at is in the judgment of Sir Thomas Bingham, as he then was—then the Master of the Rolls; he is now, of course, the senior Law Lord—and it has not been mentioned in the House before. At page 809, he began by saying:

"if, presciently, Mr. Bland had given instructions that he should not be artificially fed or treated with antibiotics if he should become a P.V.S. patient, his doctors would not act unlawfully in complying with those instructions but would act unlawfully if they did not comply, even though the patient's death would inevitably follow. If Mr. Bland were a child and a ward of the court, it would decide what was in his best interests, having regard to the views of his parents but not treating them as conclusive . . . This case is novel because Mr. Bland is not a child and a ward of court, he is immune to suffering and, as already stated, he gave no instructions concerning his treatment if he were to become a P.V.S. patient".

I skip the next passage about what is artificial feeding, which the noble Baroness, Lady Murphy, explained very clearly, and why it is part of treatment. But then, Sir Thomas Bingham, as he then was, went on to say:

"It is relevant to consider the objects of medical care . . . traditionally they have been (1) to prevent the occurrence of illness, injury or deformity . . . (2) to cure illness when it does occur; (3) where illness cannot be cured, to prevent or retard deterioration of the patient's conditions; (4) to relieve pain and suffering in body and mind. I doubt if it has ever been an object of medical care merely to prolong the life of an insensate patient with no hope of recovery where nothing can be done to promote any of these objects. But until relatively recently the question could scarcely have arisen since the medical technology to prolong life in this way did not exist".

Then, Sir Thomas Bingham, as he then was, quoted case law from around the world—the United States, New Zealand, Canada—all to the same effect, and the Bland principles reflect those. I would ask those who are interested to look particularly at the New Zealand case that he summarises on pages 810 and 811 which, in my view, are wholly in accordance with Bland and wholly in accordance with the dignity of the individual, with the sanctity of life and with patient autonomy.

The problem about these amendments is that they would take away the Bland principles, even though I understand it to be said that that is not their intention. We know that certainly the noble Baroness, Lady Knight, is no friend of the Bland decision. Previously, I think that she was not very keen on it. But that is not the point. The point is that whether or not

17 Mar 2005 : Column 1457

one is a friend of the Bland decision, in my view, the Bland decision, which is the law of the land, is entirely correct and should not be overturned.

Baroness Knight of Collingtree: My Lords, the record of what we say here is very important. Does the noble Lord not accept—perhaps he was not in his place when I said it—that I have said at least once if not twice that I agreed with the Bland decision? He is wrong in what he has just said.

Lord Lester of Herne Hill: My Lords, I am delighted to hear that and glad to know it, because these amendments cannot stand with Bland.

Baroness Oppenheim-Barnes: My Lords, before the noble Lord sits down, I wonder whether he is aware that in, for example, the United States, one can legally appoint another person to take these decisions on their behalf if their mental or even their physical condition is such that they are unable to make their views known.

Lord Lester of Herne Hill: My Lords, in the United States they use a slightly different test from ours; they use a substituted judgment test rather than a best interests test. But it comes to very much the same thing, and the ethical principles set out in Bland repeat what the Supreme Court of the United States and other courts have said in the United States and Canada. There is no real substantive difference between them. They are all to the same effect. They are all contrary to these amendments.

Lord Patten: My Lords, I do not often trouble your Lordships' House with speeches, but I am troubled by a number of the issues that are raised in these amendments. I also think that the noble Lord, Lord Alton of Liverpool, is right in predicting that there may be a bit of trouble—to use "trouble" again—in another place unless we can find some way of perhaps getting some accommodation between all of us who wish to see this Bill on the statute book. But that said, I think that these amendments which we are considering would ensure that basic care, which includes nutrition and hydration, however provided—as the noble Baroness, Lady Knight of Collingtree, has said, it is not just through tubes but through the mouth—is not withdrawn inappropriately.

I am not a medical man or a lawyer, but I am completely bemused by the classification of "foods and fluids" as medical treatment. I simply do not understand that, despite having read the helpful letters that have been circulated. I have yet to hear a convincing explanation why nutrition and hydration, however so delivered, should be classified as medical treatment and not as basic care—the sort of care that we heard about earlier regarding dealing with bed sores and other issues.

Exactly what medical ailment is being treated? Since when has hunger or thirst been considered an illness? Those things constitute deprivations, not illnesses. It has

17 Mar 2005 : Column 1458

even been established in the case of animals that freedom from hunger and freedom from thirst constitute two of the five welfare considerations to which all domestic animals are entitled. Surely it is not unreasonable for the same criteria to be applied to human beings as are applied in law to animals. If starving a sheep to death is worth a six-month prison sentence—as was reported some months back—how can it be logical, ethical or compassionate to justify the starving to death of a human being? I simply do not understand and I would like to be relieved of my burden of misunderstanding or stupidity by the Minister.

I hasten to add at this point that none of us wants to make unlawful the withdrawal of food and fluids delivered by artificial means from a patient who is in the process of dying, and where the placing of feeding tubes would be regarded as entirely and unduly intrusive and inappropriate—the kind of situation to which the noble Lord, Lord Detchant, to whom I always listen very carefully, has referred in the past—or where, indeed, the risk of placement of feeding tubes would be excessive.

However, in the Leslie Burke case, the High Court declared that it was hard to envisage any circumstances in which withdrawal of assisted nutrition and hydration (ANH)from a sentient patient—the kind of patient to whom the noble Lord, Lord Walton, referred—whether competent or incompetent, would be compatible with the European Convention on Human Rights.

The learned judge—I note that a very learned noble Lord, who is much more learned in the law than I—wishes to intervene.

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Lord Lester of Herne Hill: My Lords, is the noble Lord aware that the decision of my old opponent in the Bland case, Mr Justice Mumby, as he now is, whose arguments were entirely rejected by the House of Lords in the Bland case, but who is now a learned judge, is now under appeal to the Court of Appeal with the consent of Mr Justice Mumby, and that the medical profession itself wishes to be joined and heard as to why that judgment, with which I respectfully disagree in certain respects, is wrong?

Lord Patten: My Lords, I was not aware of the fact of which the noble Lord has just informed your Lordships. However, nothing in what he said prevents me continuing the argument which I was putting before the Chamber as a non-lawyer.

It is worth repeating that in the Leslie Burke case the High Court declared that it was hard to envisage any circumstances in which withdrawal of assisted nutrition and hydration from a sentient patient, whether competent or incompetent, would be compatible with the European Convention on Human Rights. It would be interesting to see what happens during that process but in the mean time I refer to what we have on the record. The learned judge in the Burke case also referred to the suffering of patients caused by dehydration and starvation. Will the Minister confirm what safeguards are in place in this Bill to ensure that patients affected by it do not suffer through the premature and inappropriate

17 Mar 2005 : Column 1459

withdrawal of nutrition and hydration? That to me is a fundamental issue. I suspect that it is also a fundamental issue for many members of all parties in another place.

I am deeply troubled—I am not often deeply troubled, just as I do not often trouble your Lordships' House with a speech—by the fact that the Bill does not provide for judicial scrutiny of decisions to withdraw assisted nutrition and hydration. Therefore, a case might reasonably be made that it is in breach of Article 8 of the European Convention.

Lord Walton of Detchant: My Lords, I hope that the noble Lord will forgive me for interrupting. I wish to put three questions to him. Does he agree that the administration of food and fluid through a feeding tube which invades the human body can be construed as medical treatment? I wholly agree with him that the giving of food and fluid to a sentient patient who is perfectly capable of giving or withholding consent is a part of basic care; that I do not deny. However, the noble Lord may remember that many years ago in connection with the Northern Ireland hunger strikers the whole issue was raised whether doctors had the right to force feed them and to force them to take fluid. After a great deal of ethical consideration, it was decided that they did not have that right. In other words, it still stands that the sentient, competent patient has the absolute right to refuse medical treatment even if he or she also refuses food and fluid.

The other point is that under the Bland judgment, as regards any patient who is in a permanent vegetative state, the tube cannot be removed without the approval of the High Court. This Bill does nothing to change that ruling.

Lord Patten: My Lords, I entirely agree with the noble Lord in every sense that anything which invades the person is a medical treatment, but it may also be the critical way of delivering basic care. On the second point which the noble Lord made, when I was fortunate enough to join your Lordships' House in 1997, I promised myself never to use the words "I remember". However, I am afraid that I am about to break that promise to myself because I do remember in 1981 and 1982, when I was Parliamentary Under-Secretary of State in Northern Ireland—where I had been sent by the noble Baroness, Lady Thatcher, for disobedience for creating too much trouble on the Back Benches—sitting by the bed of the second of the hunger strikers, God rest his soul, when he was two days away from dying of starvation. The hunger strikers drank Highland Spring water. It was a sad and terrible thing to see. Of course, any hunger striker has the right to do exactly what they will with their own bodies in the sense that it was done in the Maze Prison in those dreadful and sad days. I hope that I never have to say "I remember" again in the time I am spared for the service of your Lordships' House.

However, I return to what deeply troubles me, and that is I do not think that the Bill provides for judicial scrutiny of decisions to withdraw ANH. Therefore, it may be in breach of Article 8 of the European Convention on Human Rights. The Joint Committee

17 Mar 2005 : Column 1460

on Human Rights appears to be aware of the Bill's deficiency in relation to that. Paragraph 2.51 of the Joint Committee's 23rd report of Session 2003–04 states that,

"in relation to the withdrawal of ANH, the presumption in favour of life-sustaining treatment is not sufficiently strong in the Bill to satisfy the requirements of Articles 2, 3 and 8 as explained by the High Court in Burke".

In its most recent report—the fourth report of Session 2004–05—which I commend to your Lordships, the Joint Committee urges the Government to amend the Bill to make it clear that if ANH is to be withdrawn or withheld, the document making that refusal or conferring the authority to make that refusal, whether an advance decision or lasting power of attorney, must make it clear that it applies to the refusal of ANH. Otherwise, ANH should continue to be provided, the committee states. The Joint Committee considers that reference to "life-sustaining treatment" is too vague and that people may not appreciate that a decision to refuse life-sustaining treatment would mean that they would be deprived of nutrition and hydration. We are dealing with human beings who may not understand technical terms at the time that they make this commitment. Therefore, I would like to know exactly what action the Government have taken in response to the Joint Committee's report. I am sure that the noble Baroness will tell us that in her response.

The noble Lord, Lord Alton of Liverpool, said that we live in a eugenic society. We have done so for many decades; it is just that it seems to be bubbling up to the surface now. We used to talk about people being "pro-life" and "the politics of pro-life". I do not mean party politics, but the way in which life issues get brought into the political process.

It is interesting for those of us who read the newspapers regularly to see how young female correspondents and commentators, often in their twenties and thirties, are now raising those issues, changing their minds, and changing the ground of argument, as they were once so much in favour of keeping the eugenic society under wraps on matters of abortion that the noble Lord, Lord Alton, referred to. The politics of death, which is the term that I prefer to use, will not necessarily roar but will come quite fast up the political agenda. I know that some people do not like to have some of those issues brought into politics. We had a case of that a week or so ago, when the Prime Minister said that he did not wish to have a particular pro-life/anti-life issue raised in the general election campaign.

None of us who are democrats should ever attempt—as Martin McGuinness has most recently done with the sisters and the fiancée of Mr McCartney who was killed in Northern Ireland—to rule something out of political debate. Anyone who has stood in any election in recent decades will know that those matters of life and death come up from the floor in question and answer sessions, very often promoted by the Church. None of us can rule the key issues out of political debate. The Minister would not seek to prevent that; she is much too sensitive and much too talented, and I better stop there in case I damage her career.

17 Mar 2005 : Column 1461

The issues of life and death and the politics of death will be part and parcel of the next few weeks and the next few years, and we are seeing a major sea change in people's attitudes to those issues. I hope that the Minister can find some way to allow all of us in both Houses who wish to see the Bill on the statute book to vote for it.

Baroness Ashton of Upholland: My Lords, this has been a long and interesting debate. I begin by saying to the noble Baroness, Lady Chapman, who opened the debate, that I was grateful for her words. I want to say something to her at a personal level. When I came into your Lordships' House, I found that I had to get to grips with the fact that the effect of individual words, because we are legislators, is different from that in the world that I came from. I wondered, as the noble Baroness was talking about dealing with words, whether the same thing is happening to her—that sort of journey into understanding that an individual word put in a law can have a huge effect. I shall return to that as I discuss the amendment.

I say to the noble Baroness, Lady Knight, that I would never want to weary her. I fear that sometimes the noble Baroness feels when I say that something is unnecessary, or use what she described as "anodyne" words, that somehow it is a failure to recognise the underlying interest and cause that she speaks for. I want her to know absolutely—I said it on Tuesday and I will say it again—that I fully understand and respect the issues that the noble Baroness has sought to raise. I say again to those noble Lords who have not been present throughout our debates that because of the work of the noble Baroness, it has become a bigger issue in the Department of Health and in the work that we are doing on this Bill to think carefully about how well basic care is provided for patients. I do not dispute or deny any of the individual, sometimes horrific, stories that she has told us, but that is about people not fulfilling their duties properly, and it is something that we need to address. I simply say that it is not addressed by the amendments.

I say to the noble Lord, Lord Alton, that I would never seek to bring anything that could be described as a threat to him. I have tried in the course of the passage of the Bill to meet and discuss with anyone who has asked me about any of the issues that have been around. We have tried to provide information, and we have had two sessions with palliative care experts in the House for noble Lords. I am sorry that the noble Lord, Lord Patten, was not there, I plan to send him the little briefing pack about why ANH is a treatment, which I think he would welcome. I have held open sessions every day that the Bill has been in the House. I have visited hospitals and talked to doctors and to as many experts as I possibly could. On Tuesday, I put forward the best case that I could, supported by some in your Lordships' House and opposed by others, about why I felt that it was unnecessary to do some of the things that the noble Lord, Professor Finnis and the Archbishop of Cardiff have sought.

17 Mar 2005 : Column 1462

12.45 p.m.

There was an opportunity at that stage for those who put forward the amendment to seek the opinion of noble Lords. The noble Lord, Lord Walton, has indicated that he withdrew because he was satisfied, and the noble Lord, Lord Carlile, is of the same mind. The noble Lord, Lord Brennan, indicated to me last night that he would not be pursuing the issue. All I can do is try to persuade noble Lords of the issues. I will do no more than that, and I will not do it in any way other than the appropriate manner that noble Lords would expect; that is what debates are for. The noble Lord must consider whether and how he wishes to pursue this. It is no use saying to me, "In another place there will be concerns". Yes, there will be concerns. Noble Lords will be talking, as they do, to their opposite numbers, as am I. We are in your Lordships' House specifically to deal with the issues before us and to make our decisions and our judgments. Yes, I will continue to talk, but I have no intention of reversing my position as I laid it out on Tuesday. I would not want the noble Lord to think that I would do any other.

I want to make clear the position of the Department of Health on the Burke judgment, because is important. The side issues around the Burke judgment were not around the provision of artificial nutrition and hydration, which we agree when it is in the best interests of a patient should always be provided; there is no issue about that. It was that alongside it came whether a patient could demand any treatment. There are two problems here that the Department of Health is interested in. The first is around clinical judgment. If a patient determines the treatment that they request that is different to a doctor saying, "This is what you need. You can choose to have it or not, but this is what I recommend". Secondly, there is the resource question that we need to get underneath within that. That is why the Department of Health has joined the Burke appeal, not because of the ANH issue, which it is clear about.

The noble Lord said, "Does the Bill support euthanasia?". It does not. Do the Government in this Bill, or do I, support a position of assisted suicide? No, my Lords, we do not, I do not, and I would not put a Bill before your Lordships' House that did anything to change the law on murder, manslaughter, or assisted suicide. I would resign my position. I would not do it, the Government would not do it, and I would not pretend to your Lordships' House if that were the case. This does not do it. People who have talked and debated with us have come to that conclusion. People of great eminence, not least the noble Lord, Lord Walton, and others who have looked carefully either from, as it has tended to be, a legal perspective or a medical perspective, have increasingly said to me, "I have looked, I have listened, I have looked again, and I agree". The noble Baroness, Lady Finlay, who cannot be with us, sent me a letter—I shall not bore your Lordships' House by reading it out—and she is clear that this Bill does not have the loophole.

17 Mar 2005 : Column 1463

Clause 58 is clear; the law on murder, manslaughter and assisted suicide is unaffected. An advance decision cannot require a doctor to do anything, and certainly does not require a doctor to take any step to aid or abet suicide. An advance decision refuses consent to treatment. We all have a right to refuse consent if we have the capacity to do so. The Bill turns what is already in law—the ability to refuse consent—from common law into statute. We have said that when it is about life-sustaining treatment it must be written; it must be specific, and it must be witnessed.

For example, the noble Lord, Lord Alton, and I have talked about a young man of 19 with no apparent condition who comes in with an advance decision written and witnessed saying that he does not want anything done. Where the doctor is sure, because it is obvious that this person has tried to commit suicide, they can treat. The difference is that they can treat without any question of their being taken to court or sued under this Bill. That is a huge and important difference.

The second reason is that even if the decision was not of that type, if the doctor believes that the circumstances have changed in any way—that the treatment has moved on because it was written some time ago or that the individual has done something that suggests that they would not do that or whatever reason—he has only to have any doubt and he can treat, and continue to treat, while seeking advice from the courts if necessary. The Bill makes it much safer and much more protective for people than the current position. That is why it should be on the statute book as soon as possible.

The noble Baroness, Lady Oppenheim-Barnes, who I am pleased to see has joined our debates, raised a question about relatives. In the Bill there is a new right—which, I confess, I thought existed already—that the next of kin will be consulted. I did not know that there was no right in law for that whatever. In the Bill there is a new right for relatives and loved ones to have their voices heard when the doctor is deciding what is in that individual's best interests. I think that it is really important that if my husband, my son, my daughter or my stepchildren were in that position I would be able to be consulted and so would they—as loved ones. That is a very important safeguard. However, if, in that consultation, the doctor had concerns that a loved one was not acting in the best interests of the patient, he can treat. Again, there is a fundamental difference in the position.

I could spend a long time explaining to the noble Lord, Lord Patten, why ANH is a treatment, but I am not going to, because I shall send him the presentation by Professor Rob George, the palliative care expert, which is much better. It is not about classification. What matters in the Bill is ensuring that what is offered to the patient is in his best interests. The whole premise within the Bill is that if you are acting on behalf of someone who lacks capacity, you have to act in his best interests. You cannot do anything that is not in the person's best interests.

17 Mar 2005 : Column 1464

For me, the only thing that could override best interests would be if I had written an advance decision that said, in certain circumstances and in a particular way, I would not want this. So, if I am a Jehovah's Witness I may wish to refuse a blood transfusion for religious reasons, which is my right, and decide to write that in an advance decision. Then, if I end up in a road accident and need a blood transfusion, which is clearly in my best interests, my decision on religious grounds can override that. I personally might not like that; the noble Lord might not like that; but that is the right of an individual.

I also wish to be clear that when it is in the best interests—

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Lord Patten: My Lords, could the Minister now, or at a later stage in her speech, to which I am listening with great care, address the specific question that I asked about why food and water are regarded as a treatment, not basic care?

Baroness Ashton of Upholland: My Lords, I was trying to get around that by offering to send the noble Lord specific details of the two sessions held in your Lordships' House with a palliative care expert. He explained specifically why artificial nutrition and hydration were regarded as a treatment. I was trying not to weary your Lordships House because some of us have considered this matter many times. If the noble Lord wishes me to go through that, I am able to do so. However, I felt that it might be of more use for the noble Lord to be able to reflect on the particulars and to talk to the palliative care expert who has made himself available to discuss these matters with any noble Lord who wishes.

Lord Patten: My Lords, I am grateful to the Minister for giving way a second time and I shall not trouble her again. But I would ask her to reflect on the fact that there may be all sorts of meetings held by all sorts of people with all sorts of views—particular experts in this place, another place or in buildings outside—but it is in this Chamber, in your Lordships' Chamber, where these issues are debated. It is fundamentally undemocratic to suggest that a Minister should not reply to a point, because it happens to have been exhaustively debated in a couple of sessions held by experts in some other place. That is completely wrong.

Lord Lester of Herne Hill: My Lords, before the noble Baroness replies to that, is she aware that the answer was given by the Law Lords, the Court of Appeal and the judge of first instance in Bland? That is the law of the land and it would be pointless to go into it now. The noble Lord and everyone else can read what they have said. That is the law.

Baroness Ashton of Upholland: My Lords, I was also going to say that I covered this matter in Committee. I am not denying the Chamber the opportunity to discuss it, but we have debated these amendments before. Sadly, the noble Lord was not here and was not able to read Hansard. I am sorry that that was the case,

17 Mar 2005 : Column 1465

but I was merely trying to say that I have a way of short-circuiting a whole process, which is to give him a presentation. He could ring the palliative care expert if he wished. He would be available, which I thought would benefit the noble Lord, who could return to the matter if he wished to at another stage. I am very happy to go through the reasons. I trust that the noble Lord will understand that I was not trying to circumvent democracy in any way, shape or form.

The noble Lord, Lord Walton, also specifically addressed this point as an eminent medical professional in describing the invasive nature of the treatment. If you wish to give someone ANH, you must obtain his consent. But there are real consequences for someone who has ANH treatment; for example, you have to watch that he does not become waterlogged, which can be a real problem. Kidney functions must be observed and blood must be regularly taken. For some conditions, ANH is detrimental—for example, with some forms of stomach cancer, where the provision of that food would enable the cancer to grow.

These are all issues that the medical profession believe put ANH into the category of medical intervention and, therefore, treatment—the reason being that you are bypassing the functions of the body and having to monitor the body in particular ways. The noble Lord may not agree with that view. I am not a medical expert, but I have gone to the medical experts and brought them to your Lordships' House so that they could make the position clear. It is also true that there are real side-effects for ANH, of which noble Lords will be aware. There is great discomfort on occasions, bloating or diarrhoea—many burdens that can be felt by the individual when this treatment is provided. So it is carried out with great care and in the right circumstances.

The critical point is that it is carried out when it is in the right and best interests of the patient. To a large extent I agree with the concerns of the noble Baroness, Lady Knight, and the noble Lord, Lord Alton. We should be giving people food and water and artificial nutrition and hydration when it is in their interests. We should not deny people those things. That goes back to the argument or discussion we had on Tuesday about the whole issue of basic care. It is a medical treatment because of the way that it has to be carried out and because of the consequences involved—

Baroness Knight of Collingtree: My Lords, I am grateful to the noble Baroness and I shall be brief. Will she answer two questions? She mentioned clearly that the nearest and dearest have a right to state their opinion. Does that opinion override and take priority over the decision that might have been made by any of the other consultees? As the noble Lord, Lord Patten, said, it seems that the Bill is incompatible with Article 2 of the human rights convention which states that everyone's right to life shall be protected by law. Is that the case? Is the noble Baroness engaged in any consultation about that?

17 Mar 2005 : Column 1466

Baroness Ashton of Upholland: My Lords, we are moving off into other areas. Regarding the first question, we have enshrined the right of a loved one to be consulted, which does not exist at all at the moment. We have also put in the Bill provision for a lasting power of attorney, so you can give to your loved one the ability to act on your behalf in a whole range of issues, including medical treatment. In all of those contexts, we have said that when you are treating someone the best interests of the patient are paramount. So if you have appointed a lasting power of attorney, but, on listening to that person, the doctor feels that he or she is not acting in the best interests of the patient, he can say, "I am not satisfied, I am going to treat; and I am going to go to court to obtain a decision on this".

That is the position. As I have tried to explain, we have made the position much clearer, much safer, but it is skewed and errs on the side of saying: when there is doubt, you treat. What you cannot do, whoever you are, is not to act in the best interests of the patient, because that would be completely wrong.

Our view is that the Bill is entirely compatible with Article 2. We are in discussion with the Joint Committee and will continue to be, but we think that there are no issues that have not been addressed. We are grateful to the committee, which has carried out a great deal of work.

Perhaps I may now deal with the point that underlies much of this issue—and it is worth stating what is in the Bill. I do not think that we can address the kind of negligence issues that have been raised by the noble Baroness in terms of basic care. I have said on many occasions, and I do not wish to weary the noble Baroness or anyone else, that those issues will need to be, and should be, addressed properly. What we have put in the Bill is a new criminal offence of neglect. That will capture professionals, as well as others, who withhold vital care and treatment from a patient in need. That is a substantial step forward, which recognises the importance of that issue.

Lord Alton of Liverpool: My Lords, I welcome that provision and I am grateful to the Government for having included it. If, for example, a cup of tea was put aside and the patient could not reach it because of his incapacity, that would now be a criminal offence. I think that the Minister is right to remind us that that provision is in the Bill.

Baroness Ashton of Upholland: My Lords, I am very grateful to the noble Lord. The provision is important because it is precisely about that point, and we should recognise that. The noble Baroness should take some credit for it, and rightly so.

I want to finish by setting out our three basic reasons for resisting the amendments. The issue of the way in which they are drafted goes back to what I said to the noble Baroness, Lady Chapman, at the beginning of the debate about the effect of words. Often when we discuss amendments, I know what underlies them but it is partly my job to explain what the amendments would do if they

17 Mar 2005 : Column 1467

were included in the law. They would, in fact, force on people in their final days non-beneficial provision of artificial nutrition and hydration and other forms of life-saving treatment, regardless of what was in the patients' best interests. I return to that point as the central plank of my argument.

Sometimes in a palliative care setting—the noble Baroness, Lady Murphy, will know this better than most—it is in a person's best interests for treatment to be withheld because it would confer no real benefit. Doctors balance benefits and burdens when determining whether a treatment is in the best interests of a patient. I remember that in Committee the noble Baroness, Lady Finlay, said that such decisions are determined almost on an hourly basis as the patient moves towards death in his final days. One is then balancing all the time.

In some end-of-life situations, it cannot be assumed that all or any treatments should be given just because they are available. That is not always the right thing for the patient, but the amendment would require that. I do not think that decisions to withhold life-sustaining treatment are taken lightly; they are taken with great love and care. In situations where the patient is dying, it is critical that he does not suffer a painful or undignified death. In palliative care situations, patients are not, and will not be, denied necessary hydration. Suffering is caused only where the care is negligent, and I repeat that that offence is now included in the Bill.

Secondly, under the amendment, patients would not be able to make an advance decision to refuse any form of life-sustaining treatment. That would lead to the situation that I described on Tuesday—it may seem a rather bizarre example but that would be the effect—concerning someone who had, for religious reasons, decided not to receive a particular treatment. That would be okay while the person had capacity but, under the amendment, when he lost consciousness and thus capacity, the advance decision would not count and he would be given the treatment. So it is possible that someone who was going in and out of consciousness would not have his religious views respected, and I would not wish to see that happen. Not only would the amendment affect those who have religious concerns but it would limit the personal autonomy for which we all strive and would create a disparity between what one can refuse contemporaneously and what one can refuse in advance.

Thirdly—this has been said many times and so I shall be brief—the amendment would overturn the Bland judgment. We would not wish to see that happen to that judgment, and the subsequent 36 cases, because it provides a good way of resolving a difficult and heart-breaking situation.

I have taken some time and I hope that my explanation has been helpful to the House. In the spirit of our continuing debates, I hope that I have answered as many of the points as possible and that the noble Baroness, Lady Chapman, will feel able to withdraw her amendment.

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Baroness Chapman: My Lords, I thank the Minister for her very detailed response. It is not my intention to

17 Mar 2005 : Column 1468

overturn the Bland judgment, and I understand what she is saying. I still have concerns about non-dying patients having some treatments withdrawn but, because I hear what the noble Baroness is saying, I shall go away and rethink the matter. For now, I beg leave to withdraw the amendment.

Amendment, by leave, withdrawn.

[Amendment No. 9A not moved.]

Clause 5 [Acts in connection with care or treatment]:

[Amendment No. 10 not moved.]

Clause 6 [Section 5 acts: limitations]:

Baroness Ashton of Upholland moved Amendment No. 11:

Page 4, line 28, at end insert—

"( ) But D does more than merely restrain P if he deprives P of his liberty within the meaning of Article 5(1) of the Human Rights Convention (whether or not D is a public authority)."

The noble Baroness said: My Lords, we now turn to a group of amendments which respond directly to particular concerns raised by the Joint Committee on Human Rights. The committee wanted the Bill to confirm expressly that actions amounting to the deprivation of liberty do not fall within the definition of "restraint" used in the Bill. The amendments achieve that.

Amendments Nos. 11, 37 and 48 clarify that Clauses 6, 11 and 20 do not provide a defence against deprivation of liberty. That means that no one acting in connection with care or treatment under Clause 5, nor an attorney or deputy, may deprive a person who lacks capacity of his liberty. "Restraint" includes only restrictions of liberty.

Amendments Nos. 109, 112 and 108 are merely consequential amendments to ensure that the Bill defines the necessary terms of "public health authority" and the "human rights convention". We recognise that the distinction between restriction of liberty and deprivation is complex, and the Bournewood case is relevant here.

The European Court judgment in the Bournewood case made clear that the question of whether someone has, in fact, been deprived of liberty depends on the particular circumstances of the case. Specifically, the court said at paragraph 89 of the judgment:

"The distinction between a deprivation of, and restriction upon, liberty is merely one of degree or intensity and not one of nature or substance".

As noble Lords are aware, in the Bournewood case the European Court said that further procedural safeguards must be in place whenever deprivation of liberty is used in a person's best interests. I know that noble Lords will want to raise many more detailed concerns in relation to the Bournewood judgment, and I look forward to discussing them fully in relation to our Amendment No. 107. Meanwhile, I hope that this group of amendments addresses the concern of noble Lords and the committee that "restraint", as defined in the Bill, does not cover actions amounting to deprivation of liberty. I beg to move.

On Question, amendment agreed to.

17 Mar 2005 : Column 1469

Clause 7 [Payment for necessary goods and services]:

Lord Goodhart moved Amendment No. 12:

Page 5, line 2, at end insert—

"(3) Subject to subsections (1) and (4), a contract purportedly entered into by a person who lacks capacity to enter into the contract is not enforceable against that person and may be set aside on an application to a court made by or on behalf of that person.
(4) Subsection (3) shall not apply if the following conditions are satisfied—
(a) the terms of the contract are fair to the person lacking capacity,
(b) no other party to the contract knew or should have known that that person lacked or might lack capacity, and
(c) failure to enforce the contract against that person or the setting aside of the contract will cause loss or hardship to another party to the contract.
(5) It shall be for a party seeking to enforce the contract or objecting to its being set aside to prove that the conditions in subsection (4) are satisfied."

The noble Lord said: My Lords, this amendment is of much less serious importance than the one that we have just been discussing. It raises an issue brought to my attention by the CAB.

In English law, a contract entered into by a person lacking capacity can be set aside on his or her behalf only if the other party to the contract knew of the incapacity when he or she entered into the contract. In Scotland, I understand that any contract entered into by a person lacking capacity is unenforceable by the other party, even if the other party was not aware of the lack of capacity at the time of making the contract. According to the CAB, that system works satisfactorily in Scotland. Businesses in Scotland do not pursue claims against customers who turn out to have lacked capacity. It seems to me that, in fact, English law does not go far enough, although Scottish law may go a little too far in making all contracts unenforceable in that situation. I moved an amendment in Committee. I withdrew it after debate and have now returned with what I think is a somewhat improved version.

In its briefing, the CAB refer to two contexts where there is an abuse of people lacking capacity and where remedies in English law are inadequate. The first and obvious one is where someone grossly overcharges a person lacking capacity for supplying goods or services or grossly underpays for property which he acquires from the person lacking capacity. The other context, which is perhaps a little less obvious, is where the person lacking capacity buys at a reasonable price goods or property which are inappropriate or for which the person buying them has no need.

In Committee, I referred to one particular example from my own experience at the Bar involving a man who owned a small hobby farm and bought gigantic cowsheds to install on the farm, threatening ruin to his family. Steps had to be taken to make that impossible.

17 Mar 2005 : Column 1470

Our amendment starts, with proposed new subsection (3) of Clause 7, by providing that any contract entered into by a person lacking capacity is unenforceable against that person and can be set aside by him or her. Of course, the person lacking capacity, or persons acting on his behalf, would always be free to enforce the contract against the other party if it was favourable to the person lacking capacity.

Subsections (4) and (5) of the amendment provide for an exception from the rule that a contract is voidable where certain conditions are satisfied. I shall take my cowsheds example and show how those conditions apply.

The first condition is that the terms of the contract are fair when looked at independently of the surrounding circumstances. As far as I know, the cowshed case involved sheds that were sold at the market price and the terms of the contract were perfectly normal; they were such as would have been insisted on by the supplier with anyone else. So the first condition there is satisfied.

The second condition is that the other party was not aware of the buyer's lack of capacity and had no reason to suspect it. I cannot say whether that condition was satisfied in the cowshed case. Was the buyer's behaviour so strange as to raise doubts about his capacity? Was enough known by the provider of the cowsheds about the size of the farm or the herd involved to indicate that the sheds were wholly inappropriate? We do not know whether there was anything which required investigation.

But, even if there is no cause for suspicion and both the first and second conditions are satisfied, the third condition also has to be satisfied. In the cowshed case, the supplier of the sheds must still show that he would be worse off if the contract were set aside than if the contract had never been entered into. This condition would be satisfied, of course, if the supplier had started building the sheds, had paid employees for working on them and had used materials which could not be recovered. The condition would not be satisfied if the contract could be cancelled at an early stage, before work was done on site or other substantial expenses had been incurred in performing the contract.

I believe the amendment gives protection to people lacking capacity while protecting also the interests of other parties to the contract who have acted properly and would suffer loss through its cancellation. I hope the Government will look on the amendment favourably and accept the principle behind it. I beg to move.

Baroness Ashton of Upholland: My Lords, it was amusing to see the noble Lord, Lord Roper, arrive in the middle of the cowshed explanation.

I have met with officials from the Department of Trade and Industry and my own officials to talk through these issues. I know that this is something about which the noble Lord, Lord Goodhart, feels strongly. I acknowledge, as does the noble Lord, that there is a tricky balance between empowerment and protection. We have also had discussions with the CAB, which we know is interested in this matter.

17 Mar 2005 : Column 1471

On the one hand, we are trying to protect people who lack capacity from being bound by an inappropriate contract into which they may have entered; on the other hand, we are trying to empower people to take as many decisions as they possibly can. These include, perhaps, people with fluctuating capacity due to mental health problems, or people in the early stages of a degenerative disease who can make some decisions and not others. These matters have to be, in a sense, weighed in the balance.

I cannot accept the amendment at this stage because, when I spoke to the officials about this matter, we were very uncertain about what would happen; we did not feel that we had the evidence before us of what the consequences might be. We need to consider whether the existing protections are inadequate and what would be the genuine practical benefits of the amendment. We also need to consider what its potential impact would be on business. That is a matter of great concern to the Department of Trade and Industry in particular.

I am also worried about the risk of disempowering people; that traders might take risk averse action if they are fearful that somehow they will not be able to enforced a contract. We have spoken before about discriminatory issues and how people feel about other people. For example, a person with a learning disability, who is trying to make a contract with someone for the supply of goods, might find himself in a position where the trader is fearful that it will be decided that it is not a real contract and therefore will not do business with that person.

I am sure the noble Lord, Lord Goodhart, will accept that there is also the possibility that his proposal could be used in fraud; that people could claim that they lacked capacity. We must remember that, under the Bill, lacking capacity could mean that you were blind drunk in an A&E ward. You can lack capacity for all kinds of reasons. Therefore there could be fraud where people claim that at a particular moment they had a mental health problem, lacked capacity, and therefore are not liable for what they have just purchased or what they have just done.

The impact goes wider than consumer contracts; it could also affect personal relationships between individuals. These issues affect all vulnerable people, not only those who lack capacity, and I am keen to consider also the wider group.

On a previous occasion I referred to some of the issues we have been addressing, particularly in the Department of Trade and Industry, in regard to doorstep selling—an issue about which I feel very strongly—the unfair commercial practices directive and the Consumer Credit Bill.

I recognise that this is an important matter. I have committed my department—I wish to put this on the record—to carrying out scoping research work to assess whether there is a problem arising from the current law and, if so, the extent of that problem. This will take into account people who lack capacity and the broader group of vulnerable consumers more generally.

17 Mar 2005 : Column 1472

The DCA will also commit to working with the Department of Trade and Industry as part of the implementation strategy of the Bill to ensure that policy development within the DTI on consumer strategy, credit and indebtedness is sensitive to the needs of consumers who lack capacity.

I hope that that commitment will satisfy the noble Lord that I accept and recognise the principles he is seeking to develop. However, I cannot accept the amendment because I fear that we might accidentally do something around the empowerment issues, or something which will have a detrimental effect on business, because we have not had time to scope out the problem. On the basis of the commitment I have given, I hope the noble Lord will feel able to withdraw his amendment.

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Lord Goodhart: My Lords, I am grateful to the noble Baroness. I welcome the fact that her department will undertake a scoping inquiry into the matter. It is an issue of some importance. Although there is a possibility that a situation under the amendment could be a source of abuse, equally there is no doubt that the law as it now stands could be a source of abuse in the other direction.

I hope that in due course something will come of this. However, as I am sure the noble Baroness anticipated, I never intended to push the amendment to a vote. I hope that not too many other farms will be covered in enormous cowsheds in the future. I beg leave to withdraw the amendment.

Amendment, by leave, withdrawn.

Clause 9 [Lasting powers of attorney]:

Baroness Andrews moved Amendment No. 13:

Page 5, line 36, leave out "section" and insert "sections 1 (the principles) and"

The noble Baroness said: My Lords, this is not quite such an entertaining amendment—there is not a cowshed in sight—but, nevertheless, it is important.

In moving Amendment No. 13, I shall speak also to Amendments Nos. 16, 42 and 47, all of which concern attorneys, deputies and the court. I am very pleased to bring the amendments forward because currently the Bill makes specific reference only to Clause 4, the "Best interests" clause. The amendments are a response to the very helpful concerns raised by the noble Earl, Lord Howe, the noble Lord, Lord Kingsland, and the noble Baronesses, Lady Greengross and Lady Barker.

We believe that ensuring that attorneys, deputies and the court follow the principles in Clause 1 is vital if people who may lack capacity are to be given the opportunity to make as many of their own decisions as they can. This, of course, is the burden of the Bill. They are already required to do so by the provisions of the Bill, but we agree with noble Lords that further emphasis would be helpful. This is what we have done.

Let me reiterate that the principles are designed to empower and enable people who, in the past, might have had their lives taken over, their freedoms restricted and their decisions taken from them, albeit on the very good intentions of others. We want to ensure that people are enabled to make as many decisions for themselves as possible, so that they can

17 Mar 2005 : Column 1473

lead as full a life as possible. The extension of those five key principles set out in Clause 1 make that very much more likely. Therefore, I beg to move.

Earl Howe: My Lords, I thank the Government for having responded so positively and constructively to the concerns that I and others raised in Committee. This added emphasis adds value to the Bill. I am grateful to the Government for listening.

On Question, amendment agreed to.

Schedule 1 [Lasting powers of attorney: formalities]:

[Amendments Nos. 14 and 15 not moved.]

Baroness Andrews moved Amendment No. 16:

Page 37, line 5, leave out from "the" to "4" in line 6 and insert "duties imposed on a donee of a lasting power of attorney under sections 1 (the principles) and"

On Question, amendment agreed to.

[Amendments Nos. 17 and 18 not moved.]

Baroness Ashton of Upholland moved Amendment No. 19:

Page 38, line 5, after "severally" insert "in respect of any matter"

The noble Baroness said: My Lords, these amendments concern the Court of Protection and deal with some small, but quite significant, issues, some of which were raised by my noble friend Lord Christopher. We touched on this on Tuesday. Since then, I have had the benefit of a discussion with the master of the court, Master Lush, and we have sought to resolve some of the outstanding issues that he had. We shall resolve them once the Bill is on the statute book.

These amendments allow the Court of Protection to decide whether a lasting power of attorney is valid. That means that the court will be able to "blue pencil" a section of a lasting power of attorney that is ineffective or illegal and leave the remainder of the lasting power of attorney to stand. I have discussed this issue with my noble friend Lord Christopher and I feel sure that he would welcome this amendment, were he here. It is certainly something that the master of the court was concerned that we should deal with. The court can direct the public guardian not to register a lasting power of attorney whose flaws would make it inoperable. That is an important safeguard.

Amendment No. 29 enables the Court of Protection to make a decision where there is an objection to a lasting power of attorney. That is particularly important when objections are not matters of fact; for example, if someone objects because they think that the proposed attorney lacks capacity.

In Amendments Nos. 19, 35, 36, 40, 41 and 45 we are ensuring that a donor of a lasting power of attorney has all possible options when wanting to appoint more than one donee. So a donor can specify, on different matters, that all the donees must act together or that any or all of them may act. The donor could say, for example, that any of their chosen attorneys can act in relation to most matters, but, if they were selling the

17 Mar 2005 : Column 1474

donor's house, they must all act together. Amendment No. 45 gives the same flexibility to the Court of Protection when it appoints deputies.

Amendment No. 43 will help to ensure that the arrangements for supervising court-appointed deputies are robust, but I hope not too bureaucratic. The court will be able to grant powers to the deputy on condition that it first obtains the public guardian's consent for certain actions. It is important that the deputies are, of course, properly supervised, but it would be disproportionately burdensome and costly to require them to apply to the court all the time for authority to act. That supervisory role should properly be undertaken by the public guardian.

Finally, Amendments Nos. 117 and 118 clarify that it will no longer be possible to create an enduring power of attorney once the lasting power of attorney provisions in the Bill come into effect. I beg to move.

Earl Howe: My Lords, once again, I thank the Government for introducing these amendments, which I agree are beneficial to the Bill. They provide welcome flexibility. The safeguards are still there, but at the same time the Government have ensured that the bureaucracy and procedural aspects are kept to the absolute minimum. I am very happy to endorse the inclusion of the amendments.

On Question, amendment agreed to.

Baroness Ashton of Upholland moved Amendment No. 20:

Page 38, line 16, leave out "11" and insert "10A"

On Question, amendment agreed to.

[Amendments Nos. 21 to 25 not moved.]

Baroness Ashton of Upholland moved Amendment No. 26:

Page 38, line 43, at end insert—

"Instrument not made properly or containing ineffective provision

10A (1) If it appears to the Public Guardian that an instrument accompanying an application under paragraph 4 is not made in accordance with this Schedule, he must not register the instrument unless the court directs him to do so.
(2) Sub-paragraph (3) applies if it appears to the Public Guardian that the instrument contains a provision which—
(a) would be ineffective as part of a lasting power of attorney, or
(b) would prevent the instrument from operating as a valid lasting power of attorney.
(3) The Public Guardian—
(a) must apply to the court for it to determine the matter under section 23(1), and
(b) pending the determination by the court, must not register the instrument.
(4) Sub-paragraph (5) applies if the court determines under section 23(1) (whether or not on an application by the Public Guardian) that the instrument contains a provision which—
(a) would be ineffective as part of a lasting power of attorney, or
(b) would prevent the instrument from operating as a valid lasting power of attorney.
(5) The court must—

17 Mar 2005 : Column 1475

(a) notify the Public Guardian that it has severed the provision, or
(b) direct him not to register the instrument.
(6) Where the court notifies the Public Guardian that it has severed a provision, he must register the instrument with a note to that effect attached to it."

On Question, amendment agreed to.

[Amendments Nos. 27 and 28 not moved.]

Baroness Ashton of Upholland moved Amendment No. 29:

Page 39, line 17, leave out sub-paragraph (2) and insert—

"(2) If the Public Guardian is satisfied that the ground for making the objection is established, he must not register the instrument unless the court, on the application of the person applying for the registration—
(a) is satisfied that the ground is not established, and
(b) directs the Public Guardian to register the instrument."

On Question, amendment agreed to.

[Amendments Nos. 30 and 31 not moved.]

Baroness Ashton of Upholland moved Amendments Nos. 32 to 34:

Page 40, line 28, at end insert—

"17A (1) Sub-paragraph (2) applies if the court determines under section 23(1) that a lasting power of attorney contains a provision which—
(a) is ineffective as part of a lasting power of attorney, or
(b) prevents the instrument from operating as a valid lasting power of attorney.
(2) The court must—
(a) notify the Public Guardian that it has severed the provision, or
(b) direct him to cancel the registration of the instrument as a lasting power of attorney."
Page 41, line 10, at end insert—

"Severance of ineffective provisions

21A If in the case of a registered instrument the court notifies the Public Guardian under paragraph 17A(1)(a) that it has severed a provision of the instrument, the Public Guardian must attach to it a note to that effect."
Page 41, line 13, leave out "or 21" and insert ", 21 or 21A"

On Question, amendments agreed to.

Clause 10 [Appointment of donees]:

Baroness Ashton of Upholland moved Amendments Nos. 35 and 36:

Page 6, line 9, at end insert ", or

(c) jointly in respect of some matters and jointly and severally in respect of others"
Page 6, line 10, leave out "If" and insert "To the extent to which"

On Question, amendments agreed to.

Baroness Andrews: My Lords, I beg to move that further consideration on Report be now adjourned. In moving the Motion I suggest that the Report stage begin again not before 2.27 p.m.

17 Mar 2005 : Column 1476

Moved accordingly, and, on Question, Motion agreed to.

Gender Recognition (Approved Countries and Territories) Order 2005

Lord Evans of Temple Guiting rose to move, That the draft order laid before the House on 20 January be approved [7th Report from the Joint Committee].

The noble Lord said: My Lords, in laying this order for affirmative resolution, the Government are fulfilling commitments they made to both Houses following the recommendations of the Delegated Powers and Regulatory Reform Committee. The noble Baroness, Lady Buscombe, and the noble Lords, Lord Goodhart and Lord Carlile, proposed amendments to that effect.

Members of this House might find it useful if I briefly outline the main objectives of the Gender Recognition Act before considering the detail of this order. The Act provides transsexual people with legal recognition of an everyday reality: the gender to which they now belong—their acquired gender. This is no mere legal technicality. It determines who an individual can marry, their pension rights and much else.

The effect of legal recognition will be that the transsexual person is entitled to be treated for all purposes as a person of the acquired gender, and gains the legal rights and responsibilities appropriate to that gender. The Act sets out clear criteria against which a transsexual person applying for legal recognition will be assessed. Each application will be properly scrutinised by a Gender Recognition Panel, composed of people with legal and medical qualifications. That application process is robust, credible and sustainable, and was recognised as such by Parliament during the passage of the Bill.

In drawing up that application process we had to be mindful of the fact that many other countries already grant legal recognition to transsexual people in their acquired gender. This is something we cannot ignore when so many UK citizens live and work overseas and just as many overseas citizens live and work in the UK. That is why Parliament agreed to include in the Act a process whereby a person who has gained legal recognition overseas can also gain legal recognition in the UK.

However, Parliament also agreed that it was only fair to provide such individuals with a simpler process for gaining recognition in the UK. They will have already changed their gender and obtained legal recognition for that change. It would be unfair and unnecessary if, at the end of that long journey, they were required to repeat the full legal process in the UK.

At the same time, Parliament and the Government were rightly concerned to ensure that the criteria set out in the Act were not compromised. If we were not alive to that danger, a person who did not expect to receive recognition in the UK could potentially go overseas to a country with much softer criteria. If by virtue of that overseas recognition that person also gained

17 Mar 2005 : Column 1477

recognition in the UK, others would follow and the integrity and credibility of the process in the Gender Recognition Act would be damaged.

This order protects the integrity of the application process in the Gender Recognition Act. We have undertaken careful research to identify those countries and territories which have a process for legal recognition at least as rigorous as our own, and it is our intention to publish details of that research on the Gender Recognition Panel website.

The precise criteria for legal recognition of a change of gender are of course not standardised across the world. In drawing up this list we applied two key criteria: first, we allowed only countries or territories that provide legal recognition for gender change—the UK Act is about legal recognition and we felt that we should only approve others which had taken the same decisive step; and, secondly, we allowed only countries or territories where the process of legal recognition is such as to demonstrate the permanence of the decision to change gender.

Of course that meant that there were countries which did not meet these tests. For example, one country which did not pass muster was Bosnia-Herzegovina. There, while there is a unique citizen's code which refers to "change in gender", the local police station makes the decision on change of name and change of gender. The legal adviser we contacted said that it was probable that such a decision would be based on documentation issued by a competent hospital. This was not good enough.

The order can be revised as countries or territories establish new schemes for legal recognition. The links we have forged with contacts overseas through the Foreign and Commonwealth Office will enable us to keep the list of countries or territories up to date.

Once alerted, we will investigate, and if we are satisfied that the criteria for recognition meets with our requirements in terms of legality and permanence, an amending order will be brought before the House.

Using the same network of contacts, we will also be able to monitor changes in policy which might cause us to withdraw a country or territory from the approved list. However, as countries which appear in this order recognise gender change in law it would be unusual for there to be any resiling from this position.

The order has been consulted on and has received the support of the transsexual community.

In summary, the order provides clarity as to those countries or territories with a process for legal recognition which we can trust. A transsexual person who has been recognised in any of the countries or territories on this list will have undergone a process of gender reassignment with the intention of living permanently in their acquired gender. I commend the order to the House.

Moved, That the draft order laid before the House on 20 January be approved [7th Report from the Joint Committee].—(Lord Evans of Temple Guiting.)

Lord Henley: My Lords, I thank the noble Lord for that very full and helpful explanation of exactly what is

17 Mar 2005 : Column 1478

behind the order. By giving that very full explanation most of my questions have been answered. In particular, I wanted to ask about the details of how the Government intend to check on the rigorousness of tests in other countries overseas. For example, in Bosnia-Herzegovina it seems that one just goes along to the local police station to have one's change of gender ratified. I am grateful for the explanation that that is not appropriate. The country cannot be put on the list at the moment, unless it improves its tests in the future.

The noble Lord went on to say that there would be further orders in due course as evidence appeared from other countries on whether their tests were suitably rigorous, and the Department for Constitutional Affairs would be able to recognise them. How often will it be necessary to come to the House with further orders adding countries? I cannot remember whether under the Act it is only the first such order that needs to have affirmative resolution. Subsequent orders might not be possible with this particular order because of what happened at the time of the passing to the Act, but perhaps subsequent orders might be introduced under the negative procedure. Otherwise, the noble Lord will have to come to the House presumably with some regularity as he adds Bosnia-Herzegovina, then Idaho or India or whatever other country or state of the United States has been left out. I put that forward as an idea. It is certainly something that might be thought of in the future.

I have one further minor question. In the Explanatory Memorandum we are told that a regulatory impact assessment has been prepared. I am sorry I misread that. I see that one has not been prepared. I failed to notice the "not". I had some doubts as to what on earth any regulatory impact assessment could look at in this order. But I am glad to see that one has not been prepared on this occasion.

With that perhaps I may say that I welcome this order. I shall be interested to know how many further orders we will have to see in the future and how often.

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Lord Goodhart: My Lords, we fully supported the legislation under which the order is made. We are very happy to support this legislation.

I am glad that the order includes a large number of territories. It includes the whole of Australia, almost the whole of Canada, 46 out of the 50 states of the USA, together with New Zealand, all the major European states and most of the minor ones. There are obvious gaps. For instance, the list does not as yet include any state that is wholly within Asia. It includes Turkey and Russia, both of which are partly within Asia. It includes no states from Latin America and it includes only South Africa from the states of Africa.

So I hope that in due course it will be possible to come back; that the changes in the law which have been adopted here by the Gender Recognition Act and in many other countries will spread to those parts of the world as well; and that it will be possible therefore

17 Mar 2005 : Column 1479

to get extensions from time to time with the approved countries. We feel that this is certainly a very big step in the right direction. We are entirely happy with it.

Lord Evans of Temple Guiting: My Lords, I am grateful for the welcome the order has received. There were a few questions from the noble Lords, Lord Henley and Lord Goodhart, with which I shall deal. The noble Lords might be interested in the criteria that we apply to territories when we engage in discussion with them. The speaking note is a long one. I shall not try and précis it because that will not do it justice, but I will make sure that both noble Lords have a copy of it because it is very interesting.

I move on quickly to the recognition of the noble Lord, Lord Goodhart, that the list of countries is a very good one, although there are sad omissions. It will also be interesting for the noble Lords to see the list of countries and those with which we have decided we cannot make an arrangement at the moment.

The noble Lord, Lord Henley, helpfully asked whether subsequent orders will be by affirmative or negative resolution. They will have to be made by a affirmative resolution: that was the arrangement that we made. However, we do not expect to be coming back to the House regularly. It is really too early to tell, but there may be an order once in every parliament. I am grateful for the welcome that the order has received. It is terrifically important and I commend it to the House.

On Question, Motion agreed to.

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Fibrillation & Cardiac Arrhythmia via HYPOglycemia ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Tue, 24 Jun 2008 21:39:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.
CARDIAC ARRHYTHMIA = HYPOglycemia patterns ?????

J Small Anim Pract. 2005 Sep;46(9):445-8.Links

Comment in:: J Small Anim Pract. 2005 Sep;46(9):423-4.

HYPOglycemic 'ultra-low pulse' and associated circulatory collapse in a dog and a cat.

Little CJ.

Barton Veterinary Hospital, 34 New Dover Road, Canterbury, UK ...

HYPOglycemia was accompanied by sinus bradycardia [protective ultra-low pulse] and circulatory collapse in a dog and a cat.

In each case, when the

HYPOglycemia was corrected by intravenous infusion of a glucose solution ... the substantial reduction of pulse [to very low fatal/levels] and circulatory failure were soon abolished, indicating that these alleged 'abnormalities' were caused by the HYPOglycemia.

Similar observations have been made in Human Patients. To the author's knowledge, this is the first report documenting HYPOglycemia induced substantial reduction of pulse [to very low fatal/levels] and circulatory failure ... in veterinary medicine.

PMID: 16167596

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Eur J Emerg Med. 2003 Dec;10(4):331-3. Links

Ultra-low pulse related to HYPOglycemia.

Navarro-Gutiérrez S, González-Martínez F, Fernández-Pérez MT, García-Moreno MT, Ballester-Vidal MR, Pulido-Morillo FJ.

sergionavarrog@hotmail.com
Department of Emergency Medicine, Hospital Virgen de la Luz, Cuenca, Spain ...

Alterations in blood glucose levels are known to be involved in electrocardiogram changes.

Various types of arrhythmias have been reported.

We present here the case of an 81-year-old Woman presenting

with transient atrial fibrillation while being treated for HYPOglycemia with dextrose infusion, and subsequently developing a 'healthy' sinus rhythm.

The presence of alterations in glucose blood levels should always be considered as a potential cause of transient atrial fibrillation.

PMID: 14676515

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Acad Emerg Med. 1996 Jul;3(7):700-7.Links

HYPOglycemia manifested by sinus bradycardia: a report of three cases.

Pollock G, Brady WJ Jr, Hargarten S, DeSilvey D, Carner CT.

Department of Emergency Medicine, University of Pittsburgh, PA, USA ...

Three cases are reported of HYPOglycemia manifested by profound sinus 'ultra-low potentially fatal pulse rates' and fatigue, which

responded to i.v. dextrose with prompt normalization of the cardiac rhythm.

The cases involved 3 different Patients and disease processes:-

1. a young Female who had anorexia nervosa and profound malnutrition; and

2.. an elderly, non-Diabetic Male who subsequently experienced a transient ischemic attack [FOLLOWING HYPERINSULINEMIA-INDUCED RELATIVE-HYPOGLYCEMIA DISTRESS ?]: and

3... a Patient who had diabetes mellitus managed with chronic, subcutaneous insulin administration.

It is vitally important that the emergency Physician recognize unusual clinical manifestations of HYPOglycemia and fully evaluate such scenarios when HYPOglycemia may occur.

Untreated, HYPOglycemia may result in significant chronic morbidity, and rarely, in death.

Bradyarrhythmias--particularly sinus bradycardia -- should be added to the list of potential clinical manifestations of HYPOglycemia.

PMID: 8816187

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Ann Emerg Med. 1990 May;19(5):565-7. Links

Transient atrial fibrillation precipitated by HYPOglycemia.

Odeh M, Oliven A, Bassan H.

Department of Internal Medicine B, Bnai Zion Medical Center, Haifa, Israel ...

Two non-insulin-dependent Diabetic Patients developed transient atrial fibrillation precipitated by HYPOglycemia

that reverted to 'normal' sinus rhythm after administration of IV dextrose.

Atrial fibrillation as a complication of HYPOglycemia in Diabetic Patients has previously been reported in only two Patients ... with insulin-dependent diabetes mellitus.

PMID: 2331103

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

Postgrad Med J. 1987 Oct;63(744):895-7.Links

Transient atrial fibrillation precipitated by HYPOglycemia: two case reports.

Collier A, Matthews DM, Young RJ, Clarke BF.

Diabetic and Dietetic Department, Royal Infirmary, Edinburgh, UK ...

We describe

two insulin-dependent Diabetic Females who presented with severe HYPOglycemia associated with atrial fibrillation which reverted to 'healthy' sinus rhythm after intravenous dextrose.

Atrial fibrillation has not previously been reported as a complication of HYPOglycemia in ... insulin-dependent Diabetic Patients.

PMID: 3328849

http://www.ConsciousMediaNetwork.cOM/members/jbarrett.htm

ATP starvation, Co-Q10 starvation, Nicotinic Acid starvation, Glucose starvation, Water starvation, Ketosis starvation, Fuel-anemia ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Mon, 23 Jun 2008 22:40:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

Coenzyme Q10

Ubiquinone

Coenzyme Q₁₀ (also known as ubiquinone, ubidecarenone, coenzyme Q, and abbreviated at times to CoQ₁₀, CoQ, Q10, or Q) is a benzoquinone, where Q refers to the quinone chemical group, and 10 refers to the isoprenyl chemical subunits.

This vitamin-like substance is, by nature, present in most human cells except red blood cells and eye lens cells (no mitochondria) and is responsible for the production of the body’s own energy. In each human cell, food energy is converted into energy in the mitochondria with the aid of CoQ₁₀. Ninety-five percent of all the human body’s energy requirements (ATP) is converted with the aid of CoQ₁₀.^[1]^[2] Therefore, those organs with the highest energy requirements – such as the heart and the liver – have the highest CoQ₁₀ concentrations.^[3]^[4]^[5]

History

Coenzyme Q was first discovered by professor Fred L. Crane and colleagues at the University of Wisconsin-Madison Enzyme Institute in 1957.^[6]^[7] In 1958, its chemical structure was reported by Professor Karl Folkers and coworkers at Merck.^[8]^[7]

Chemical properties

The oxidized structure of CoQ, or Q, is given here. The various kinds of Coenzyme Q can be distinguished by the number of isoprenoid side-chains they have. The most common CoQ in human mitochondria is Q₁₀. The image to the right has three isoprenoid units and would be called Q₃.

If Coenzyme Q is reduced by one equivalent, the following structure results, a ubisemiquinone, and is denoted QH. Note the free-radical on one of the ring oxygens (either oxygen may become a free-radical, in this case the top oxygen is shown as such).

If Coenzyme Q is reduced by two equivalents, the compound becomes a ubiquinol, denoted QH₂:

Biochemical role

Electron transport chain ("UQ" visible in green near center.)

CoQ is found in the membranes of endoplasmic reticulum, peroxisomes, lysosomes, vesicles, and the inner membrane of the mitochondrion, where it is an important part of the electron transport chain; there it passes reducing equivalents to acceptors such as Coenzyme Q: cytochrome c - oxidoreductase:

CoQH₂+ 2 Fe^III-cytochrome c → CoQ + 2 Fe^II-cytochrome c

CoQ is also essential in the formation of the apoptosome, along with other adapter proteins. The loss of trophic factors activates pro-apoptotic enzymes, causing the breakdown of mitochondria.

Supplementation

Because of its ability to transfer electrons and therefore act as an antioxidant, Coenzyme Q is also used as a dietary supplement. When you are younger the body can synthesize Q₁₀ from the lower-numbered ubiquinones such as Q₆ or Q₈.^{[citation needed]} The sick and elderly may not be able to make enough, thus Q₁₀ becomes a vitamin later in life and in illness.^{[citation needed]}

Mitochondrial disorders

Supplementation of Coenzyme Q₁₀ is a treatment for some of the very rare and serious mitochondrial disorders and other metabolic disorders, where patients are not capable of producing enough coenzyme Q₁₀ because of their disorder. Coenzyme Q₁₀ is then prescribed by a physician.^[9]

Migraine headaches

Supplementation of Coenzyme Q₁₀ has been found to have a beneficial effect on the condition of some sufferers of migraine headaches. So far, three studies have been done, of which two were small, did not have a placebo group, were not randomized, and were open-label,^[10] and one was a double-blind, randomized, placebo-controlled trial, which found statistically significant results despite its small sample size of 42 patients.^[11] Dosages were 150 to 300 mg/day.

Cancer

It is also being investigated as a treatment for cancer, and as relief from cancer treatment side-effects.^[12]

Brain health and neurodegenerative diseases

Recent studies have shown that the antioxidant properties of Coenzyme Q₁₀ benefit the body and the brain in animal models.^[13] Some of these studies indicate that Coenzyme Q₁₀ protects the brain from neurodegenerative disease such as Parkinson's,^[14] although it does not relieve the symptoms.^[15] Dosage was 300 mg per day.

Cardiac arrest

Another recent study shows a survival benefit after cardiac arrest if coenzyme Q₁₀ is administered in addition to commencing active cooling (to 32–34 degrees Celsius).^[16]

Blood pressure

There are several reports concerning the effect of CoQ₁₀ on blood pressure in human studies.^[17] In a recent meta-analysis of the clinical trials of CoQ₁₀ for hypertension, a research group led by Professor FL Rosenfeldt (from the Cardiac Surgical Research Unit, Alfred Hospital, Melbourne, Australia) reviewed all published trials of Coenzyme Q₁₀ for hypertension, and assessed overall efficacy, consistency of therapeutic action, and side-effect incidence. Meta-analysis was performed in 12 clinical trials (362 patients) comprising three randomized controlled trials, one crossover study, and eight open-label studies. The research group concluded that coenzyme Q₁₀ has the potential in hypertensive patients to lower systolic blood pressure by up to 17 mm Hg and diastolic blood pressure by up to 10 mm Hg without significant side-effects.^[18]

Lifespan

Studies have shown that low dosages of Coenzyme Q₁₀ reduce oxidation and DNA double-strand breaks, and a combination of a diet rich in polyunsaturated fatty acids and Coenzyme Q₁₀^[19] supplementation leads to a longer lifespan in rats

Biosynthesis

The benzoquinone portion of Coenzyme Q₁₀ is synthesized from tyrosine, whereas the isoprene acetyl-CoA through the mevalonate pathway. The mevalonate pathway is used for the first steps of cholesterol biosynthesis. sidechain is synthesized from

Inhibition by statins and beta blockers

Coenzyme Q₁₀ shares a common biosynthetic pathway with cholesterol. The synthesis of an intermediary precursor of Coenzyme Q₁₀, mevalonate, is inhibited by some beta blockers, blood pressure-lowering medication,^[20] and statins, a class of cholesterol-lowering drugs.^[21] Statins can reduce serum levels of coenzyme Q₁₀ by up to 40%.^[22] Some research suggests the logical option of supplementation with coenzyme Q₁₀ as a routine adjunct to any treatment that may reduce endogenous production of coenzyme Q₁₀, based on a balance of likely benefit against very small risk.^[23]^[24]

Occurrence in nature

CoQ10 occurs in mackerel and herring fresh heart tissue in concentrations of 105-148 μg/g. In fresh mackerel "red and white tissue," CoQ10 concentrations of 67 and 15 μg/g, respectively, have been reported. In fresh herring tissue, an amount of 15–24 μg/g of CoQ10 has been reported.^[25]

CoQ10 Content of various foods:^[26]

Food	CoQ10 [μg/g]	Portion of Food [g]	CoQ10 Amount in Portion [mg]
Pork heart	203	120	24
Chicken leg	17	120	2.0
Beef heart	41	120	4.8

References

^ Ernster L, Dallner G: Biochemical, physiological and medical aspects of ubiquinone function. Biochim Biophys Acta 1271: 195-204, 1995
^ Dutton PL, Ohnishi T, Darrouzet E, Leonard, MA, Sharp RE, Cibney BR, Daldal F and Moser CC. 4 Coenzyme Q oxidation reduction reactions in mitochondrial electron transport (pp 65-82) in Coenzyme Q: Molecular mechanisms in health and disease edited by Kagan VE and Quinn PJ, CRC Press (2000), Boca Raton
^ Okamoto, T.et al (1989) Interna.J.Vit.Nutr.Res.,59,288-292
^ Aberg,F.et al (1992)Archives of Biochemistry and Biophysics, 295, 230-234
^ Shindo, Y., Witt, E., Han, D., Epstein, W., and Packer, L., Enzymic and non-enzymic antioxidants in epidermis and dermis of human skin, Invest. Dermatol., 102 (1994) 122-124.
^ Crane F, Hatefi Y, Lester R, Widmer C (1957). "Isolation of a quinone from beef heart mitochondria". Biochim Biophys Acta 25 (1): 220–1. doi:10.1016/0006-3002(57)90457-2. PMID 13445756.
^ ^a ^b Peter H. Langsjoen, "Introduction of Coezyme Q10"
^ Wolf DE, Hoffman CH, Trenner NR, Arison BH, Shunk CH, Linn BD, McPherson JF, and Folkers K. Structure studies on the coenzyme Q group. J Am Chem Soc 1958: 80:4752.
^ Berbel-Garcia, A.; et al. (July 2004). "Coenzyme Q 10 improves lactic acidosis, strokelike episodes, and epilepsy in a patient with MELAS". Clinical Neuropharmacology 27: 187–191. doi:10.1097/01.wnf.0000137862.67131.bf. PMID 15319706.
^ Rozen T, Oshinsky M, Gebeline C, Bradley K, Young W, Shechter A, Silberstein S (2002). "Open label trial of coenzyme Q10 as a migraine preventive". Cephalalgia 22 (2): 137–41. doi:10.1046/j.1468-2982.2002.00335.x. PMID 11972582.
^ Sándor PS, et al. (2005). "Efficacy of coenzyme Q10 in migraine prophylaxis: A randomized controlled trial". Neurology 64: 713–715. doi:10.1212/01.WNL.0000151975.03598.ED. PMID 15728298.
^ Katsuhisa Sakano, Mami Takahashi, Mitsuaki Kitano, Takashi Sugimura, Keiji Wakabayashi: Suppression of Azoxymethane-induced Colonic Premalignant Lesion Formation by Coenzyme Q10 in Rats. Asian Pacific J Cancer Prev, 7, 599-603, 2006
^ Matthews, R. T.; et al. (July 1998). "Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects". PNAS 95: 8892–8897. doi:10.1073/pnas.95.15.8892. PMID 9671775.
^ Biol Signals Recept. 2001 May-Aug;10(3-4):224-53
^ Alexander Storch, MD; Wolfgang H. Jost, MD; Peter Vieregge, MD; Jörg Spiegel, MD; Wolfgang Greulich, MD; Joachim Durner, MD; Thomas Müller, MD; Andreas Kupsch, MD; Henning Henningsen, MD; Wolfgang H. Oertel, MD; Gerd Fuchs, MD; Wilfried Kuhn, MD; Petra Niklowitz, MD; Rainer Koch, PhD; Birgit Herting, MD; Heinz Reichmann, MD; for the German Coenzyme Q10 Study Group (2007-05-14). Randomized, Double-blind, Placebo-Controlled Trial on Symptomatic Effects of Coenzyme Q10 in Parkinson Disease. Archives of Neurologu.
^ Damian, M. S.; et al. (July 2004). "Coenzyme Q10 Combined With Mild Hypothermia After Cardiac Arrest". Circulation, American Heart Foundation 110: 3011–3016. doi:10.1161/01.CIR.0000146894.45533.C2. PMID 15520321.
^ Cupp MJ and Tracy TS. Chapter 4: Coenzyme Q10 (Ubiquinone, Ubidecarenone), pp 53-85 in Dietary Supplements edited by Cupp MJ and Tracy TS Humana press, Totowa, New Jersey (2003)
^ Rosenfeldt FL, Haas SJ, Krum H, Hadj A, Ng K, Leong J-Y, Watts GF. Coenzyme Q₁₀ in the treatment of hypertension: a meta-analysis of the clinical trials. J Human Hypertension 21: 297-306, 2007
^ Quiles JL, Ochoa JJ, Huertas JR, Mataix J (2004). "Coenzyme Q supplementation protects from age-related DNA double-strand breaks and increases lifespan in rats fed on a PUFA-rich diet.". Exp Gerontol. 39 (2): 189–94. doi:10.1016/j.exger.2003.10.002. PMID 15036411.
^ Kishi T, Watanabe T, Folkers K (1977). "Bioenergetics in clinical medicine XV. Inhibition of coenzyme Q10-enzymes by clinically used adrenergic blockers of beta-receptors". Res Commun Chem Pathol Pharmacol 17 (1): 157–64. PMID 17892.
^ The Synthesis of Cholesterol
^ Ghirlanda G, Oradei A, Manto A, Lippa S, Uccioli L, Caputo S, Greco A, Littarru G (1993). "Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double-blind, placebo-controlled study". J Clin Pharmacol 33 (3): 226–9. PMID 8463436.
^ Sarter B (2002). "Coenzyme Q10 and cardiovascular disease: a review". J Cardiovasc Nurs 16 (4): 9–20. doi:10.1002/cncr.11242
. PMID 12597259.
^ Thibault A, Samid D, Tompkins A, Figg W, Cooper M, Hohl R, Trepel J, Liang B, Patronas N, Venzon D, Reed E, Myers C (1996). "Phase I study of lovastatin, an inhibitor of the mevalonate pathway, in patients with cancer". Clin Cancer Res 2 (3): 483–91. PMID 9816194.
^ Nathalie Soucheta and Serge Laplante, Seasonal variation of Co-enzyme Q10 content in pelagic fish tissues from Eastern Quebec
^ www.thefactsaboutfitness.com

External links

v • d • e Mitochondrial electron transport chain/oxidative phosphorylation

Primary	Complex I/NADH dehydrogenase - Complex II/Succinate dehydrogenase - Coenzyme Q - Complex III/Coenzyme Q - cytochrome c reductase - Cytochrome c - Complex IV/Cytochrome c oxidase

Other	Alternative oxidase - Electron-transferring-flavoprotein dehydrogenase

v • d • e Enzyme cofactors

Coenzymes	vitamins: NAD⁺ (B3) \| NADP⁺ (B3) \| Coenzyme A (B5) \| THF / H4F (B9), DHF, MTHF \| Ascorbic acid (C) \| Menaquinone (K) \| Coenzyme F420 non-vitamins: ATP \| CTP \| SAM \| PAPS \| GSH \| Coenzyme B \| Coenzyme M \| Coenzyme Q \| Methanofuran \| BH4 \| H4MPT

Organic prosthetic groups	vitamins: TPP / ThDP (B1) \| FMN, FAD (B2) \| PLP / P5P (B6) \| Biotin (B7) \| Methylcobalamin, Cobamamide (B12) non-vitamins: Haem / Heme \| Lipoic acid \| Molybdopterin \| PQQ

Metal prosthetic groups	Ca²⁺ \| Cu²⁺ \| Fe²⁺, Fe³⁺ \| Mg²⁺ \| Mn²⁺ \| Mo \| Ni²⁺ \| Se \| Zn²⁺

Major families of biochemicals Saccharides \| Carbohydrates \| Glycosides \| \| Amino acids \| Peptides \| Proteins \| Glycoproteins \| \| Lipids \| Terpenes \| Steroids \| Carotenoids Alkaloids \| Nucleobases \| Nucleic acids \| \| Enzyme cofactors \| Flavonoids \| Polyketides \| Tetrapyrroles

Retrieved from "http://en.wikipedia.org/wiki/Coenzyme_Q10"

Love Spirit

noreply@blogger.com (Nicholas Dynes Gracey) — Sun, 22 Jun 2008 20:45:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

Love

http://YouTube.cOM/user/adampants2007

For other uses, see Love (disambiguation).

Basic Aspects
Part of a series on Love

Love
Love (scientific views)
Human bonding
Historically
Courtly love
Greek love
Religious love
Types of emotion
Erotic love
Platonic love
Familial love
Puppy love
Romantic love
See also
Unrequited love
Problem of love
Interpersonal relationship
Sexuality
Sexual intercourse
Valentine's Day
This box: view • talk • edit

Love represents a range of human emotions and experiences related to the senses of affection and sexual attraction.^[1] The word love can refer to a variety of different feelings, states, and attitudes, ranging from generic pleasure to intense interpersonal attraction. This diversity of meanings, combined with the complexity of the feelings involved, makes love unusually difficult to consistently define, even compared to other emotional states.

As an abstract concept love usually refers to a strong, ineffable

feeling towards another person. Even this limited conception of love, however, encompasses a wealth of different feelings, from the passionate desire and intimacy of

romantic love to the nonsexual. Love in its various forms acts as a major facilitator of interpersonal relationships and, owing to its central psychological importance, is one of the most common themes in the creative arts.

Definitions

The Kiss by Gustav Klimt.

The English word love can have a variety of related but distinct meanings in different contexts. Often, other languages use multiple words to express some of the different concepts which English relies mainly on love to encapsulate; one example is the plurality of Greek words for "love". Cultural differences in conceptualizing love thus make it doubly difficult to establish any universal definition.^[2] American psychologist Zick Rubin try to define love by the psychometrics. His work states that three factors constitute love: attachment, caring and intimacy.^[3]^[4]

Although the nature or essence of love is a subject of frequent debate, different aspects of the word can be clarified by determining what isn't "love". As a general expression of positive sentiment (a stronger form of like), love is commonly contrasted with hate (or neutral apathy); as a less sexual and more emotionally intimate form of romantic attachment, love is commonly contrasted with lust; and as an interpersonal relationship with romantic overtones, love is commonly contrasted with friendship, though other definitions of the word love may be applied to close friendships in certain contexts. When discussed in the abstract, love usually refers to interpersonal love, an experience felt by a person for another person. Love often involves caring for or identifying with a person or thing, including oneself (cf. narcissism).

In addition to cross-cultural differences in understanding love, ideas about love have also changed greatly over time. Some historians date modern conceptions of romantic love to courtly Europe during or after the Middle Ages, though the prior existence of romantic attachments is attested by ancient love poetry.^[5] Because of the complex and abstract nature of love, discourse on love is commonly reduced to a thought-terminating cliché, and there are a number of common proverbs regarding love, from Virgil's "Love conquers all" to The Beatles' "All you need is love". Bertrand Russell describes love as a condition of "absolute value", as opposed to relative value. Theologian Thomas Jay Oord said that to love is to "act intentionally, in sympathetic response to others, to promote overall well-being".^[6]

A person can be said to love a country, principle, or goal if they value it greatly and are deeply committed to it. Similarly, compassionate outreach and volunteer workers' "love" of their cause may sometimes be borne not of interpersonal love, but impersonal love coupled with altruism

and strong political convictions. People can also "love" material objects, animals, or activities if they invest themselves in bonding or otherwise identifying with that item. If sexual passion is also involved, this condition is called

paraphilia.^[7]

Interpersonal love

Grandmother and grandchild, Sri Lanka

Interpersonal love refers to love between human beings. It is a more potent sentiment than a simple liking for another. Unrequited love refers to those feelings of love which are not reciprocated. Interpersonal love is most closely associated with interpersonal relationships. Such love might exist between family members, friends, and couples. There are also a number of psychological disorders related to love, such as erotomania.

Scientific views

Main article: Love (scientific views)

Throughout history, philosophy and religion have done the most speculation on the phenomenon of love. In the last century, the science of psychology has written a great deal on the subject. In recent years, the sciences of evolutionary psychology, evolutionary biology, anthropology, neuroscience, and biology have added to the understanding of the nature and function of love.

Chemistry

Biological models of sex tend to view love as a mammalian drive, much like hunger or thirst.^[8]Helen Fisher, a leading expert in the topic of love, divides the experience of love into three partly-overlapping stages: lust, attraction, and attachment. Lust exposes people to others, romantic attraction encourages people to focus their energy on mating, and attachment involves tolerating the spouse long enough to rear a child into infancy.

Lust is the initial passionate sexual desire that promotes mating, and involves the increased release of chemicals such as testosterone and estrogen. These effects rarely last more than a few weeks or months. Attraction is the more individualized and romantic desire for a specific candidate for mating, which develops out of lust as commitment to an individual mate forms. Recent studies in neuroscience have indicated that as people fall in love, the brain consistently releases a certain set of chemicals, including pheromones, dopamine, norepinephrine, and serotonin, which act similar to amphetamines, stimulating the brain's pleasure center and leading to side-effects such as an increased heart rate, loss of appetite and sleep, and an intense feeling of excitement. Research has indicated that this stage generally lasts from one and a half to three years.^[9]

Since the lust and attraction stages are both considered temporary, a third stage is needed to account for long-term relationships. Attachment is the bonding which promotes relationships that last for many years, and even decades. Attachment is generally based on commitments such as marriage and children, or on mutual friendship based on things like shared interests. It has been linked to higher levels of the chemicals oxytocin and vasopressin than short-term relationships have.^[9] In 2005, Italian scientists at Pavia University found that a protein molecule known as the nerve growth factor (NGF) has high levels when people first fall in love, but these levels return to as they were after one year. Specifically, four neurotrophin levels, i.e. NGF, BDNF, NT-3, and NT-4, of 58 subjects who had recently fallen in love were compared with levels in a control group who were either single or already engaged in a long-term relationship. The results showed that NGF levels were significantly higher in the subjects in love than as compared to either of the control groups.^[10]

Psychology

Further information: Human bonding

Psychology depicts love as a cognitive and social phenomenon. Psychologist Robert Sternberg triangular

formulated a

theory of love and argued that love has three different components: intimacy, commitment, and passion. Intimacy is a form in which two people share confidences and various details of their personal lives. Intimacy is usually shown in friendships and romantic love affairs. Commitment, on the other hand, is the expectation that the relationship is permanent. The last and most common form of love is sexual attraction and passion. Passionate love is shown in infatuation as well as romantic love. All forms of love are viewed as varying combinations of these three components.

Following developments in electrical theories, such as Coulomb's law, which showed that positive and negative charges attract, analogs in human life were developed, such as "opposites attract". Over the last century, research on the nature of human mating has generally found this not to be true when it comes to character and personality; people tend to like people similar to themselves. However, in a few unusual and specific domains, such as immune systems, it seems that humans prefer others who are unlike themselves (e.g. with an orthogonal immune system), since this will lead to a baby which has the best of both worlds.^[11] In recent years, various human bonding theories have been developed described in terms of attachments, ties, bonds, and affinities.

Some Western authorities disaggregate into two main components, the altruistic and the narcissistic. This view is represented in the works of Scott Peck, whose works in the field of applied psychology explored the definitions of love and evil. Peck maintains that love is a combination of the "concern for the spiritual growth of another", and simple narcissism.^[12] In combination, love is an activity, not simply a feeling.

Scientific models

"Sacred Love versus Profane Love" by Giovanni Baglione

Biological models of love tend to see it as a mammalian drive, similar to hunger or thirst.^{[citation needed]}hormones (such as oxytocin), neurotrophins (such as NGF), and pheromones, and how people think and behave in love is influenced by their conceptions of love. The conventional view in biology is that there are two major drives in love — sexual attraction and attachment. Attachment between adults is presumed to work on the same principles that lead an infant to become attached to its mother. The traditional psychological view sees love as being a combination of companionate love and passionate love. Passionate love is intense longing, and is often accompanied by physiological arousal (shortness of breath, rapid heart rate). Companionate love is affection and a feeling of intimacy not accompanied by physiological arousal. Psychology sees love as more of a social and cultural phenomenon. There are probably elements of truth in both views — certainly love is influenced by

Studies have shown that brain scans of those infatuated by love display a resemblance to those with a mental illness. Love creates activity in the same area of the brain that hunger, thirst, and drug cravings create activity in. New love, therefore, could possibly be more physical than emotional. Over time, this reaction to love mellows, and different areas of the brain are activated, primarily ones involving long-term commitments. Dr. Andrew Newberg, a neuroscientist, suggests that this reaction to love is so similar to that of drugs because without love, humanity would die out.

Cultural views

Persian

- "Even after all this time the sun never says to the earth you owe me. - Look what happens with a Love like that, - It lights the whole Sky." - Iranian ( Persian ) Poet and Mystic, Hafez - Rumi, Hafez and Omar Khayyam are just symbols of the passion and love that the Persian culture and language presents.

Over seven centuries ago, Sa'di, an Iranian poet, wrote the following verses:

- "The children of Adam are limbs of each other - Having been created of one essence. - When the calamity of time afflicts one limb - The other limbs cannot remain at rest. - If thou hast no sympathy for the troubles of others - Thou art unworthy to be called by the name of a man."

Love in Persian is the word Eshgh. In the Persian culture, everything is encompassed by love and all is for love, but for starters we practice loving our friends and family, then our husbands and wives, our country and culture, and eventually the ultimate love of divine love which is the ultimate goal in life.

Chinese and other Sinic cultures

The traditional Chinese character for love (愛) consists of a heart (middle) inside of "accept", "feel", or "perceive", which shows a graceful emotion.

In contemporary Chinese language and culture, several terms or root words are used for the concept of "love":

Ai (愛) is used as a verb (e.g. Wo ai ni, "I love you") or as a noun, especially in aiqing (愛情), "love" or "romance." In mainland China since 1949, airen (愛人, originally "lover," or more literally, "love person") is the dominant word for "spouse" (with separate terms for "wife" and "husband" originally being de-emphasized); the word once had a negative connotation, which it retains among many on Taiwan.

Lian (戀) is not generally used alone, but instead as part of such terms as "being in love" (談戀愛, tan lian'ai—also containing ai), "lover" (戀人, lianren) or "homosexuality" (同性戀, tongxinglian).

Qing (情), commonly meaning "feeling" or "emotion," often indicates "love" in several terms. It is contained in the word aiqing (愛情); qingren (情人) is a term for "lover".

In Confucianism, lian is a virtuous benevolent love. Lian should be pursued by all human beings, and reflects a moral life. The Chinese philosopher Mozi developed the concept of ai (愛) in reaction to Confucian lian. Ai, in Mohism, is universal love towards all beings, not just towards friends or family, without regard to reciprocation. Extravagance and offensive war are inimical to ai. Although Mozi's thought was influential, the Confucian lian is how most Chinese conceive of love.

Gănqíng (感情), the "feeling" of a relationship, vaguely similar to empathy. A person will express love by building good gănqíng, accomplished through helping or working for another and emotional attachment toward another person or anything.

Yuanfen (緣份) is a connection of bound destinies. A meaningful relationship is often conceived of as dependent strong yuanfen. It is very similar to serendipity. A similar conceptualization in English is, "They were made for each other," "fate," or "destiny".

Zaolian (Simplified: 早恋, Traditional: 早戀, pinyin: zǎoliàn), literally, "early love," is a contemporary term in frequent use for romantic feelings or attachments among children or adolescents. Zaolian describes both relationships among a teenaged boyfriend and girlfriend, as well as the "crushes" of early adolescence or childhood. The concept essentially indicates a prevalent belief in contemporary Chinese culture that due to the demands of their studies (especially true in the highly competitive educational system of China), youth should not form romantic attachments lest their jeopardize their chances for success in the future. Reports have appeared in Chinese newspapers and other media detailing the prevalence of the phenomenon and its perceived dangers to students and the fears of parents.

Japanese

In Japanese Buddhism, ai (愛) is passionate caring love, and a fundamental desire. It can develop towards either selfishness or selflessness and enlightenment.

Amae (甘え), a Japanese word meaning "indulgent dependence", is part of the child-rearing culture of Japan. Japanese mothers are expected to hug and indulge their children, and children are expected to reward their mothers by clinging and serving. Some sociologists have suggested that Japanese social interactions in later life are modeled on the mother-child amae.

Ancient Greek

Greek distinguishes several different senses in which the word love is used. For example, Ancient Greek has the words philia, eros, agape, storge and xenia. However, with Greek as with many other languages, it has been historically difficult to separate the meanings of these words totally. At the same time the Ancient Greek text of the Bible has examples of the verb agapo being used with the same meaning as phileo.

Agape (ἀγάπη agápē) means love in modern day Greek. The term s'agapo means I love you in Greek. The word agapo is the verb I love. It generally refers to a "pure", ideal type of love rather than the physical attraction suggested by eros. However, there are some examples of agape used to mean the same as eros. It has also been translated as "love of the soul".

Eros (ἔρως érōs) is passionate love, with sensual desire and longing. The Greek word erota means in love. Plato refined his own definition. Although eros is initially felt for a person, with contemplation it becomes an appreciation of the beauty within that person, or even becomes appreciation of beauty itself. Eros helps the soul recall knowledge of beauty, and contributes to an understanding of spiritual truth. Lovers and philosophers are all inspired to seek truth by eros. Some translations list it as "love of the body".

Philia (φιλία philía), a dispassionate virtuous love, was a concept developed by Aristotle. It includes loyalty to friends, family, and community, and requires virtue, equality and familiarity. Philia is motivated by practical reasons; one or both of the parties benefit from the relationship. Can also mean "love of the mind". Storge (στοργή storgē) is natural affection, like that felt by parents for offspring.

Xenia (ξενία xenía), hospitality, was an extremely important practice in Ancient Greece. It was an almost ritualized friendship formed between a host and their guest, who could previously be strangers. The host fed and provided quarters for the guest, who was only expected to repay with gratitude. The importance of this can be seen throughout Greek mythology, in particular Homer's Iliad and Odyssey.

Turkish (Shaman & Islamic)

In Turkish the word "Love" comes up with several meanings. A person can love the god, a person, the parents or the family. But that person can "Love" just one person from the opposite sex which they call the word " Ask ". Ask is a feeling for to love, as it still is in Turkish today. The Turks used this word just for their romatic loves in a romantic or sexual sense. If a Turk says that he is in Love (Ask) with somebody, it is not a love that a person can feel for his or her parents. It is just for one person and it indicates a huge infatuation.

Ancient Roman (Latin)

The Latin language has several different verbs corresponding to the English word 'love'.

Amare is the basic word for to love, as it still is in Italian today. The Romans used it both in an affectionate sense, as well as in a romantic or sexual sense. From this verb come amans, a lover, amator, 'professional lover', often with the accessory notion of lechery, and amica, 'girlfriend' in the English sense, often as well being applied euphemistically to a prostitute. The corresponding noun is amor, which is also used in the plural form to indicate 'love affairs' or 'sexual adventures'. This same root also produces amicus, 'friend', and amicitia, 'friendship' (often based on mutual advantage, and corresponding sometimes more closely to 'indebtedness' or 'influence'). Cicero wrote a treatise called On Friendship (de Amicitia) which discusses the notion at some length. Ovid wrote a guide to dating called Ars Amatoria (The Art of Lovers), which addresses in depth everything from extramarital affairs to overprotective parents.

Complicating the picture somewhat, Latin sometimes uses amare where English would simply say to like; this notion, however, is much more generally expressed in Latin by placere or delectare, which are used more colloquially, and the latter of which is used frequently in the love poetry of Catullus.

Diligere often has the notion 'to be affectionate for', 'to esteem', and rarely if ever is used of romantic love. This word would be appropriate to describe the friendship of two men. The corresponding noun diligentia, however, has the meaning 'diligence' 'carefulness' and has little semantic overlap with the verb.

Observare is a synonym for 'diligere'; despite the cognate with English, this verb and its corresponding noun 'observantia' often denote 'esteem' or 'affection'.

Caritas is used in Latin translations of the Christian Bible to mean 'charitable love'. This meaning, however, is not found in Classical pagan Roman literature. As it arises from a conflation with a Greek word, there is no corresponding verb.

Religious views

Christian

The Christian understanding is that love comes from God. The love of man and woman, eros in Greek, and the unselfish love of others, agape, are often contrasted as 'ascending' and 'descending' love, respectively, but are ultimately the same thing. ^[13]

There are several Greek words for Love that are regularly referred to in Christian circles.

Agape - In the New Testament, agapē is charitable, selfless, altruistic, and unconditional. It is parental love seen as creating goodness in the world, it is the way God is seen to love humanity, and it is seen as the kind of love that Christians aspire to have for one another.
Phileo - Also used in the New Testament, Phileo is a human response to something that is found to be delightful. Also known as "brotherly love".
Two other words for love in the Greek language -- Eros (sexual love) and storge (needy child-to-parent love) were never used in the New Testament.

Christians believe that to Love God with all your heart, mind, and strength and Love your neighbor as yourself are the two most important things in life (the greatest commandment of the Jewish Torah, according to Jesus - c.f. Gospel of Mark chapter 12, verses 28-34). Saint Augustine summarized this when he wrote "Love God, and do as thou wilt".

Paul the Apostle glorified love as the most important virtue of all. Describing love in the famous poem in 1 Corinthians he wrote, "Love is patient, love is kind. It does not envy, it does not boast, it is not proud. It is not rude, it is not self-seeking, it is not easily angered, it keeps no record of wrongs. Love does not delight in evil but rejoices with the truth. It always protects, always trusts, always hopes, and always perseveres." - 1 Cor. 13:4-7 (NIV)

John the Apostle wrote, "For God so loved the world that he gave his one and only Son, that whoever believes in him shall not perish but have eternal life. For God did not send his Son into the world to condemn the world, but to save the world through him. Whoever believes in him is not condemned, but whoever does not believe stands condemned already because he has not believed in the name of God's one and only Son." - John 3:16-18 (NIV)

John also wrote, "Dear friends, let us love one another for love comes from God. Everyone who loves has been born of God and knows God. Whoever does not love does not know God, because God is love." - 1 John 4:7-8 (NIV)

Saint Augustine says that one must be able to decipher the difference between love and lust. Lust, according to Saint Augustine, is an over indulgence, but to love and be loved is what he has sought for his entire life. He even says, “I was in love with love.” Finally, he does fall in love and is loved back, by God. Saint Augustine says the only one who can love you truly and fully is God, because love with a human only allows for flaws such as, “jealousy, suspicion, fear, anger, and contention.” According to Saint Augustine to love God is “to attain the peace which is yours.” (Saint Augustine Confessions)

Christian theologians see God as the source of love, which is mirrored in humans and their own loving relationships. Influential Christian theologian C.S. Lewis wrote a book called The Four Loves.

Benedict XVI wrote his first encyclical on God is love. He said that a human being, created in the image of God who is love, is able to practice love: to give himself to God and others (agape), by receiving and experiencing God's love in contemplation (eros). This life of love, according to him, is the life of the saints such as Teresa of Calcutta and the Blessed Virgin Mary, and is the direction Christians take when they believe that God loves them.^[14]

Buddhist

In Buddhism, Kāma is sensuous, sexual love. It is an obstacle on the path to enlightenment, since it is selfish.

Karuṇā is compassion and mercy, which reduces the suffering of others. It is complementary to wisdom, and is necessary for enlightenment.

Adveṣa and maitrī are benevolent love. This love is unconditional and requires considerable self-acceptance. This is quite different from the ordinary love, which is usually about attachment and sex, which rarely occur without self-interest. Instead, in Buddhism it refers to detachment and unselfish interest in others' welfare.

The Bodhisattva ideal in Mahayana Buddhism involves the complete renunciation of oneself in order to take on the burden of a suffering world. The strongest motivation one has in order to take the path of the Bodhisattva is the idea of salvation within unselfish, altustic love for all sentient beings.

Indic and Hindu

In Hinduism kāma is pleasurable, sexual love, personified by the god Kama. For many Hindu schools it is the third end in life (artha).

In contrast to kāma, prema or prem refers to elevated love. However, the term bhakti is used to mean the higher, divine love.

Karuna is compassion and mercy, which reduces the suffering of others.

Bhakti is a Sanskrit term from Hinduism meaning 'loving devotion to the supreme God'. A person who practices bhakti is called bhakta. Hindu writers, theologians, and philosophers have distinguished nine forms of devotion that they call bhakti, for example in the Bhagavatha-Purana and according to Tulsidas. The philosophical work Narada Bhakti Sutras written by an unknown author (presumed to be Narada) distinguishes eleven forms of love.

Arabic and Islamic views

In a sense, love does encompass the Islamic view of life as universal brotherhood which applies to all who hold the faith. There are no direct references stating that God is love, but amongst the 99 names of God (Allah), there is the name Al-Wadud or 'the Loving One', which is found in Surah 11:90 as well as Surah 85:14. It refers to God as being "full of loving kindness". In Islam, love is more often than not used as an incentive for sinners to aspire to be as worthy of God's love as they may. One still has God's love, but how the person evaluates his own worth is to his own and God's own counsel. All who hold the faith have God's love, but to what degree or effort he has pleased God depends on the individual itself.

Ishq, or divine love, is the emphasis of Sufism. Sufis believe that love is a projection of the essence of God to the universe. God desires to recognize beauty, and as if one looks at a mirror to see oneself, God "looks" at itself within the dynamics of nature. Since everything is a reflection of God, the school of Sufism practices to see the beauty inside the apparently ugly. Sufism is often referred to as the religion of Love. God in Sufism is referred to in three main terms which are the Lover, Loved, and Beloved with the last of these terms being often seen in Sufi poetry. A common viewpoint of Sufism is that through Love humankind can get back to its inherent purity and grace. The saints of Sufism are infamous for being "drunk" due to their Love of God hence the constant reference to wine in Sufi poetry and music.

Jewish

In Hebrew Ahava is the most commonly-used term for both interpersonal love and love of God. Other related but dissimilar terms are Chen (grace) and Hesed, which basically combines the meaning of "affection" and "compassion" and is sometimes rendered in English as "loving-kindness".

Judaism employs a wide definition of love, both between people and between man and the Deity. As for the former, the Torah states: "Love your neighbor like yourself" (Leviticus 19:18). As for the latter, one is commanded to love God "with all your heart, with all your soul and with all your might" (Deuteronomy 6:5), taken by the Mishnah (a central text of the Jewish oral law) to refer to good deeds, willingness to sacrifice one's life rather than commit certain serious transgressions, willingness to sacrifice all one's possessions and being grateful to the Lord despite adversity (tractate Berachoth 9:5). Rabbinic literature differs how this love can be developed, e.g. by contemplating Divine deeds or witnessing the marvels of nature.

As for love between marital partners, this is deemed an essential ingredient to life: "See life with the wife you love" (Ecclesiastes 9:9). The Biblical book Song of Songs is considered a romantically-phrased metaphor of love between God and his people, but in its plain reading reads like a love song.

The 20th century Rabbi Eliyahu Eliezer Dessler is frequently quoted as defining love from the Jewish point-of-view as "giving without expecting to take" (from his Michtav me-Eliyahu, vol. 1). Romantic love per se has few echoes in Jewish literature, although the Medieval Rabbi Judah Halevi wrote romantic poetry in Arabic in his younger years (he appears to have regretted this later).

References

^ Oxford Illustrated American Dictionary (1998) + Merriam-Webster Collegiate Dictionary (2000).
^ Kay, Paul. "What Is the Sapir-Whorf Hypothesis?". American Anthropologist, New Series, Volume 86, No. 1, March, 1984. pp. 65-79
^ Rubin,Zick. "Measurement of Romantic Love". Journal of Personality and Social Psychology,16, 265-273, 1970
^ Rubin, Zick.Liking and Loving: an invitation to social psychology. New York: Holt, Rinehart & Winston. 1973
^ Ancient Love Poetry
^ "[http://www.templetonpress.org/bookreviews_detail.asp?book_id=73 Science of Love The Wisdom of Well-Being]". 'Scientific and Medical Network, Gloucestershire, United Kingdom, 2005. Retrieved on April 30, 2008.
^ DiscoveryHealth, Paraphilia, <http://health.discovery.com/centers/sex/sexpedia/paraphilia.html>. Retrieved on 16 December 2007
^ Lewis, Thomas; Amini, F., & Lannon, R. (2000). A General Theory of Love. Random House. ISBN 0-375-70922-3.
^ ^a ^b Winston, Robert (2004). Human. Smithsonian Institution.
^ Emanuele, E. Polliti, P, Bianchi, M. Minoretti, P. Bertona, M., & Geroldi, D. (2005). “Raised plasma nerve growth factor levels associated with early-stage romantic love.” Abstract. Psychoneuroendocrinology, Nov. 09.
^ Berscheid, Ellen; Walster, Elaine, H. (1969). Interpersonal Attraction. Addison-Wesley Publishing Co.. CCCN 69-17443.
^ Peck, Scott (1978). The Road Less Traveled. Simon & Schuster, 169. ISBN 0-671-25067-1.
^ Pope Benedict XVI, papal encyclical, Deus Caritas Est.
^ Pope Benedict XVI, papal encyclical, Deus Caritas Est.

Sources

Henry Chadwick and Edzrin. "Saint Augustine Confessions". Oxford University Press, 1998.
Helen Fisher. Why We Love: the Nature and Chemistry of Romantic Love
Irving Singer, The Nature of Love, in three volumes, Random House (v.1, 1966), reprinted and later volumes from The University of Chicago Press, 1984. ISBN 0226760944
R. J. Sternberg. A triangular theory of love. 1986. Psychological Review, 93, 119–135
R. J. Sternberg. Liking versus loving: A comparative evaluation of theories. 1987. Psychological Bulletin, 102, 331–345
Dorothy Tennov. Love and Limerence: the Experience of Being in Love. New York: Stein and Day, 1979. ISBN 0812861345
Wood, Wood and Boyd. The World of Psychology. 5th edition. 2005. Pearson Education, 402–403

External links

Look up love in Wiktionary, the free dictionary.

Wikiquote has a collection of quotations related to:

Love

Look up I love you in Wiktionary, the free dictionary.

The Science of Love

Federal Motor Carrier Safety Administration [FMCSA] What is good for trucking is good for the heart ... keep on trucking ... keep on pumping ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Sat, 21 Jun 2008 21:19:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

Safe for hearts and safe for trucking or is it safe for trucking and safe for hearts or is safe only for trucking ???

WHAT'S THE SAFE 'FUEL-LEVEL' FOR HEARTS THEN ?

and what was the safe fuel-level for TIM RUSSERT ?

My Friend, Jeff - the Trucker

Posted Mar 29th 2007 1:16PM by Allison Love Beatty

Filed under: Type 2, Adult Onset, Lifestyle, Research, Opinion, Services

About a year ago, I met a guy named Jeff Mather. Well, we never met, personally. But we spoke many times over the phone about diabetes and how it has affected our paths in life. Jeff had lost his job, the one he had for over 10 years. The job he wanted to have since he was a little kid. According to Federal Safety Guidelines, if a trucker takes insulin - they are no longer safe to drive across state lines.

Jeff wrote letters every day. He posted to online forums. He contacted politicians and pleaded to every diabetic organization in existence to get him back on the road. And sure enough - his perseverance paid off. He took his predicament all the way from Washington D.C to National Public Radio. The story on NPR included details on how Jeff was able to qualify to drive again.

While diabetes advocates are pleased that it's now easier for truckers to keep their jobs when they go on insulin, they're not entirely happy with the way that the Federal Motor Carrier Safety Administration (FMCSA) will decide whether a trucker is safe to drive. In order for a trucker to be considered "safe" to drive, his HgA1c must be between 7 and 10. This means that in order to keep trucking - one must sustain a blood sugar between 140 mg/dL and 200 mg/dL. Yes, this is flawed. I was going to use another choice F phrase to describe it.

FMCSA expressed it wants to see a higher test result because they feel people with lower scores who are aggressively managing their diabetes with insulin, may be more likely to have periods of very low blood sugar, or hypoglycemia, that could make them pass out or feel woozy. Diabetes expert Christopher Saudek, at Johns Hopkins Hospital, says the agency's reasoning is flawed. And he says it puts diabetics in a bind.

"Essentially what you're saying with this kind of a rule is that if you are controlling your diabetes at all well, if you get it to 6.8 or 6.5, then you're liable to lose your job," Saudek says. "So congratulations. Your A1c is in a good range, but you aren't going to be able to drive your truck anymore. That doesn't make any sense."

Jeff, I'm so proud of you for not giving-up. You're driving your truck and I'm sure you're doing it in good health. Enjoy all that you've worked so hard to regain. Best of luck to you!

A. Has Jeff Mather been diagnosed with ‘Type 2 diabetes’ or ‘Type 1 diabetes’(?) and if Jeff has been diagnosed with Type 2 diabetes … Where is the peer reviewed research the proves that Jeff’s health will be ever be improved by reducing his HgA1c?

Transient supernormal glycaemia ‘TSG’ occurs in every Human Being as a healthy and natural response to stress [‘adaptive medicine’] and may well increase HgA1c … so what? … when glucose levels surge up for a transient period [and then down again] an above average HgA1c can just as easily be viewed as a marker for a very healthy ‘stress adapted’ Human Being who has the benefit of being ‘insulin-resistant’. My guess is that Jeff Mather was way tougher & healthier, than the average 36 year old, before his injections of insulin at age 37.

B. What is the most definitive study which substantiates the benefit of reducing HgA1c in drug/insulin treated acute&chronic 'insulin-resistant diabetes' [Type 2] … as compared with treatment-free [drug/insulin] acute&chronic 'insulin-resistant diabetes' [ie in a ZERO drug (repeat zero) treatment control Group]? {ps please note the word written there says: “zero”} ie completely ignoring HgA1c value variability…

... Am seeking a ‘peer reviewed’ study that clearly disassociates drug/insulin treatment from any changes in Patient behaviour [eg diet/exercise] and/or categorically proves that drug/insulin treated acute&chronic 'insulin-resistant diabetes' is healthier than doing absolutely nothing [‘zero’] ie just accepting the higher HgA1c value and [possibly beneficial] blood glucose value [and possibly beneficial “insulin resistance”]; and

C. What is the most definitive study which provides incontrovertible evidence that the apparent insulin receptor mediated down-regulation [in response to: transient supernormal glycaemia ‘TSG’] is anything substantially other than a stress-adaptive mechanism of 'local' [on a cell-by-cell basis] intracellular cyto-protection from influx of excessive [blood] circulating glucose [ie homeostasis] eg cardio muscle protective?

... My understanding is that insulin receptor mediated down-regulation ‘IRD’ [aka “insulin resistance”] is primarily an adaptive [protective/regulatory/beneficial] reply to transient [and chronically repeated] oral indulgence/stress …

eg "...healthy young students were fed a very high fat diet containing egg yolks, heavy cream, and butter, and within 2 days all of the students had blood sugar levels high enough to be labelled diabetic..."
Sweeney J. Dietary factors that influence the dextrose tolerance test: A preliminary study. Archives of Internal Medicine 1927; 40:818.

“…After World War I, when insulin was first discovered, the medical profession thought diabetes would be totally curable as a medical problem. Diabetes was believed to be due to insulin deficiency, and everyone thought that since insulin would now be given to patients there would be no more problems. It seemed this way for a few years, but terrible things started happening to patients with diabetes who were given insulin to control their blood sugar levels. They developed eye disease, kidney disease, and, most important, accelerating atherosclerosis leading to blood vessel disease and early heart attacks. Their problems were worse than ever. Decades later, when the insulin assay became available and doctors were able to measure insulin levels in their patients’ bloodstreams, they found most interesting results: the insulin levels of type 1 (childhood-onset) diabetics were indeed low, but the levels in type 2 (adult-onset) diabetics were not only not low, but also were higher than those of people without diabetes. It became clear that type 2 diabetes is a disease of insulin resistance, not insulin deficiency. Type 2 diabetics produce plenty of insulin … I can only view today’s treatment of diabetic patients as malpractice…”
(1995) Dr Joel Fuhrman [a board-certified Family Physician practising in Belle Mead, New Jersey who specialises in preventing and reversing chronic conditions of high blood sugar; Dr Fuhrman is an active staff member of Hunterdon Medical Centre and provides nutritionally oriented medical care to Patients as well as nutritional education to other Physicians].

Warm thanks, Nicholas Dynes Gracey, BSc(Hons) Medical Biochemistry, Birmingham University, UK c/o www.TheDiabetesBlog.com @ 17:23hrs FRI.30.MAR.2007.
Posted at 1:19PM on Mar 30th 2007 by Nicholas Dynes Gracey

'keep on trucking' Jeff Mather…

Love ... Please explain why your adoption of the word "flawed" [ie where is the apparent 'flaw'?] in relation to FMSCSA wisdom:-

"...the Federal Motor Carrier Safety Administration (FMSCSA) will decide whether a trucker is safe to drive. In order for a trucker to be considered "safe" to drive, his HgA1c must be between 7 and 10. This means that in order to keep trucking - one must sustain a blood sugar between 140 mg/dL and 200 mg/dL..."
[ie similar blood sugar levels to many 'happy go lucky' UNdrugTREATED pre type 2 Diabetics?].

Jeff? How beneficial has your ‘treatment’ been?

Please Someone explain the PROVEN benefits of ANYdrugTREATED lowering of a Type 2 Diabetic's blood sugar ... ASAP

Warm thanks, Nicholas Dynes Gracey, BSc(Hons) Medical Biochemistry, Birmingham University, UK c/o www.TheDiabetesBlog.com @ 14:09hrs MON.02.APR.2007.

Posted at 9:17AM on Apr 2nd 2007 by Nicholas Dynes Gracey

http://www.thediabetesblog.com/2007/03/29/my-friend-jeff-the-trucker
post #2

http://www.thediabetesblog.com/2007/04/19/no-food-no-problem
post #3

http://www.thediabetesblog.com/2007/04/17/is-human-synthetic-insulin-a-cock-block
post #9

Posted at 8:51AM on May 10th 2007 by Nicholas Dynes Gracey

DNA dehydration NHS euthanasia CPR investigation by HealthCare Commission ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Fri, 20 Jun 2008 22:45:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

Dehydration

This article is about the medical condition. For the removal of water through chemical or physical means, see desiccation. For the chemical reaction, see dehydration reaction. For food preservation by dehydration, see drying (food).

Dehydration Classification and external resources
ICD-10	E 86.
ICD-9	276.5

Dehydration (HYPO-hydration) is the removal of water (hydro in ancient Greek) from an object. In Physiologic terms, it entails a relative deficiency of water molecules in relation to other dissolved solutes. Dehydration, thus, is slightly different from HYPO-volemia, which defines water deficiency only in terms of overall volume rather than in terms of solute concentrations.

Medical causes of dehydration in humans

In humans, dehydration can be caused by a wide range of diseases and states that impair water homeostasis in the body. These include:

External or stress-related causes
- Prolonged physical activity without consuming adequate water, especially in a hot and/or humid environment
- Prolonged exposure to dry air, e.g. in high-flying airplanes (5-15% relative humidity)
- Survival situations, especially desert conditions
- Blood loss or hypotension due to physical trauma
- Diarrhea
- Hyperthermia
- Shock (hypovolemic)
- Vomiting
- Burns
- Lacrimation
- Use of Methamphetamine and other stimulants.

Infectious diseases

Malnutrition
- Electrolyte disturbance
  - Hypernatremia (also caused by dehydration)
  - Hyponatremia, especially from restricted salt diets
- Fasting
- Recent rapid weight loss may reflect progressive depletion of fluid volume (the loss of 1 L of fluid results in a weight loss of 1 kg or 2.2 lb).^[1]
- Patient refusal of nutrition and hydration

Other causes of obligate water loss
- Severe hyperglycemia, especially in Diabetes mellitus
  - Glycosuria

Symptoms and prognosis

Symptoms may include headaches similar to what is experienced during a hangover, muscle cramps, a sudden episode of visual snow, decreased blood pressure (hypotension), and dizziness fainting when standing up due to orthostatic hypotension. Untreated dehydration generally results in delirium, unconsciousness, swelling of the tongue[1] and in extreme cases death. or

Dehydration symptoms generally become noticeable after 2% of one's normal water volume has been lost. Initially, one experiences thirst and discomfort, possibly along with loss of appetite and dry skin. This can be followed by constipation. Athletes may suffer a loss of performance of up to 30%^[2], and experience flushing, low endurance, rapid heart rates, elevated body temperatures, and rapid onset of fatigue.

Symptoms of mild dehydration include thirst, decreased urine volume, abnormally dark urine, unexplained tiredness, lack of tears when crying, headache, dry mouth, dizziness when standing due to orthostatic hypotension, and in some cases can cause insomnia.

In moderate to severe dehydration, there may be no urine output at all. Other symptoms in these states include lethargy or extreme sleepiness, seizures, sunken fontanel (soft spot) in infants, fainting, and sunken eyes.

The symptoms become increasingly severe with greater water loss. One's heart and respiration rates begin to increase to compensate for decreased plasma volume and blood pressure, while body temperature may rise because of decreased sweating. Around 5% to 6% water loss, one may become groggy or sleepy, experience headaches or nausea, and may feel tingling in one's limbs (paresthesia). With 10% to 15% fluid loss, muscles may become spastic, skin may shrivel and wrinkle, vision may dim, urination will be greatly reduced and may become painful, and delirium may begin. Losses greater than 15% are usually fatal. ^[3]

For adults over age 50, the body’s thirst sensation diminishes and continues diminishing with age. Many senior citizens suffer symptoms of dehydration. Dehydration along with hyperthermia results in seniors dying during extreme hot weather.

Dehydration is the excessive loss of water from the body. Diseases of the gastrointestinal tract can lead to dehydration in various ways. Often, dehydration becomes the major problem in an otherwise self-limited illness. Fluid loss may even be severe enough to become life-threatening.

Treatment

Nurses encouraging this patient to drink an Oral Rehydration Solution to improve dehydration he acquired from cholera.

The best treatment for minor dehydration is drinking water and stopping fluid loss. Water is preferable to sport drinks and other commercially-sold rehydration fluids, as the balance of electrolytes they provide may not match the replacement requirements of the individual. To stop fluid loss from vomiting and diarrhea, avoid solid foods and drink only clear liquids.^[4]

In more severe cases, correction of a dehydrated state is accomplished by the replenishment of necessary water and electrolytes (rehydration, through oral rehydration therapy or intravenous therapy). Even in the case of serious lack of fresh water (e.g., at sea or in a desert), drinking seawater or urine does not help, nor does the consumption of alcohol. It is often thought that the sudden influx of salt into the body from seawater will cause the cells to dehydrate and the kidneys to overload and shut down but it has been calculated that an average adult can drink up to 0.2 liters of seawater per day before the kidneys start to fail.

When dehydrated, unnecessary sweating should be avoided, as it wastes water. If there is only dry food, it is better not to eat, as water is necessary for digestion. For severe cases of dehydration where fainting, unconsciousness, or other severely inhibiting symptom is present (the patient is incapable of standing or thinking clearly), emergency attention is required. Fluids containing a proper balance of replacement electrolytes are given orally or intravenously with continuing assessment of electrolyte status; complete resolution is the norm in all but the most extreme cases.

Avoiding dehydration

Dehydration is best avoided by drinking plenty of water. The greater the amount of water lost through perspiration, the more water must be consumed to replace it and avoid dehydration. Since the body cannot tolerate large deficits or excesses in total body water, consumption of water must be roughly concurrent with the loss (in other words, if one is perspiring, one should also be drinking water frequently). Drinking water beyond the needs of the body entails little risk, since the kidneys will efficiently remove any excess water through the urine with a large margin of safety.

A person's body, during an average day in a temperate climate such as the United Kingdom, loses approximately 2.5 litres of water. This can be through the lungs as water vapor, through the skin as sweat, or through the kidneys as urine. Some water (a less significant amount, in the absence of diarrhea) is also lost through the bowels. In warm or humid weather or during heavy exertion, however, the water loss can increase by an order of magnitude or more through perspiration; all of which must be promptly replaced. In extreme cases, the losses may be great enough to exceed the body's ability to absorb water from the gastrointestinal tract; in these cases, it is not possible to drink enough water to stay hydrated, and the only way to avoid dehydration is to reduce perspiration (through rest, a move to a cooler environment, etc.).

A useful rule of thumb for avoiding dehydration in hot or humid environments or during strenuous activity involves monitoring the frequency and character of urination. If one develops a full bladder at least every 3-5 hours and the urine is only lightly colored or colorless, chances are that dehydration is not occurring; if urine is deeply colored, or urination occurs only after many hours or not at all, water intake may not be adequate to maintain proper hydration.

When large amounts of water are being lost through perspiration and concurrently replaced by drinking, maintaining proper electrolyte balance becomes an issue. Drinking fluids that are hypertonic or hypotonic with respect to perspiration may have grave consequences (hyponatremia or hypernatremia, principally) as the total volume of water turnover increases.

If water is being lost through abnormal mechanisms such as vomiting or diarrhea, an imbalance can develop very quickly into a medical emergency. In fact, the main mechanisms through which diseases such as infantile diarrhea and cholera kill their victims are dehydration and loss of electrolytes.

During sports events, water stops and water breaks are provided to avoid dehydration of athletes.

References

Ira R. Byock, M.D., Patient Refusal of Nutrition and Hydration: Walking the Ever-Finer Line. American Journal Hospice & Palliative Care, pp. 8-13. (March/April 1995)

Notes

^ Dehydration Symptoms - Benefits of Drinking Water - Signs of Fluid Imbalance
^ Bean, Anita (2006). The Complete Guide to Sports Nutrition. A & C Black Publishers Ltd., pp. 81-83. ISBN 0713675586.
^ http://faculty.washington.edu/kepeter/118/notes/pdf-set5/118water-bal-06.htm
^ "Healthwise Handbook," Healthwise, Inc. 1999

External links

Look up Dehydration in
Wiktionary, the free dictionary.

[hide] v • d • e Water-electrolyte imbalance and acid-base imbalance (E86-E87, 276)

Volume status	Dehydration/Hypervolemia - Hypovolemia

Electrolyte	Na⁺ Hypernatremia/Hyponatremia K⁺ Hyperkalemia/Hypokalemia Cl⁻ Hyperchloremia/Hypochloremia

Acid-base	Acidosis: Metabolic - Respiratory - Lactic - Ketosis Alkalosis: Metabolic, Respiratory Mixed disorder of acid-base balance

Retrieved from "http://en.wikipedia.org/wiki/Dehydration"

Categories: Metabolic disorders | Electrolyte disturbances | Nutrition | Causes of death
.
.
.

Clin J Sport Med. 1997 Jul ;7 (3):180-4 9262884 (P,S,E,B) Cited:1

Hyponatremia and weight changes in an ultradistance triathlon.

D B Speedy, J G Faris, M Hamlin, P G Gallagher, R G Campbell

SportsMed, Christchurch, Auckland, New Zealand.

OBJECTIVE: To describe the weight changes and the incidence of HYPO-natremia during an ultradistance triathlon in the athletes who attend medical care after the race.

Fasting for recovery from acute disease

noreply@blogger.com (Nicholas Dynes Gracey) — Thu, 19 Jun 2008 16:36:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.
Fasting for recovery from 'Acute Disease'

"Instead of using medicine, rather fast a day," wrote Plutarch. Someone else has said: "Wise people, falling into any ailment, take a bath, go to bed, and fast, leaving nature to do her own work of cure, and not hindering her beneficent operations."

One of the first indications of illness is a failing appetite. Indeed appetite often fails a few days before any other symptoms appear. If the illness begins "suddenly," while the stomach is full of food, or if there is a serious accident or shock to the nervous system while the stomach is full of food, the stomach is immediately emptied by vomiting. Thus does nature indicate, both in animals and in man, that in acute "disease," no food but water should be consumed. In chronic disease she indicates that the amount of food eaten should be much less than that consumed in health. Dr. Eales admonishes: "Let the sick eat only when Nature calls for food." If this rule were adhered to by all, an untold amount of suffering would be avoided and many would be saved from an untimely death. But thanks to the medical delusion that "the sick man must eat to keep up his strength," this rule is not likely to be adopted by the great majority for years to come.

The common expression applied alike to horse and man, "off his feed," describes the instinctive abstinence from food that comes when power to digest food is low or absent. The loss of digestive power and digestive conditions is proportioned to the severity of the curative actions.

Writing of the vomiting that occurs in sea-sickness, Dr. Shew asserted that "almost all persons are benefited by it" (sea sickness), and explained the benefit thus: "It is by the beneficial power of fasting that the benefit of sea sickness is caused." Only false teachings can induce people to go on eating regularly in the face of the fact that the food is vomited as promptly as it is ingested. For this false teaching we have the medical profession to thank.

FALSE TEACHINGS OF MEDICAL "SCIENCE"

Physicians have taught the people that there are specific diseases requiring specific causes and that the sick must be fed "to keep up their strength." while being "cured" of their diseases. So long as we believe that the "cure" of a common "disease" depends upon the accidental or providentially ordained discovery of some mysterious compound, we are likely to continue overlooking the plainest indications of nature and go on killing the sick in the time-honored way.

Not merely in low chronic conditions, but in acute conditions, with high temperature as well, overfeeding is prescribed and enforced. Indeed, a high calorie diet is now the rule in fevers.

Dr. Kellogg insists on sugar in some form, even in the most violent stages of acute "disease." This insistence is not based on physiology, but on his fear of bacteria. He says that bacteria "will not grow or at least are not virulent and active in producing toxins, in the presence of sugar."

Fear and false theories lead men away from nature and physiology and cause them to do many absurd and damaging things. With all due respect to Dr. Kellogg, his influence in this matter is highly pernicious and prejudicial to the health and recovery of the sick. The indications of nature are the true guide in a search for health. Ephemeral theories of mis-called science often do much harm.

INSTINCTIVE REPUGNANCE TO FOOD IN ACUTE ILLNESS

Animals will not eat when sick. It has long been known that when animals are severely injured they refuse food. Shock, severe injury of any kind, fever, pain, inflammation, poisoning, reduce or suspend digestive power and reduce the nutritive functions throughout the body. The human animal has no desire for food when ill; in fact, there is a positive repugnance to food, coupled with an inability to digest and utilize it. But, all too often, the human animal disregards his repugnance to food and the discomforts that follow eating in spite of this, and eats because he has become convinced that he will die if he does not eat.

When animals, young or old, become sick they instinctively refrain from eating. Warmth, Quiet and Fasting, with a little water, are all they want. When they take nourishment, it is a sure sign that they are recovering. They eat but little at first and gradually eat more as they grow better. They never worry about calories or protein requirements either. Warmth, Quiet (rest) and Fasting, with a little water, as demanded by thirst, are the needs of a sick man or woman.

A sick animal cannot be made to eat; but sick men, women and children can be induced to eat to "keep up their strength." Feeding, with relapses galore, until death ends the various tragedies, is common on both sides of the Atlantic. Every year the loss of life among useful men is appalling. They develop a "spring cold," then eat to keep up their strength; but the eating strengthens the toxins and weakens the body, until friends are shocked by their death.

Dr. Hazzard claims, and I believe rightly, that while appetite may be and often is present in "disease," true hunger never is. I believe that, with a few possible exceptions, this is as true of chronic as of acute "disease." Liek says that objection to fasting on the part of adults, is usually due not to the working of the instinct but to that of a faulty working intelligence. He illustrates this with a story about a fat woman doctor upon whom he performed an abdominal operation, which was followed by septic developments. Although she admitted she did not have the slightest desire for food and that even the thought of food produced nausea, she thought "she ought to eat something to keep up her strength" and "was worrying for days because she had the idea that she ought to be given strengthening food."

He very appropriately remarks that "her stomach possessed more sense than her brain." His remark would have been nearer the mark, had he said that her organic instincts possessed more intelligence than her medical instructors who educated her into the false belief that "the sick must eat to keep up their strength."

Dr. Densmore says: "Quite generally, in severe attacks, the patient has no appetite--food is positively repulsive; but when there seems to be craving for food, it will be found to be a fictitious longing caused by inflammation and not from need of nourishment. This fictitious appetite usually disappears with the first twenty-four hours fast. The effort of the true physician must be to assist Nature, and to be guided by her. If there should still be found longing for food at the expiration of forty-eight hours fasting, it will be evidence that food is needed. * * * The more serious the attack of illness, the longer duration of fast needed. From three to six days will be found advisable in extreme cases. Let nature be absolutely trusted; when the patient has been denied food long enough to overcome the inflammation which is liable to be mistaken for appetite, then give nourishment as soon and no sooner than the patient craves food."--How Nature Cures, p. 23.

I do not agree that in cases of severe acute illness where the fictitious desire for food persists beyond forty-eight hours of fasting, it indicates a real need for food. There can be no digestion of food in these cases and there is no urgent need for food so long as the patient's reserves are not exhausted.

The reappearance of a keen appetite in the sick is a sure indication of returning health and strength. The absence of desire for food, whether caused by illness, grief, anger, excitement, fatigue, or other cause, is nature's way of saying that the digestive organs are, for the time being, incapable of digesting food.

FEEDING TO KEEP UP STRENGTH

The idea that dominates the physician, the nurses and the relatives of the sick person is that the vital power or strength "must be supported with food" while the "conflict with disease" rages. This supposed need for food to support life, great in proportion to the apparent gravity of the patient's condition, would seem to make the natural or instinctive aversion to food a serious mistake of nature. "The force of custom," wrote Dr. Densmore, "is one of the strongest powers, and doctors and nurses for generations have been in the habit of urging invalids to partake of food, not infrequently to their serious injury." Because we believe that recovery from illness depends on nourishment "our unreasoning sympathy and solicitude prompt us to urge our invalid friends to partake of food. Whatever the origin of the custom, it is one universally to be condemned; when one is seriously ill a fast is indicated."--How; Nature Cures, p. 21.

One thing is certain; either nature or the physician is mistaken. The furred tongue and loss of relish for food, the absence of "hunger contractions," the mental depression; in short, the entire absence of every physiological requirement for digestion, with, in many conditions, the presence of inflammation and even ulceration in the digestive tract, makes it impossible to sustain the patient's strength by feeding.

Enforced feeding of the sick is a war against nature, dangerous in proportion to the gravity of the patient's condition. The poisonous products of undigested or imperfectly digested food must handicap the patient who is fed during an acute illness. The stuff-to-kill doctor who feeds milk, eggs, meat broths, etc., were he not so blind, should be able to see that he is killing his patient.

NO POWER TO DIGEST IN ACUTE SICKNESS

Beaumont showed that there is no digestion in serious acute illness. He says of one of his experiments, that, this "experiment has considerable pathological importance. In febrile diathesis, very little or no gastric juice is secreted. Hence the importance of withholding food from the stomach in febrile complaints. It can afford no nourishment; but is actually a source of irritation to that organ, and, consequently, to the whole system. No solvent can be secreted under these circumstances; and food is as insoluble in the stomach, as lead would be under ordinary circumstances." Certainly no food should be eaten until normal secretions have been restored.

A few years ago Prof. Carlson confirmed the findings of Beaumont and several of his successors. He showed that gastric secretion is absent during gastritis and fevers. The absence of hunger in fever has been shown to be associated with absence of the "hunger contractions" of the stomach. "Hunger contractions" have been shown to be absent in nausea, gastritis, tonsillitis, influenza and colds. In dogs these "hunger contractions" have been shown to be absent in infection and pneumonia. The absence of hunger is a concomitant of the absence of gastric and salivary secretions and the absence of the "hunger contractions." It is, in other words, an evidence of a suspension of the digestive process.

It is unfortunate that few, save Natural Hygienists have ever based their care of the acutely ill upon the fact that there is no power to digest food when there is fever, pain, inflammation and severe poisoning. The practitioners of all schools have continued to urge food upon their acutely ill patients in spite of the protests of nature and in the face of the mounting physiological knowledge of the lack of power to digest food under such circumstances.

Pain, inflammation, fever, headaches, mental disturbances, etc., take away the appetite, inhibit secretion and excretion, impair digestion and render it injurious to eat under such conditions. Pain, inflammation and fever in all forms of acute "disease" inhibit the secretion of digestive juices, "take away the appetite" and render digestion practically impossible. The dryness of the mouth in fevers is matched by a similar dryness all along the digestive tract. It can be of no advantage to urge food upon a patient suffering with an acute "disease," for there is then no digestive power to work it up.

There is an almost total absence of the digestive juices. The little of these present, are of such poor quality that they could not properly digest even small amounts of food. Along with the absence of the power to digest and the absence of the digestive juices, there is lacking the keen relish for food which is so essential to normal digestion. Pain inhibits digestion and secretion. Fever inhibits these. So does inflammation. Food taken under such conditions is not digested. Nature has temporarily suspended the digestive functions. This is necessary in order that her undivided attention can be given to the task of cure. Energy that is ordinarily consumed in the work of digesting, absorbing and assimilating food is now being used to carry on the curative processes. The muscles of the stomach and intestine are in about the same condition as the muscles of the arm.

In acute disease the digestive system is as little fit to digest food as the limbs are for locomotion--both require rest. What is to be gained by eating when there is no ability to digest food? Why should physicians insist upon the patient eating when there is no desire for food, or when there is an actual aversion to food?

Dr. Emmett Densmore laid down as the first rule to be followed when illness develops: "Partake of no food during forty-eight hours; after that time continue an absolute fast from food until the patient has pronounced natural hunger." He says that "at all such times (when there is fever and inflammation) all food must absolutely be withheld from the patient. This may be only for a day, or for many days; no food is to be taken until all symptoms of fever have entirely abated, and none then until the patient has a decided appetite and relish for it."

Jennings says: "It is of no advantage to urge food upon the stomach when there it no digestive power to work it up. There is never any danger of starvation so long as there are reserve forces sufficient to hold the citadel of life and start anew its mainsprings.

For when sustenance becomes a prime necessity, the digestive apparatus will be clothed with power enough to work up some new material, and a call made for it proportioned to the ability to use it. And if there is not power within the domain of life to save the organism, it must perish."

Trall declared that when the body is struggling to throw off the toxins of "disease," the patient "has no ability, until the struggle is decided, to digest food; and to cram his stomach with it, or to irritate the digestive organs with tonics and stimulants, is merely adding fuel to the fire."

The stuff-to-kill doctor shuts his eyes to this important fact and, ignoring all the instinctive indications that food is not desirable and all the physiological evidences that food cannot be digested if consumed, insists that "the sick must eat to keep up their strength."

NO NOURISHMENT WITHOUT DIGESTION

In all types of acute disease the whole organism is engaged in the work of eliminating toxins, not in that of assimilating food, hence, it is perfectly natural that the body should rebel against food. Anorexia, foul breath, coated tongue, nausea, vomiting, fetid discharges, the excretion of much mucus, constipation alternating with diarrhea, etc., all indicate that the organs are engaged in the work of vicarious or compensatory elimination, and are not able to digest food. It is not possible to nourish the body by feeding under such circumstances.

"Science and physiology teach," says Dr. Densmore, "that digestion of food can only be performed satisfactorily when there is secretion of the digestive juices; and also that there can be no adequate secretion of the digestive juices, where there is inflammation, or from any cause an absence of appetite. * * * If, as physiologists teach, there can be no effective digestion except from the secretion of digestive juices, and if there is almost no secretion of digestive juices where there is high temperature, we ought to expect that there would be as much emaciation of the fever patient while partaking of food as while fasting; and this is precisely what will be seen to be the result by any physician who will make the experiment. Common sense teaches that if food is taken and not digested, such food does not help nourish the system. If no food at all be taken the processes of life are carried on by consuming the tissues; and if food be taken and not digested the processes of life must be supported by the same consumption of tissues, with the further result that the undigested food must be excreted from the body, which at a glance will be seen to be a strain upon the vital powers, calling for an additional consumption of tissue, and inevitably delaying the restoration of the patient."--How Nature Cures--p.p. 21-22.

RECTAL AND SKIN FEEDING

It may be objected to all of this that the patient should be fed so-called pre-digested foods. Our reply is that there are no predigested foods and little ability to absorb them if there were. Efforts to feed so-called pre-digested foods have proven failures, even when the foods were not vomited. Well did Dr. Dewey say: "Pre-digested foods! If they nourish the sick, why not feed the well? Why not abolish our kitchens at an immense saving in the time, expense and worry of cooking and live on them at an immense saving of the tax of digestion and the digestive juices? Brethren of the Medical Profession, make haste to let the world know when you have found a case in which you have made use of the lower bowel so to nourish the sick body that it didn't waste while the cure was going on."

Rectal feeding is absurd. It feeds nothing. The colon is busy excreting, not absorbing, and the so-called food injected into the colon, not being digested, could not be used if it were absorbed. The least it can do is ferment and putrefy and add to the discomforts and expenditures of the patient. Lavage or stomach tube or duodenal feeding are delusions.

When such large quantities of fluid are being poured out, there is no absorption from the stomach and intestine. To feed under such conditions, when there is no absorption, and also no digestion, is not to nourish the body. Food adds to the putrescence and to the danger.

The body never performs any of what Dr. Tilden calls "Hindu tricks," in this matter of taking nourishment. It does not digest and absorb food when digestion is suspended and the membranes of the stomach and intestine are exuding matter instead of absorbing it. It is exuding fluid to aid in expelling the mass of putrescence in the food tube, and to protect the walls of the tube and any irritated surface. Sometimes nature even rejects water, expelling it by vomiting as often as it is forced down. How foolish in such cases to continue to force food and drugs on the patient and water into his stomach. Nature is trying to protect herself by this vomiting. She even guards against water by creating a bad taste in the mouth that causes the patient to refuse water. Dr. Lindlahr likened the process to a sponge. During health, the sponge (intestine) is busy absorbing, during a fast or in acute "disease" the sponge is being squeezed.

Skin feeding is another absurdity. The skin will not absorb food, and it would not be prepared for use by the organism, if it did do so, as was shown in our study of digestion in a previous volume. I have heard doctors tell of feeding patients through the skin. Milk baths, olive oil rubs and other unphysiological procedures are employed, and then, if the patient does not die, the doctor tells us how long he kept his patient alive by such absurd practices. Had the doctor not been ignorant of the internal resources of the body he would have known that the patient would have lived just as long without such mis-called feeding. Skin foods are delusions. Intravenous feeding is also a delusion.

GASTRO-INTESTINAL DECOMPOSITION

If bacteriologists desire to make cultures of "pathogenic" organisms, they use meat broths, meat jellies and boiled milk. These substances provide equally as good culture media for microbes in the digestive tract, when fed to patients who are acutely ill, as when used in the laboratory, and generate just as much putrescence. The doctor who would not feed a putrid culture medium to a patient, will blindly feed the patient the culture medium and see it become putrid in the digestive tract.

Dr. Josian Oldfield says, in Fasting for Health and Life: "If friends were only present at the post mortem and could see and smell for themselves the foul and filthy contents of the stomach and intestines of those nurse-bullied dying patients, they would pray, as I pray, that when their last days are come they may be allowed to die in quietude and cleanliness, taking only sips of pure water, and such fruit juices as their thirsty cells crave for, until peaceful dissolution takes place."

What Dr. Oldfield overlooks is that the members of his own profession, who are present at the post mortems and are allowed to see and smell the putrescence in the digestive tract, prescribed the foods the nurse or fond relative forced upon the patient and that these same medical men trained the nurse and taught the relatives.

Food that is not digested undergoes decomposition, forming a mass of toxins more or less of which are absorbed to further poison and sicken the patient. A veritable cess pool is formed under the diaphragm that is much more dangerous to the individual than any cess pool that may be in the neighborhood.

To get rid of this rotting, fermenting mass of food and the toxins it has formed requires a needless expenditure of energy. Nature is trying to conserve energy. This is precisely the reason she has temporarily suspended the digestive functions. It is little less than criminal to force the organism to divide its energies and attention between the work of curing and the added task of eliminating a rotting septic mass from the digestive tract.

The only sensible thing to do is to keep the digestive tract free of all such matter. Nature herself indicates this in the strongest possible manner, for not only is all desire for food cut off, but the most tempting dishes are not relished by the sick person. There is a positive disinclination to take food.

Bear in mind that the food decomposed and poisoned the patient because his digestive power had been greatly impaired, and that to give more food, under such conditions, is only to add to the poisoning.

The "disease" will last until the poisons have been eliminated and the decomposing food has been voided. Fever, vomiting and purging are nature's methods of getting rid of the poison, and when these cases are fasted and not fed, such troubles soon end. There is no danger in them. Feeding and drugging are the elements of danger. Never permit a patient to be drugged, and never permit the physician to reduce (suppress) his fever.

One of our rules for caring for the sick is to stop the absorption of all toxins from the outside. Feeding during acute "disease" does just the opposite. It keeps the digestive tract full of decaying animal and vegetable matter, which the body must void or absorb. Putrescence arising from gastro-intestinal decomposition, grafted onto the pre-existing enervation, toxemia and dyscrasia, forms the cause of practically all the so-called "diseases" from which man suffers.

In health the body is "potentized with immunizing power" and can to a large extent, render innocuous the toxic substances arising from decomposition. The secretions of the stomach and intestine take care of such substances for us every day of our lives. When wrong eating and poor hygiene have broken down the body's resistance and deranged digestion, so that decomposition produces toxins in excess of the immunizing power of these secretions, trouble begins; the body must defend itself against these toxins, and this defense we call "disease."

When the decomposition overwhelms the immunizing power of the digestive secretions, vomiting and purging, so commonly regarded as evil, are the conservative and defensive measures which nature employs in expelling the putrescence.

To absorb the fermenting and putrefying contents of the digestive tract into the bloodstream would mean death. This does not occur. The absorbents reverse their ordinary activities and, instead of taking up the fluid contents of the digestive tract, pour a large amount of fluid (blood-serum), into the stomach and intestine to dilute and neutralize the decomposing matter and wash it away. The great quantity of fluid flushes the entire alimentary canal and the vomiting and purging complete the work of carrying the toxic matter from the body's cavities.

THE STOMACH AND INTESTINES IN ACUTE ILLNESS

A standard medical author thus describes the stomach in acute gastritis: "The gastric mucous membrane of such a stomach is red and swollen, it secretes little gastric juice, and this contains very little acid but much mucus. The patient has uncomfortable feelings in his abdomen, with headache, lassitude, some nausea, often vomiting. The vomiting relieves him considerably, for it removes the irritating substance. The tongue is coated, and the flow of saliva is increased. If this decomposing, fermenting, irritating mass is not vomited, but reaches the bowel, colic and diarrhea are the result. As a rule the patient is well in about one day, although he may not have much appetite for the next two or three days."

With the stomach in this condition, with appetite lacking, and with no digestive juice secreted, eating would be worse than folly. It would seem criminal to add more food to the "decomposing, fermenting, irritating mass" in the stomach. Fasting in such a condition is the only rational procedure. Yet in typhoid fever, with the stomach in an even worse condition, with the intestines in a much worse state and with temperature high, most medical men insist upon heavy feeding; a high calorie diet being generally recommended and employed.

Not in acute gastritis and typhoid only, but in cholera and other intestinal ills, it is the custom to insist upon plenty of good nourishing food. Indeed, food is literally forced upon the sick. Part of the recognized formula of nursing invalids is to tickle their palates with food dainties. Food is urged upon their unwilling stomach in spite of strong protests.

NAUSEA AND VOMITING

Nausea and vomiting are common symptoms in acute disease of all forms. If food is taken it is commonly vomited. Where vomiting does not take place, the food is likely to be thrown out by means of a diarrhea. What can be more ill-advised than to persuade a patient to take food, knowing that it will be vomited immediately? By rejecting food, does the body not indicate in the strongest possible manner, that food is not needed and cannot be used? Yet food is literally forced upon the sick patient, "by order of the physician," in spite of the fact that his whole system rebels against it, and in spite of the nausea and vomiting that follow taking it. Physicians resort to sedatives, anti-emetics and tonics in their efforts to force the rebellious digestive system into submission.

FEEDING INCREASES SUFFERING

To feed under such conditions causes the temperature to rise and the pains and general discomfort of the patient to increase. Much of the restlessness and uneasiness usually observed in fever patients of all kinds is due to feeding and drugging. The fasting patient is comparatively comfortable and rests well, and makes a more rapid and satisfactory recovery.

Dr. Jennings says: "The more you feed a sick man, the sicker you make him." Again, "Don't aggravate the troubles of a sick fellowman by forcing him to swallow food against the protest of his stomach."

Let us see what happens if we feed in acute "disease." The first thing the patient and physician note is an increase in symptoms. The fever goes up, the pulse increases, pain and other symptoms become more intense; the patient is caused much unnecessary suffering, and the patient's relatives are caused much needless anxiety.

Graham declared that "the more they nourish (feed) a body while diseased action is kept up in it, the more they increase the disease." Again "when the body is seriously diseased * * * entire and protracted fasting would be the very best means in many cases of removing disease and restoring health. I have seen wonderful effects result from experiments of this kind."--Science of Human Life. He also called attention to the fact that eating increases the pain, inflammation, discomfort, fever and irritableness of the sick and that it does so in proportion to the amount of food eaten and in direct ratio to its supposed nutritive qualities, while fasting reduces the "violence" of the "disease" and renders recovery more certain. All forms of acute disease are cut short and made comfortable by fasting. Fever rapidly abates and inflammation quickly subsides.

COMPENSATION

Disease is labor, action, struggle--it is often violent action. Rapid heart action, rapid breathing, vomiting, diarrhea, etc., etc., represent increased effort. This uses up energy. It often leaves the patient exhausted at the end of his strenuous effort. It may so completely exhaust him as to end his life. Disease frequently means a greater expenditure of energy than the normal activities of health require, hence the urgent need for conservation of energy in every possible way. So great is the intensity of the effort, so fully are the powers of life concentrated upon the work in hand, there is no energy available with which to carry on the work of digestion. The suspension of digestive secretions, cessation of the rhythmic contractions of the stomach and intestines and the withdrawal of the desire for food are, therefore, compensatory measures, equally with the prostration of the patient, designed to conserve energy on the one hand that it may be available for use on the other.

Dr. Jennings wrote of this conservative measure seen in all acute disease: "The great, extensive, and complicated nutritive apparatus, that requires a large amount of force to convert raw material into living structure, is put at rest, that the forces saved thereby may be transferred to the recuperative machinery within their respective limits, so that there is no call for food, and none should be offered until the crisis is passed, or a point is reached where some nutritive labor can be performed, and there is a natural call for nutriment. * * * And food has no more to do with the production of vitality, than the timber, planks, bolts and canvas for the ships have in supplying ship-carpenters and sailors. In the mass of diseases--such as simple, continued, or remittent fever, scarlet fever, measles, mild bilious fevers--and most of the disorders that are termed febrile, that require a few days to do up their recuperative work in, the proper course of treatment to be pursued, is exceedingly plain and simple. So long as there is no call for nutriment, a cup of cool water is all that is needed for the inner man."--Tree of Life, pp. 186-187.

The urgent demand for increased effort which the presence of toxins occasions is the reason for the increased, even violent effort. But violent effort in one direction requires reduced effort, by way of compensation, in other directions. Fasting by the acutely ill is definitely a compensatory measure and its urgency is in direct proportion to the severity of the symptoms. There remains digestive power in a cold, in pneumonia there is none. By this is meant that the more ill is the patient the greater is the need to refrain from eating. Curious as it may appear at first thought, health and hunger come together.

PHYSIOLOGICAL REST

"Nothing is remedial," wrote Trall, "except conditions which economize the vital expenditures." The amount of work done by the heart, liver, lungs, kidneys, glands, etc., is largely determined by the amount of food eaten. Why should these organs and the stomach and intestines be given more work to do by eating? Haven't they enough work to perform under the circumstances? Nature demands physiological rest, not physiological over-work. Her call for rest comes in unmistakable terms. Why, then, shall the organs be forced to do extra work by the use of stimulants or by feeding? To stop the use of food for a time affords the most complete rest to the whole vital economy.

Fasting, or physiological rest is the surest way of economizing vital expenditures. Walter pointed out that "the patient often grows stronger through the process of fasting and always better." It should be understood that when food is eaten by the sick man or woman, much of the vital energies must be diverted from the work of purification to that of ridding the body of the unwanted and unusable food. Even in those mild acute diseases, such as the cold, in which but part of the body's energies have been mobilized for the work of disease, and in which considerable digestive power remains, with, perhaps, some desire for food, fasting often means the difference between a mild illness with quick recovery of physiological equilibrium and a severe illness that is long drawn out, or that may end in death.

PREVENTION

Tilden says: "All acute disease could be prevented if anticipated by a fast of sufficient duration to lower the accumulated toxins below the toleration point. An anticipatory fast establishes a dependable immunization to any so-called disease. If started too late, it will eliminate or render very mild the worst types of epidemics. If this were generally known and acted upon by towns and cities in ordering the people to fast for a few days, and to follow the fast by light eating, epidemics would be shorn of their virulence, and in time rendered impotent or prevented entirely. Only the vulnerable--those pronouncedly toxemic--are attacked (?) by epidemics."

Fasting does not remove the cause of "disease"--toxemia. It merely allows the body to do its work of elimination more efficiently by not putting any hindrances in the way. Fasting does not stop the processes commonly called "disease"--nor does it shorten their duration — feeding and treatment do often suppress these processes, always impede them, and almost always lengthen their duration. The lengths of time the courses of self-limited "diseases" are said to run are times they run under the feeding and treating plans. Under fasting and resting they never run so long.

Nature indicates in the strongest possible manner her desire to fast in acute "disease". In proportion to its severity, so-called "disease" means a loss of digestive conditions and digestive power. Anorexia, nausea, vomiting and the absence of all relish for food should convince anyone, who is not a convert to the doctrine of "total depravity," that no food should be given. Due to our distrust of our natural instincts, we all too often disregard the patent demands of Nature and eat in spite of the closed-for-repairs sign she has hung out--an action invariably pursued by Nature.

If fasting were instituted at the first sign of trouble, few acute diseases would ever become very severe and many of them would be so mild as to lead to the thought that the patients would not have been very sick anyway. Unfortunately, it is the custom to continue eating when symptoms appear. As Dr. Page ably put it, Natural Cure, p. 146: "Nearly all patients continue eating regularly, until food becomes actually disagreeable, even loathsome, often; and after this every effort is exhausted to produce some toothsome compound to 'tempt the appetite.' Furthermore, and often worst of all, after the entire failure of this program, the patient can, and usually does, take to gruel or some sort of 'extract' which he can drink by holding his breath. All this tends to aggravate the acute symptoms, and to fasten the disease in a chronic form upon the rheumatic patient, or to insure rheumatic fever; and the same principle holds in nearly all acute disorders, it is well to remember."

Dr. Chas. E. Page says: "There is neither pleasure nor nourishment in forced feeding--only pain, poisoning and starving. The fasting cure universally and rationally applied, would save thousands of lives every year. For example, there would be practically no 'typhoid fever,' as all fevers would be aborted in a few days of stomach rest; and never a death or prolonged illness from whooping-cough, which is always a stomach cough from inflammation of that organ. In my busy practice of forty years, no fever has developed into 'typhoid'; nor has there been any whooping beyond a few days, and never a death."

NO DANGER OF STARVATION

There is no danger of the patient dying of starvation in the process of getting well. Let us bear in mind that the body is possessed of reserve food stores which will meet its needs for nutriment for a prolonged period. In acute "diseases" the body can supply its nutritive needs from these food reserves with less effort and with less waste of energy and substance than is required to supply them from raw materials.

We believe that man requires food all the time because we have learned to think of him as an engine or a machine that can run only so long as he is supplied with fuel. This absurd mechanistic view of life insists upon ignoring every prompting of instinct and treating man as an inanimate machine is treated.

Let the sick eat only when Nature calls for food. A large number of cases will recover, whether they feed or fast, but there is also a very large number of cases who will die, if they are fed, who would otherwise recover. To fast or to feed--this is often the issue of to live or to die.

PAIN

Pains that seem unbearable without the use of narcotics and anodynes rapidly lessen while one fasts, so that within a short time to a few days the patient is comfortable. Repeatedly have I watched the almost unbearable pains of acute articular rheumatism subside and the patient become comfortable after three or four days of fasting. In the last stages of cancer, when nothing is done for the patient except to dose him with opium, and when pains induced by opium are as great (or greater) as those resulting from the cancer, a fast will restore comfort and permit the patient to die in peace.

TORTURE OF HOPELESS CASES

"Feed the patient anything his fancy may desire; he is going to die anyway," is the advice frequently given by physicians when the patient has been brought so low that death seems inevitable. This is shameful cruelty and often results in death in cases that would otherwise recover. Why make the dying man more miserable? Why increase his suffering? "Do take a little more, dear, just to please me," coaxes the misguided wife or mother. Or a dominating, but ignorant nurse uses all of her mental power and masterful force to get the weak, perhaps dying patient to swallow more boiled milk, more meat broth, or more egg custard, which decomposes rather than digests in the patient's digestive tract.

FASTING IN FEVERS

Trall insisted that "strictly speaking, fever and food are antagonistic ideas. No simple fever, if well-managed, requires dieting in any way, save the negative one of starvation, until its violence is abated."--Hydropathic Encyclopedia, Vol. I, p. 447. Again he says: "If you give food in the early stage of a fever, you do not feed the system, you only aggravate the fever. Why? Because the vital powers are so occupied in the remedial effort that they cannot digest or assimilate. That is why so many fever patients are fed to death by the nurses and doctors * * * In fever it (the living system) cannot digest food."--Jennings-Trall Debate.

Fever indicates poisoning, usually decomposition in the intestines. It means that there is a mass of rotting food in the food tube poisoning the body. It means something else--namely: nutrition is suspended until the poisoning is overcome. It means that no food should be given to the patient until all fever and other symptoms are gone. It means that nothing but water, as demanded by thirst, should be given to the patient.

So long as there is fever and diarrhea, no food, of whatever character, can be of any use to the body. If the patient appears to be hungry, it is thirst. Give him water, for food will not relieve the thirst.

The following quotation from Trall is to the point in this connection: "Food should not be taken at all until the violence of the fever is materially abated, and then very small quantities of the simplest food only should be permitted, as gruel, with a little toasted bread or cracker, boiled rice, mealy potatoes, baked apples, etc. There is not a more mischievous or more irrational error abroad in relation to the treatment of fever than the almost universal practice of stuffing the patient continually with stimulating slops, under the name of mild nourishing diet, beef tea, mutton broth, chicken soup, panada, etc. The fever will always starve out before the patient is injured by abstinence, at least under hydropathic treatment, and the appetite will always return when the system is capable of assimilating food."--Hydropathic Encyclopedia, Vol. II, p. 84.

In speaking of the treatment of smallpox, Dr. Shew declared, Hydropathic Family Physician, p. 249: "Most fever patients are allowed to eat too much. Some may be allowed too little; but this must be the exception to the rule. In all severe fevers, the system absolutely refuses nourishment; that is, it is not digested or made into blood. Hence all nutriment, in such cases, is worse than useless, since if it does not go to nourish the system, it must only prove a source of irritation and harm. If the disease is severe, then it would be best as long as the fever lasts, to give no nourishment whatever. In mild cases it would of course be otherwise, although it would harm no one to fast a few days, but would, on the contrary, do them good. When nourishment is given, it should be of some bland and anti-feverish kind. Good and well-ripened fruit in its season would be especially useful, taken always at the time of a regular meal."

TYPHOID

Typhoid fever patients become comfortable in three to four days if the fast is instituted at the "onset" of the "disease," and in from seven to ten days are convalescing. The patient will have such a comfortable sickness and recover so speedily that friends and relatives will declare he was not sick. And, indeed, he will not be very sick.

It requires feeding and drugging to convert those simple natural processes we call acute "diseases" into serious and complicated troubles. It is not possible to have a typical case of typhoid fever, as described in allopathic text-books, without typical text-book treatment. Unthwarted nature never builds such complications and such serious "diseases" as are described in allopathic works. All this mass of pathology is built by drugging, serum squirting and feeding.

In a voluminous work on diet, contributed to by a number of medical authorities in dietetics and edited by G. A. Sutherland, M.D., F.R.C.E., and entitled A System of Diet and DieteticsDiet In Fever and Acute Infectious Disease, contributed by Claude E. Ker, M.D., F.R.C.P., Ed., which are worth quoting. He says, in discussing the "starvation treatment" in enteric fever (typhoid fever): (published by the Physicians and Surgeons Book Co., of New York City) I find a few interesting paragraphs in the chapter on

"The same idea which underlies the empty bowel theory is no doubt responsible for the attempts made to treat enteric fever with either no food by the mouth at all, or at the most with very little quantities. Thus Queirolo has recommended that feeding should be entirely rectal, a lemonade made up with a little hydrochloric acid being the only drink allowed, provided that the bowel of a patient so treated was first emptied by a dose of calomel, or other suitable purgative. Such method of dieting should secure complete rest for the affected parts and absolutely exclude the possibility of fermenting masses of partially digested material lying in the gut. The nutritive value, however, of rectal feeding in a prolonged disease is so limited that this method may be fairly regarded as a treatment by starvation.

"Similar in its objects and effects is the method suggested by Williams, who, believing that the exhausting diarrhea of the fever is due to improper feeding, endeavors to secure that the bowels shall, as far as possible, remain empty. Only water is allowed in severe cases, sometimes for days at a time, and he regards half a pint of milk in twenty-four hours as a liberal diet, seldom apparently exceeding this amount until the temperature is normal. The method seems drastic, but I have reason to know that the cases do remarkably well. I have often marvelled at the amount of starvation which a typhoid case can safely tolerate after a hemorrhage, and it is only rational to suppose that the patient would support starvation even better before such a depressing complication had occurred. Under such a regime Williams probably more nearly attains the ideal of the 'empty bowel' than any other observer. It seems almost incredible that patients so treated should occasionally gain weight and that they do not in any case waste more than patients more liberally fed; but it is, after all, obvious that, if food is not assimilated there is no benefit to be derived from it, and in many cases of enteric fever assimilation is undoubtedly extremely poor.

"The theoretical objection to both these methods of treatment is that, if ulceration has once started such a remarkably low diet would apparently give the intestinal lesions only a poor chance of repair. On the other hand, it is possible that the absence of irritation would go far to counterbalance this defect, apparently as the patient seems to stand the starvation so well. If plenty of water was supplied this would be more easily understood, but some of Williams' patients were limited, for a time at least, to one pint of water per diem, which seems to be a most inadequate amount."

Dr. Ker is unwilling to recommend what he mistakenly calls the "starvation treatment," but thinks there is much to be learned from such things and adds: "It encourages us to starve for two or three days, if necessary, severe cases with marked gastric and intestinal disturbances, probably very much to their advantage. It is, however, unnecessarily severe for the average patient, even while we admit that in enteric fever there is no certainty as to what may happen from day to day."

We have it stated that the exhausting diarrhea of typhoid is probably due to improper feeding.

We have it admitted that a "starvation treatment" seems complete rest for the affected parts of the intestine.

We have it admitted that typhoid patients may "starve" for days and make remarkable improvement during this time.

We have it admitted that they may do this even after a hemorrhage.

We also have it admitted that in this "disease" "assimilation is undoubtedly extremely poor." (It is so poor that there is none). We have it admitted that "starvation" leaves no rotting food in the intestines to irritate and poison the inflamed and ulcerated intestinal wall.

Every one of these things, Hygienists have been pointing out for a hundred years. We have been denounced as "quacks" and "ignorant pretenders" for so doing and our methods have been rejected by the medical profession as a whole, and, even now, the authorities, in adopting our methods in part, and in reporting favorably upon them, neglect to give credit where credit is plainly due.

Dr. Ker overlooks the important fact that where typhoid patients are not fed, ulceration is not likely to occur, and that hemorrhages are extremely rare, while he seems to be wholly unaware of the body's ability to heal wounds, broken bones, open sores, ulcers, etc., while fasting.

The theoretical objection offered to fasting, in enteric fever, is based on ignorance. It completely ignores the preceding statement that "assimilation is undoubtedly extremely poor," and it appears to be made in utter ignorance of the body's own internal resources. The author does not seem to be cognizant of the fact that repair of tissues does go on during a fast. What is more, he overlooks the fact that if feeding is stopped at the "onset" of the "disease" there is not likely to be any ulceration or any hemorrhage. Besides this, the patient is more comfortable and the "disease" of shorter duration--providing no drugging is resorted to. It is encouraging to note that he does not offer, as an objection, the old notion that fasting lowers one's resistance to germs.

The fault I find with the method of Queirolo is that he does not stop feeding at the outset instead of waiting until the "disease" becomes well developed and not that it is "too severe for the average patient." On the contrary, it is the easiest, safest and best plan. The feeding and drugging plan is the drastic plan; the plan than intensifies and prolongs the patient's suffering. It is no ordeal to do without food in acute illness. The ordeal consists in eating at such times. All we ask when acutely sick is to be let alone and to be free of worry of any kind.

PNEUMONIA

If fasting is instituted at the very outset in pneumonia, the patient will not be very sick, the exudate into the lungs will not be great and resolution will be hastened. Death in pneumonia will be very rare.

APPENDICITIS

All medical authorities admit the great value of fasting in appendicitis and recommend its employment, if the patient refuses an operation, or, if for some other reason an operation is considered inadvisable. The pains of appendicitis practically cease after about three days of fasting.

RHEUMATISM

Page quotes Casey A. Wood, M.D., Professor of Chemistry in the Medical Department of Bishop's College, Montreal, in an article in the Canada Medical Record, entitled "Starvation in the treatment of Acute Articular Rheumatism," as giving the "history of seven cases where the patients were speedily restored to health by simply abstaining from food from four to eight days, and he says he could have given the history of forty more from his own practice." No drugs were used.

"In no case did this treatment fail." The cases reported "included men and women of different ages, temperaments, occupations, and social positions." Dr. Wood says: "From the quick and almost invariably good results to be obtained by simple abstinence from food, I am inclined to the idea that rheumatism is, after all, only a phase of indigestion." Dr. Page adds: "In chronic rheumatism he obtained less positive results, but did not venture to try fasts of longer duration." Dr. Wood concludes by saying that "this treatment, obviating as it does, almost entirely, danger of cardiac complications, will be bound to realize all that has been claimed for it--a simple, reliable remedy for a disease that has long baffled the physician's skill."

COUGHS

Most coughs can be stopped by a twenty-four to seventy-two hours fast; then, if the errors in eating are corrected, the cough is gone forever. Relief comes in the very worst cases of bronchial asthma in from twenty-four to seventy-two hours of fasting so that the sufferer can lie down and sleep in comfort.

DIARRHEA - DYSENTERY

Vomiting, restlessness, diarrhea and gross fatness are some of the symptoms of the surfeit disease and its proper cure is--not soothing syrups, but--fasting. Imagine feeding a patient who is having twenty to thirty bowel movements in twenty-four hours; or one that is vomiting frequently! Dysentery medicines may be entirely dispensed with if the sufferer will resort to fasting.

Oswald says: "For the incipient stages of the disorder the great specific is fasting. Denutrition, or the temporary deprivation of food, exercises an astringent influence, as part of its general constructive effect. The organism, stinted in the supply of its vital resources, soon begins to curtail its current expenditure. The movements of the respiratory process decrease; the temperature of the body sinks, the secretion of bile and uric acid is diminished, and before long the retrenchments of the assimilative process react on the functions of the intestinal organs; the colon contracts, and the smaller intestines retain all but the most irritating ingesta."

WASTING BY THE ACUTELY ILL DESPITE FEEDING

Dewey emphasized the fact that the bodies of the acutely ill always waste, no matter what they are fed nor how much. Indeed, he insisted that in typhoid and other severe fevers, the patient that is fed wastes most. This fact that in acute disease wasting goes on whether food is eaten or not, and that in fact, it is frequently true that the more the patient is fed, the greater the wasting, shows unmistakably that no food is absorbed and used during acute illness. Certainly, if it cannot be digested, it will not be absorbed and if it is not absorbed, it will not be assimilated, and if it is not assimilated, it can do the patient no good.

Ker believes in feeding to "keep up the strength of the patient," as do all "orthodox" medical men. Feeding in acute "disease" does not keep up strength and does not prevent the wasting of the patient.

"In all diseases," says Dr. Dewey, "in which there is a high pulse and temperature, pain or discomfort, aversion to food, a foul, dry mouth and tongue, thirst, etc., wasting of the body goes on no matter what the feeding, until a clear, moist tongue and mouth and hunger mark the close of the disease, when food can be taken with relish and digested. This makes it clearly evident that we cannot save the muscles and fat by feeding under these adverse conditions."

The wasted bodies of patients who have been fed through acute illness is the strongest kind of evidence, to those who are capable of seeing, that the food they were fed was not digested and assimilated, and that their own tissues were drawn upon to provide the materials necessary to carry on the processes of life. We may go a step further and say that in practically every instance the wasting will be greater and the "disease" will be of longer duration if the patient is fed than if he is fasted. Liek says: "From my observations on children and animals, I have come to the conclusion that, particularly in acute diseases, fasting greatly favors the process of healing."

If the food eaten is not digested, of what value can it be to the sick man or woman? A two hundred pound man may become sick with typhoid fever. He will lose weight no matter how much he is fed, until, when he is well, he is but a shadow of his former self. In fact, the more he is fed the sicker he becomes, the more prolonged his illness, and the more he will lose in weight. What more conclusive evidence is needed to prove that the food eaten does harm and not good? What is true of typhoid is also true of other "diseases."

WEAKNESS

Weakness in acute "disease" is not properly attributed to the fast. Indeed, the fasting patient will not become as weak as the eating patient. He is more likely to grow stronger as the fast progresses. I am pleased to present the following orthodox testimony, on this point, by Dr. Liek, who says: "Those who are sick feel weak. Those who have been operated upon and who wake up from the narcosis are greatly enfeebled. According to the text books, we can overcome that weakness with strengthening food. Nothing is more obvious. Hence, we inquire for the most nourishing and strengthening foods and give them to patients. That idea is, of course, completely mistaken. The patient has been weakened not by a short fast, but by the disease, by the after-effects of the narcosis, the shock of the operation, etc." It should be obvious that the weaker the patient is, the less able is he to take and digest nourishment. The weaker he is the greater is the need for rest.

death after hospital overdose treatment ...How ? Dehydration and/or insulin induced HYPOglycemia and/or HYPOvolemia ??

noreply@blogger.com (Nicholas Dynes Gracey) — Thu, 19 Jun 2008 12:35:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

Natural causes verdict on Cheshire woman who died a day after taking overdose ?

Published Date: 19 June 2008

ORIGINAL By Hayley Maguire

http://www.ChesterEveningLeader.co.uk/news/Natural-causes-verdict-on-Cheshire.4200763.jp

Source: Evening Leader Chester
Location: Mold

OBSERVATIONS ADDED IN UPPER/CASE ...

A MOTHER died at her home from medical complications a day after BEING TREATED FOR taking an overdose.

Jayne Elizabeth Wildsmith died at the Countess of Chester Hospital on July 30 after suffering a pulmonary embolism and deep vein thrombosis.

TWICE ??

Cheshire coroner Nicholas Rheinberg heard Mrs Wildsmith, 45, of Denbigh Close, Ellesmere Port, had a long history of depression, suffered with asthma and diabetes and was obese.

Mr Rheinberg read a statement by Mrs Wildsmith's GP, Dr Catherine Elizabeth Wall, who said the depression was exacerbated by a problem with alcohol.

Mrs Wildsmith told Dr Wall on July 9 she had stopped taking her medication and was feeling much better.

She returned to the doctor's on July 27 saying she was feeling anxious and having suicidal thoughts [SSRI ? / STATINS ?].

On July 29 she was admitted to hospital after taking an overdose.

Sarah Jayne Edwards, of Derwent Court, Ellesmere Port, gave evidence at the Chester inquest and said her sister had been divorced since 1992.

Mrs Wildsmith's son, Martin Edwards, said he was awoken by his mother on July 30. She told him she had taken an overdose and had called an ambulance.

Mr Edwards said his mother arrived home at 6.30pm [ON WHAT DATE ?] and had to be helped out of the taxi.

HYPOGLYCEMIA / DEHYDRATION SYMPTOMS ...

"She was staggering and was slurring her words," he said.

"I couldn't smell any alcohol and thought it was the result of the overdose."

He said he gave her some soup before taking her to bed and checked on her every 15 minutes.

After the third check, she seemed fine and he went to bed himself.

The next day he got up at noon and checked on his mother at 1.30pm [ON WHAT DATE ?].

"She was lying as I had left her. I tried to wake her and felt her hand and it was cold," he said.

Dr Sally Ann Hales, pathologist at Countess of Chester Hospital, said Mrs Wildsmith's obesity and osteoarthritis were contributory factors in her death.

The cause of death was given as pulmonary embolism arising partly as a result of immobility.

Mr Rheinberg, who recorded a verdict of death by natural causes, said Mrs Wildsmith's overdose was a "dramatic gesture" and not a serious attempt to take her own life.

The full article contains 381 words and appears in Evening Leader Chester newspaper ...

http://www.ChesterEveningLeader.co.uk/news/Natural-causes-verdict-on-Cheshire.4200763.jp

Last Updated: 19 June 2008 11:50 AM
Source: Evening Leader Chester
Location: Mold

HYPOvolemia ...

In physiology and medicine, HYPOvolemia (also HYPOvolaemia) is a state of decreased blood volume; more specifically, decrease in volume of blood plasma.

Volumetric thirst can be caused by a number of things including bleeding and diarrhea. Volumetric thirst arises when the volume of blood plasma decreases.

Causes

Common causes of HYPOvolemia can be dehydration,
bleeding, vomiting^[1], severe burns and drugs such as diuretics or vasodilators typically used to treat hypertensive individuals. Rarely, it may occur as a result of a blood donation^[2], sweating^[1], and alcohol consumption^[1].

Effects

Severe hypovolemia leads to hypovolemic shock.

A low blood volume can result in multiple organ failure, kidney damage and failure, brain damage, coma and death (desanguination).

Bodily response

To respond to hypovolemia is a task for the body fluid balance systems as well as osmotic balance systems.

Following an acute response, this function is accomplished by two sets of receptors; one in the kidneys and the other in the heart.

Acute response ...

Further information: Baroreflex

The first response to HYPOvolemia is an inversed baroreflex, where a lack of activation of baroreceptors results in elevation of total peripheral resistance and cardiac output via increased contractility of the heart, heart rate, and arterial vasoconstriction,^[3]which tends to increase blood pressure.

Kidney

Main article: Renin-angiotensin system

The kidneys have a specialized set of cells that enable the recognition of changes in blood flow to the kidneys.^[1]

Naturally, these cells detect the presence of hypovolemia and react accordingly to the loss of blood volume.

These cells secrete a hormone called renin when there is a decrease in the flow of blood to the kidneys.^[1]

Renin flows into the blood and there, initiates the conversion of a protein called angiotensinogen to angiotensin.^[1]

In order to exert its effects on the body, angiotensin I must be converted by enzymes into its active form, angiotensin II.

Physiologically, angiotensin II stimulates the release of hormones by the posterior pituitary gland (ADH, also known as vasopressin) and the adrenal cortex (aldosterone).

Aldosterone causes the kidneys to reabsorb sodium, leading to the reabsorption of water. ADH (vasopressin) also causes the kidneys to reabsorb water.

Angiotensin II increases blood pressure by contracting arterial muscles.

Heart

Further reading:Atrial natriuretic peptide

The next set of receptors responsible for detecting volumetric insufficiency are located in the heart atria. Commonly referred to as stretch receptors, these atrial baroreceptors detect the amount of blood that is being pumped back into the heart from the veins.^[1] The body constantly returns blood to the heart through veins. Therefore, when the volume of blood being transported back to the heart is decreased, these receptors detect the change in the amount of blood thereby reducing the release of atrial natriuretic peptide.

Thirst

Main article: Extracellular thirst

Both the activation of the renin angiotensin system and the decrease in atrial natriuretic peptide, along their other functions, contribute to elicit thirst, by affecting the subfornical organ.^[4]

Other response ...

Furthermore, as intravascular fluid decreases, blood pressure is reduced and the body attempts to compensate by moving fluid from other cellular compartments into the vasculature.
Fluid is transferred from all of the fluid compartments in the body, including intracellular, interstitial and other extravascular compartments.^[1]

Diagnosis

Clinical symptoms may not present until 10-20% of total whole-blood volume is lost.

Hypovolemia can be recognized by elevated pulse, diminished blood pressure, and the absence of perfusion as assessed by skin signs (skin turning pale) and/or capillary refill on forehead, lips and nail beds. The patient may feel dizzy, faint, nauseated, or very thirsty. These signs are also characteristic of most types of shock.

Note that in children, compensation can result in an artificially high blood pressure despite hypovolemia. This is another reason (aside from initial lower blood volume) that even the possibility of internal bleeding in children should always be treated aggressively.

Also look for obvious signs of external bleeding while remembering that people can bleed to death internally without any external blood loss.

Also consider possible mechanisms of injury (especially the steering wheel and/or use/non-use of seat belt in motor vehicle accidents) that may have caused internal bleeding such as ruptured or bruised internal organs. If trained to do so and the situation permits, conduct a secondary survey and check the chest and abdominal cavities for pain, deformity, guarding or swelling. (Injuries to the pelvis and bleeding into the thigh from the femoral artery can also be life-threatening.)

Treatment

Minor HYPOvolemia from a known cause that has been completely controlled (such as a blood donation from a healthy patient who is not anemic) may be countered with initial rest for up to half an hour.

Oral fluids including moderate sugars (apple juice is good) and rich in electrolytes are needed to replenish the organism of lost sodium ions.

Furthermore the advice is to the donor to eat good solid meals with proteins for the next few days.

Typically, this would involve a fluid volume of less than one liter (1000 ml), although this is highly dependent on body weight.

Larger people can tolerate slightly more blood loss than smaller people.

More serious HYPOvolemia should be assessed by a nurse or doctor. When in doubt, treat HYPOvolemia aggressively.

First Aid

External bleeding should be controlled by direct pressure. If direct pressure fails, other techniques such as elevation and pressure points should be considered. The tourniquet should be used in the case of massive hemorrhage i.e. arterial bleeds, such as the femoral artery, as a last resort, for the use of a tourniquet can easily kill all the tissue below its application upon a limb, making amputation necessary. If a first-aider recognizes internal bleeding, the life-saving measure to take is to immediately call for emergency assistance.

Field Care

Emergency oxygen should be immediately employed to increase the efficiency of the patient's remaining blood supply. This intervention can be life-saving.

The use of intravenous fluids (IVs) may help compensate for lost fluid volume, but IV fluids cannot carry oxygen in the way that blood can. See also emergency medical services for a discussion of techniques used in IV fluid management of hypovolemia.

Hospital Treatment

If the HYPOvolemia was caused by medication, the administration of antidotes may be appropriate but should be carefully monitored to avoid shock or the emergence of other pre-existing conditions.

Blood transfusions coupled with surgical repair are the definitive treatment for hypovolemia caused by trauma. See also the discussion of shock and the importance of treating reversible shock while it can still be countered.

History

HYPOvolemia has historically been termed desanguination (from Latin sanguis, blood), meaning a massive loss of blood. The term was widely used by the Hippocrates in traditional medicine practiced in the Greco-Roman civilization and in Europe during the Middle Ages. The word was possibly used to describe the lack of personality (by death or by weakness) that often occurred once a person suffered hemorrhage or massive blood loss.

References

^ ^a ^b ^c ^d ^e ^f ^g ^h Carlson, N. R. (2005). Foundations of Physiological Psychology: Custom edition for SUNY Buffalo. Boston, MA: Pearson Custom Publishing.
^ Danic B, Gouezec H, Bigant E, Thomas T (2005). "Incidents of blood donation". Transfus Clin biol Jun;12(2):153-9. PMID 15894504
^ [Influence of age on the cardiovascular response during graded haemorrhage in anaesthetized rats] Andrej Banic 1, Gisli H. Sigurdsson 2, Anthony M. Wheatley 3 1Department of Plastic Surgery, University of Berne, Inselspital, CH-3010 Bern, Switzerland
^ M.J. McKinley and A.K. Johnson (2004). "The Physiological Regulation of Thirst and Fluid Intake". News in Physiological Sciences 19 (1): 1-6.

External links

CRISP Thesaurus 00004050
DDB 29217

v • d • e Water-electrolyte imbalance and acid-base imbalance (E86-E87, 276)

Volume status	Dehydration/Hypervolemia - HYPOvolemia

Electrolyte	Na⁺ Hypernatremia/Hyponatremia K⁺ Hyperkalemia/Hypokalemia Cl⁻ Hyperchloremia/Hypochloremia

Acid-base	Acidosis: Metabolic - Respiratory - Lactic - Ketosis Alkalosis: Metabolic, Respiratory Mixed disorder of acid-base balance

Golfers & Gardeners eat trichlorfon pesticides ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Thu, 19 Jun 2008 09:58:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.
Diabetes: Why golfers are more likely to become diabetic | What Doctors Don't Tell You: "... Diabetes: Why golfers are more likely to become diabetic ..."

19 June 2008

People who like to get out on the golf course for a round or two – thinking they are doing some good for their health – are actually increasing their chances of diabetes.

Researchers have discovered that the pesticides commonly used on golf courses and other public areas can double the risk of diabetes. Pesticides that contain the chemical trichlorfon are especially associated with diabetes, and are to be added to the other known risks, such as obesity and diet.

Trichlorfon is an organo-phosphate insecticide that is used by professional Groundsmen to maintain turf, such as golf courses, and it is also sold to the public. Not surprisingly, the greatest at-risk group is gardeners and others who regularly work with the pesticides.

Researchers from America’s National Institutes of Health estimate that the risk can be as high as 200 per cent in workers who are exposed to the pesticides for more than 100 days in their working life.

(Source: National Institutes of Health: http://www.niehs.nih.gov/news/releases/2008/longterm.cfm)"

Long-term Pesticide Exposure May Increase Risk of Diabetes

Licensed pesticide applicators who used chlorinated pesticides on more than 100 days in their lifetime were at greater risk of diabetes, according to researchers from the National Institutes of Health (NIH). The associations between specific pesticides and incident diabetes ranged from a 20 percent to a 200 percent increase in risk, said the scientists with the NIH's National Institute of Environmental Health Sciences (NIEHS) and the National Cancer Institute (NCI).

"The results suggest that pesticides may be a contributing factor for diabetes along with known risk factors such as obesity, lack of exercise and having a family history of diabetes," said Dale Sandler, Ph.D., chief of the Epidemiology Branch at the NIEHS and co-author on the paper. "Although the amount of diabetes explained by pesticides is small, these new findings may extend beyond the pesticide applicators in the study," Sandler said. Some of the pesticides used by these workers are used by the general population, though the strength and formulation may vary. Other insecticides in this study are no longer available on the market, however, these chemicals persist in the environment and measurable levels may still be detectable in the general population and in food products. For example, chlordane, which was used to treat homes for termites, has not been used since 1988, but can remain in treated homes for many decades. More than half of those studied in the National Health and Nutrition Examination Survey in 1999-2002 had measurable evidence of chlordane exposure. "This is not cause for alarm," added Sandler "since there is no evidence of health effects at such very low levels of exposure."

Overall, pesticide applicators in the highest category of lifetime days of use of any pesticide had a small increase in risk for diabetes (17 percent) compared with those in the lowest pesticide use category (0-64 lifetime days). New cases of diabetes were reported by 3.4 percent of those in the lowest pesticide use category compared with 4.6 percent of those in the highest category. Risks were greater when users of specific pesticides were compared with applicators who never applied that chemical. For example, the strongest relationship was found for a chemical called trichlorfon, with an 85 percent increase in risk for frequent and infrequent users and nearly a 250 percent increase for those who used it more than 10 times. In this group, 8.5 percent reported a new diagnosis of diabetes compared with 3.4 percent of those who never used this chemical. Trichlorfon is an organophosphate insecticide classified as a general-use pesticide that is moderately toxic. Previously used to control cockroaches, crickets, bedbugs, fleas, flies and ticks, it is currently used mostly in turf applications, such as maintaining golf courses.

"This is one of the largest studies looking at the potential effects of pesticides on diabetes incidence in adults," said Freya Kamel, Ph.D., a researcher in the intramural program at NIEHS and co-author in the paper appearing in the May issue of the American Journal of Epidemiology. "It clearly shows that cumulative lifetime exposure is important and not just recent exposure," said Kamel. Previous cross-sectional studies have used serum samples to show an association between diabetes and some pesticides.

Diabetes occurs when the body fails to produce enough insulin to regulate blood sugar levels or when tissues stop responding to insulin. Nearly 21 million Americans have diabetes. The cause of diabetes continues to be a mystery, although genetics and environmental factors such as obesity and lack of exercise appear to play roles.

To conduct the study, the researchers analyzed data from more than 30,000 licensed pesticide applicators participating in the Agricultural Health Study, a prospective study following the health history of thousands of pesticide applicators and their spouses in North Carolina and Iowa. The 31,787 applicators in this study included those who completed an enrollment survey about lifetime exposure levels, were free of diabetes at enrollment, and updated their medical records during a five-year follow-up phone interview. Among these, 1,171 reported a diagnosis of diabetes in the follow-up interview. The majority of the study participants were non-Hispanic white men.

Researchers compared the pesticide use and other potential risk factors reported by the 1,171 applicators who developed diabetes since enrolling in the study to those who did not develop diabetes. Among the 50 different pesticides the researchers looked at, they found seven specific pesticides — aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor and cynazine - that increased the likelihood of diabetes among study participants who had ever been exposed to any of these pesticides, and an even greater risk as cumulative days of lifetime exposure increased.

All seven pesticides are chlorinated compounds, including two herbicides, three organochlorine insecticides and two organophosphate pesticides.

"The fact that all seven of these pesticides are chlorinated provides us with an important clue for further research," said Kamel. Previous studies found that organochlorine insecticides such as chlordane were associated with diabetes or insulin levels. The new study shows that other types of chlorinated pesticides, including some organophosphate insecticides and herbicides, are also associated with diabetes. The researchers also found that study participants who reported mixing herbicides in the military had increased odds of diabetes compared to non-military participants.

Reference:
Montgomery MP, Kamel F, Saldana TM, Alavanja MCR, Sandler DP. Incident diabetes and pesticide exposure among licensed pesticide applicators: Agricultural Health Study 1993 – 2003, Amer J Epidemiol, 2008;167:1235-46.

###

The Agricultural Health Study (http://aghealth.nci.nih.gov/) (AHS) is a prospective study of licensed pesticide applicators from North Carolina and Iowa recruited in 1993-1997 at the time of license renewal. The cohort includes 4,916 commercial applicators from Iowa and 52,395 private applicators, mostly farmers, from both states. More than 75 percent or 32,347 spouses of married private applicators also enrolled in the cohort. The study is a collaboration of the National Institute of Environmental Health Sciences (NIEHS), the National Cancer Institute (NCI), the Environmental Protection Agency (EPA) and the National Institute for Occupational Safety and Health (NIOSH).

For more information about cancer, please visit the NCI Web site at http://www.cancer.gov(http://aghealth.nci.nih.gov/) , or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

The primary mission of the National Institute of Environmental Health Sciences(http://www.niehs.nih.gov/) (NIEHS), one of 27 Institutes and Centers at the National Institutes of Health, is to reduce the burden of human illness and disability by understanding how the environment influences the development and progression of human disease. For additional information, visit the NIEHS Web site at http://www.niehs.nih.gov/.

The National Institutes of Health (NIH) — The Nation's Medical Research Agency - includes 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical, and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov/ (http://www.nih.gov/) .

▼ Down:

14 Apr 2008: Brain Study May Lead to Improved Epilepsy Treatments

fuel starving fetal brains grow slower how ? AND what happens to baby C-peptide, proinsulin & proglucagon ?

noreply@blogger.com (Nicholas Dynes Gracey) — Thu, 19 Jun 2008 07:51:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

Eur J Obstet Gynecol Reprod Biol. 2008 Mar;137(1):47-9. Epub 2007 Nov 14. LinkOut

Fetal growth in women managed with insulin pump therapy compared to conventional insulin.

The Princess Royal Maternity Hospital, 16 Alexandra Parade, Glasgow, G31 2ER, UK.

dawn.kernaghan@btinternet.com

OBJECTIVE: Fetal HYPERinsulinemia secondary to maternal HYPERglycemia is considered to be the driving force behind ALLEGEDLY excessive fetal growth.

It has been HYPOthesised that insulin pump therapy (continuous subcutaneous insulin infusion, CSII) would improve maternal glycemic control and normalies fetal growth parameters.

To this end, this study compares maternal glycemic control and fetal growth of women receiving insulin pump therapy with those receiving conventional insulin therapy.

STUDY DESIGN: Prospective non-randomised study of 42 women with pre-existing diabetes attending a joint obstetric diabetic clinic.

Each woman was offered the choice of commencing insulin pump therapy or remaining on a conventional insulin regime.

Estimated fetal weight and fetal growth velocity were calculated from routinely collected third trimester ultrasound biometry and expressed as standard deviation (Z) scores.

RESULTS: Eighteen women commenced insulin pump therapy.

There was no difference in pre-conception glycosylated haemoglobin A1c concentrations (HbA1c) between pump and conventional therapy groups (mean HbA1c 7.62 versus 8.01; p=0.49) or third trimester glycemic control (mean HbA1c 6.63 versus 6.44; p=0.51).

Women using pump therapy had similar mean growth velocity Z scores (1.5 versus 1.36; p=0.83), similar mean estimated fetal weight Z scores prior to delivery (2.80 versus 2.16; p=0.16) and similar mean birthweight Z scores (2.09 versus 2.00; p=0.86) compared to women using conventional insulin therapy.

CONCLUSION: This small, non-randomised study ALLEGEDLY suggests that the use of insulin pump therapy offers no benefit in terms of normaliesing fetal growth velocity, fetal size, birthweight or improving maternal glycemic control compared to conventional insulin therapy.

PMID: 18006209 [ORIGINAL PubMed]

Troponin shows fuel-anemia heart attack

noreply@blogger.com (Nicholas Dynes Gracey) — Wed, 18 Jun 2008 09:01:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

Troponin

Troponin is a complex of three proteins that is integral to muscle contraction in skeletal and cardiac muscle, but not smooth muscle. Troponin is attached to the protein tropomyosin and lies within the groove between actin filaments in muscle tissue. In a relaxed muscle, tropomyosin blocks the attachment site for the myosin crossbridge, thus preventing contraction. When the muscle cell is stimulated to contract by an action potential, calcium channels open in the sarcoplasmic reticulum and release calcium into the sarcoplasm. Some of this calcium attaches to troponin, causing a conformational change that moves tropomyosin out of the way so that the cross bridges can attach to actin and produce muscle contraction.

Troponin is found in both skeletal muscle and cardiac muscle, but the specific versions of troponin differ between types of muscle. The main difference is that the TnC subunit of troponin in skeletal muscle has four calcium ion binding sites, whereas in cardiac muscle there are only three.

Discussions of troponin often pertain to its functional characteristics and/or to its usefulness as a diagnostic marker for various heart disorders.

Functional characteristics

Role of troponins

Both cardiac and skeletal muscles are controlled by changes in the intracellular calcium concentration. When calcium rises, the muscles contract, and when calcium falls the muscles relax.

Troponin is a component of thin filaments (along with actin and tropomyosin), and is the protein to which calcium binds to accomplish this regulation. Troponin has three subunits, TnC, TnI, and TnT. When calcium is bound to specific sites on TnC, tropomyosin rolls out of the way of the actin filament active sites, so that myosin (a molecular motor organized in muscle thick filaments) can attach to the thin filament and produce force and/or movement. In the absence of calcium, tropomyosin interferes with this action of myosin, and therefore muscles remain relaxed.

Troponin I has also been shown to inhibit angiogenesis in vivo and in vitro.

Individual subunits serve different functions:

Troponin C binds to calcium ions to produce a conformational change in TnI
Troponin T binds to tropomyosin, interlocking them to form a troponin-tropomyosin complex
Troponin I binds to actin in thin myofilaments to hold the troponin-tropomyosin complex in place

Diagnostic use

Certain subtypes of troponin (cardiac troponin I and T) are very sensitive and specific indicators

of damage to the

heart muscle (myocardium). They are measured in the blood to differentiate between unstable angina and myocardial infarction (heart attack) in patients with chest pain. A patient who had suffered from a myocardial infarction would have an area of damaged heart muscle and so would have elevated cardiac troponin levels in the blood.^[1]

It is important to note that cardiac troponins are a marker of all heart muscle damage, not just myocardial infarction. Other conditions that directly or indirectly lead to heart muscle damage can also therefore increase troponin levels:^[2]

Cardiac:
Non-cardiac:
- Critical illness, e.g. sepsis
- High-dose chemotherapy
- Primary pulmonary hypertension
- Pulmonary embolism
- Renal failure
- Subarachnoid hemorrhage
- Scorpion venom
- Stroke
- Very heavy exercise (marathon)

Detection of cardiac troponin

Cardiac troponin T and I are measured by immunoassay methods.^[3] Due to patent regulations a single manufacturer distributes cTnT. A host of diagnostic companies make cTnI immunoassay methods available on many different immunoassay platforms.^[4]

Detection of cardio-toxicity and cardio-protection

Drug-induced cardiotoxicity is common to all classes of therapeutic drugs. It is essential that cardiotoxicity is detected with a high degree of sensitivity and specificity. The newly developed troponins are especially useful in this context^[5] Similarly, cardioprotective effects of therapeutic intervention is paramount in preserving myocardial integrity, especially during general surgery. Sensitive assays for cardiac troponin can be used to monitor the protective effects of intervention. ^[6]

Cardiac troponin I, in a community-based cohort study indicating the importance of silent cardiac damage, has been shown to predict first CHD event in men free from CVD at baseline, and death. ^[7]

Sources

^ Antman EM, Tanasijevic MJ, Thompson B, Schactman M, McCabe CH, Cannon CP, Fischer GA, Fung AY, Thompson C, Wybenga D, Braunwald E. Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes. N Engl J Med 1996;335:1342-9. PMID 8857017.
^ Ammann P, Pfisterer M, Fehr T, Rickli H. Raised cardiac troponins. BMJPMID 15117768. 2004;328:1028-9.
^ Melanson SEF, Tanasijevic MJ, Jarolim P. Cardiac Troponin Assays Circulation. 2007;116:e501-e504.
^ Collinson PO, Boa FG, Gaze DC. Measurement of cardiac troponin. Ann Clin BiochemPMID 11587122. 2001;38:423-449.
^ Gaze DC, Collinson PO. Cardiac troponins as biomarkers of drug- and toxin-induced cardiac toxicity and cardioprotection. Expert Opin Drug Metab Toxicol 2005;1:715-725. PMID 16863435.
^ Gaze DC. The role of existing and novel cardiac biomarkers for cardioprotection. Curr. Opin. Invest. Drugs 2007;8:711-7. PMID 17729182.
^ B Zethelius, N Johnston, P Venge. Troponin I as a Predictor of Coronary Heart Disease and Mortality in 70-Year-Old Men Circulation. 2006;113:1071-1078

Human C-peptide helps protect cells

noreply@blogger.com (Nicholas Dynes Gracey) — Tue, 17 Jun 2008 18:52:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

Diabetologia. 2008 May 21. [Epub ahead of print] Links

Human C-peptide antagonises high glucose-induced endothelial dysfunction through the nuclear factor-kappaB pathway.

Luppi P, Cifarelli V, Tse H, Piganelli J, Trucco M.

Division of Immunogenetics, Department of Pediatrics, Rangos Research Center, Children’s Hospital of Pittsburgh, 3460 Fifth Avenue, Pittsburgh, PA, 15213, USA, luppip@pitt.edu.

AIMS/HYPOTHESIS: Endothelial dysfunction in diabetes is predominantly caused by hyperglycaemia leading to vascular complications through overproduction of oxidative stress and activation of the transcription factor nuclear factor-kappaB (NF-kappaB).

Many studies have suggested that decreased circulating levels of C-peptide may play a role in diabetic vascular dysfunction.

To date, the possible effects of C-peptide on endothelial cells and intracellular signalling pathways are largely unknown.

We therefore investigated the effect of C-peptide on several biochemical markers of endothelial dysfunction in vitro.

To gain insights into potential intracellular signalling pathways affected by C-peptide, we tested NF-kappaB activation, since it is known that inflammation, secondary to oxidative stress, is a key component of vascular complications and NF-kappaB is a redox-dependent transcription factor.

METHODS: Human aortic endothelial cells (HAEC) were exposed to 25 mmol/l glucose in the presence of C-peptide (0.5 nmol/l) for 24 h and tested for expression of the gene encoding vascular cell adhesion molecule-1 (VCAM-1) by RT-PCR and flow cytometry.

Secretion of IL-8 and monocyte chemoattractant protein-1 (MCP-1) was measured by ELISA. NF-kappaB activation was analysed by immunoblotting and ELISA.

RESULTS: Physiological concentrations of C-peptide affect protection in relation to ... high glucose-induced endothelial dysfunction by...

(1) decreasing VCAM-1 expression and U-937 cell adherence to HAEC;

(2) reducing secretion of IL-8 and MCP-1; and

(3) suppressing NF-kappaB activation.

CONCLUSIONS/INTERPRETATION: During hyperglycaemia, C-peptide directly affects VCAM-1 expression and both MCP-1 and IL-8 HAEC secretion by reducing NF-kappaB activation.

These effects suggest a physiological anti-inflammatory (and potentially anti-atherogenic) activity of C-peptide on endothelial cells.

PMID: 18493738

Human proinsulin C-peptide reduces high glucose-induced proliferation and NF-kappaB activation in vascular smooth muscle cells. [Atherosclerosis. 2008]

Alpha-lipoic acid inhibits TNF-alpha-induced NF-kappaB activation and adhesion molecule expression in human aortic endothelial cells. [FASEB J. 2001]

Avenanthramides, polyphenols from oats, inhibit IL-1beta-induced NF-kappaB activation in endothelial cells. [Free Radic Biol Med. 2008]

Vascular endothelial growth factor activates nuclear factor-kappaB and induces monocyte chemoattractant protein-1 in bovine retinal endothelial cells. [Diabetes. 1999]

The Cure For All Diabetes T0 T1 T2 T3 ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Mon, 16 Jun 2008 22:21:00 +0000

"Every Day And In Every Way I Am Getting Better And Better"...
.
.
.

whipple triad HYPOglycemia fuel anemia

noreply@blogger.com (Nicholas Dynes Gracey) — Sun, 15 Jun 2008 18:07:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
.
.
.

"The brain is the major player in hypoglycemia."

Be aware that the glucometers that people use for diabetes are most accurate in

the low 100s and have very poor accuracy when it is reading concentrations

below 60 mg/dl. Additionally there is quite a bit of individual variation, so

don't think you are safe until you get to the 30s, because you may not be.

WOMEN
fasting 68-110 mg/dl
24 hrs fasting 34-81 mg/dl
48 hrs fasting 37-62 mg/dl
72 hrs fasting 15-68 mg/dl
MEN
fasting 66-111 mg/dl
24 hrs fasting 55-103 mg/dl
48 hrs fasting 50-99 mg/dl
72 hrs fasting 50-85 mg/dl.

Some normal women can get very low glucose levels and have no hypoglycemic symptoms.
Therefore a low glucose level does not give someone the diagnosis of
hypoglycemia.

So what do doctors consider proof of hypoglycemia? For the well accepted
diagnosis of hypoglycemia, a patient needs to have something called "Whipple's
triad." Whipple's triad is:

1) symptoms of hypoglycemia (see lesson one for these)
2) a low glucose level at the same time as the symptoms and
3) improvement and/or resolution of the symptoms with administration of
carbohydrate (injected or eaten).
http://www.fred.net/slowup/hcauses.txt

Some patients with diabetes can experience hypoglycemia at slightly higher blood glucose levels. Patients whose blood glucose levels are high for long periods of time may have symptoms of low blood glucose and feel poorly when levels approach 100 mg/dL. These patients should intensify their diabetic regimen to get blood glucose levels into a range that is closer to normal. This will lower the blood glucose level at which a patient feels symptoms. http://www.uptodate.com/patients/content/topic.do?topicKey=~gVqTkbDbnrE/v

You may have symptoms of low blood sugar if your blood sugar drops from a high level to a lower level. For example, if your blood sugar level has been higher than 300 mg/dL for a week or so and the level drops suddenly to 100 mg/dL, you may have symptoms of low blood sugar even though your blood sugar is in the normal range. However, if you have had diabetes for many years, you may not have symptoms of low blood sugar until your blood sugar level is very low.

http://www.revolutionhealth.com/conditions/diabetes/blood-sugar/blood-sugar-overview/index

Although low blood sugar is defined as less than 70 mg%, some patients

with chronic diabetes may have symptoms of low blood sugar when it is

below 100 mg%. You may want to check your blood sugar often. Some

people with diabetes may have rapid drop in the blood sugar. If you have

this problem, discuss with your physician how often you should check your

blood sugar for safe driving.

http://www.rancho.org/patient_education/diabetes_drive_safely.pdf

People may have symptoms of hypoglycemia without really having low blood sugar. In such cases, dietary changes such as eating frequent small meals and several snacks a day and choosing complex carbohydrates over simple sugars may be enough to ease symptoms. http://www.labtestsonline.org/understanding/analytes/glucose/test.html

Fasting Blood Sugar Levels	Before Meals means:
0-70	Danger. Too low. Get sugar immediately.
70-90	Possibly too low. Get sugar if you feel hungry, nervous, or weak.
90-160	Normal. This is the ideal range.
160-240	Too high. Work on bringing blood sugar down (see above).
240-300	This is very high and indicates that diabetes is out of control.
300-up	Danger. Call your doctor immediately.

What to do for Hypoglycemia

If patients with hypoglycemia are awake, they should immediately drink a glass of fruit juice or a non-diet soft drink (one that has sugar in it). Other alternatives include eating a handful of candy, 3 or 4 teaspoons of honey, or 3-4 glucose tablets. They should check their blood sugar again in 15 minutes and then several more times over the next few hours until their blood sugar is well above 100 and stays above 100. If the blood sugar drops low again, then medical advice should be sought immediately. http://depts.washington.edu/uwcoe/healthtopics/diabetes.html

When you have low blood sugar (usually below 70), hormones are released that tend to increase the blood sugar level for 12-24 hours. This is a normal body response to the low level. Do not increase your diabetes medication to cover the high level � this should balance out after 24 hours. If it does not, consult your doctor. Also, if you overtreat a low blood sugar response with too much juice, soda or other forms of carbohydrate, your blood sugar may rebound into an abnormally high range.

http://www.querycat.com/faq/adf034fc82e4aa9e2f9813f427f49d70

Acute symptoms occur at certain lower blood sugar levels. These include hand tremors or an inner shakiness which accompany hunger. Often these are accompanied by sweating anywhere on the body, sometimes most intensely during the night. Frequent is heart pounding or 'palpitations' and acute anxiety in the pit of the stomach. Nightmares are common. This combination disturbs sleep and causes more fatigue. More frightening however is the accentuation of these symptoms into full-blown "panic attacks". These acute events last fifteen to thirty minutes and are induced by the sudden release of larger amounts of adrenaline.

http://www.angelfire.com/hi/TheSeer/bloodsugar.html

A rare type of hypoglycemia, known as reactive hypoglycemia, may occur in children and teens without diabetes. In reactive hypoglycemia, blood glucose levels drop to 70 mg/dl approximately four hours after a meal is eaten, causing the same symptoms of low blood sugars that can occur in people with diabetes.

http://www.answers.com/topic/hypoglycemia?cat=health

Scale amount 1:
Above 180 mg/dL

A blood sugar level greater than 180 mg/dL, one to two hours after the start of a meal, or greater than 130 mg/dL before a meal, shows that your diabetes is not under good control.

Call your doctor to talk about your blood sugar level if you high blood sugar several times a week. You may need a check-up, or you may need a change in your Action Plan.
Your goal is a blood sugar of less than 180 mg/dL after a meal.

Scale amount 2:
100 to 140 mg/dL
This is your target blood sugar range at bedtime.

Scale amount 3:
90 to 130 mg/dL
This is your target "fasting" blood sugar range before you eat.

Scale amount 4:
70 mg/dL or below
You may have low blood sugar or hypoglycemia.

Here's a rule of thumb: If your blood sugar is less than 70 mg/dL and you have symptoms, like dizziness, shakiness, sweating, and a pounding heartbeat, you have low blood sugar.
You also have low blood sugar if your levels are less than 70 mg/dL, even if you have no symptoms.

If it's low, eat or drink something sugary. You can take glucose tablets, hard candy, or fruit juice.

Rest for 15 minutes. Then, recheck your blood sugar. If it's still low, eat something sugary again. Rest and then, check blood sugar again. Repeat steps until blood sugar is over 70 mg/dL.

Seek medical attention if you get low blood sugar several times a week. http://www.diabetes.com/ip010007.html

IF BLOOD SUGAR IS LESS THAN 60,

DRINK OR EAT ONE OF THE FOLLOWING:

4 oz. fruit juice

4 oz. regular soda

4 packs sugar

6-7 lifesavers

3-4 glucose tablets

If you are unable to eat or drink, an injection of glucagon should be given, and someone should call your local emergency number for help.

WAIT 10-15 MINUTES THEN TEST AGAIN!

IF BLOOD SUGAR IS 60-80

DRINK OR EAT ONE OF THE FOLLOWING:

8 oz. milk

1 slice bread

6 saltines

1 roll

3 graham crackers

WAIT 10-15 MINUTES THEN TEST AGAIN!

If the result is STILL LESS THAN 80

Repeat the treatment.

Wait 10-15 minutes and re-test.

Continue this until blood sugar is 80.

If the result is over 80, and if it is more than 1/2 hour until your next meal, have a

snack (such as crackers and peanut butter) so your sugar doesn't get too low again.

IF YOU HAVE SYMPTOMS BUT YOUR BLOOD SUGAR IS 90 OR ABOVE

• Have a small snack such as crackers or milk.

• Re-check your blood sugar after 20 minutes or so if the symptoms

persist.

Sometimes, if your blood sugar changes quickly, you may experience low blood sugar symptoms but still have a normal glucose.

http://pfrc.med.nyu.edu/handouts/pdf/describe/diabeteslbs.pdf

in vivo ketogenesis via GLUCAGON

noreply@blogger.com (Nicholas Dynes Gracey) — Sat, 14 Jun 2008 21:10:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
.
.
.
Regulation of in vivo ketogenesis: role of free fa...[Diabetes Metab. 1996]

Diabetes Metab. 1996 Oct;22(5):299-304.Links

Regulation of in vivo ketogenesis: role of free fatty acids and control by epinephrine, thyroid hormones, insulin and GLUCAGON.

Beylot M.

Laboratoire de Physiopathologie Métabolique et Rénale, Faculté de Médecine Alexis Carre, Lyon, France.

The production of ketone bodies (KB) is dependent on the amount of free fatty acids (FFA) supplied to the liver and on the hepatic metabolic fate of fatty acids and their orientation towards oxidation and ketogenesis or reesterification.

In vivo ketogenesis can thus be regulated at the pre-hepatic (lipolysis) or hepatic level. We first investigated the role of FFA availability on the rate of KB production and then the effects of epinephrine, thyroid hormones, insulin and glucagon on the relationship between FFA availability and KB production.

An increase in FFA availability augmented KB production not only by a mass effect but also by a diversion of hepatic fatty acid metabolism towards ketogenesis.

The ketogenic effect of epinephrine and thyroid hormones depended only on their stimulatory action on lipolysis and FFA availability.

An excess of thyroid hormones had no direct effect on hepatic ketogenesis, whereas the direct action of epinephrine on liver was rather anti-ketogenic.

Glucagon stimulated hepatic ketogenesis, whereas a short-term increase in insulinemia [EG via Transient Supernormal Glycemia ("TSG")] within the physiological range appeared to have no restrictive action.

PMID: 8896990

Human ketone body production and utilization studied using tracer techniques: regulation by free fatty acids, insulin, catecholamines, and thyroid hormones. [Diabetes Metab Rev. 1989]
Turnover and splanchnic metabolism of free fatty acids and ketones in insulin-dependent diabetics at rest and in response to exercise. [J Clin Invest. 1984]
Effects of free fatty acids, insulin, glucagon and adrenaline on ketone body production in humans. [Ciba Found Symp. 1982]
Hormonal regulation of ketone-body metabolism in man. [Biochem Soc Symp. 1978]
Effects of free fatty acid availability, glucagon excess, and insulin deficiency on ketone body production in postabsorptive man. [J Clin Invest. 1983]
» See all Related Articles...

Patient Drug Information

Thyroid (Armour® Thyroid) Thyroid is a hormone produced by the body. When taken correctly, thyroid is used to treat the symptoms of hypothyroidism (a condition where the thyroid gland does not produce enough thyroid hormone). Symptoms of hypothyr...

» read more ...
Glucagon (GlucaGen Diagnostic Kit®) Glucagon is a hormone produced in the pancreas. Glucagon is used to raise very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs.
» read more ...

eat one meal at night avoid toxins exercise properly

noreply@blogger.com (Nicholas Dynes Gracey) — Sat, 14 Jun 2008 09:41:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
.
.
.
Tina Marie Welcomes World-Renowned Author and Talk Show Host Ori Hofmekler on Her Weekly 'Holistic Living' Talk Show on the Voice America Network

Phoenix, AZ June, 2008 -- Internet broadcasting pioneer, producing and syndicating online audio and video, today announced that the world renowned author of "The Warrior Diet", Ori Hofmekler will join Tina Marie on her Holistic Living radio show on the VoiceAmerica, online internet talk radio network, on June 17th, 2008.

Ori Hofmekler will share “The Warrior Diet” ; a call for action. Based on survival science and anthropological research, the book proposes a radical yet surprisingly effective solution to weight gain, obesity, diabetes and their related diseases. Its premise: eat one main meal at night, avoid chemicals, exercise properly. On the show, Ori will share his innate knowledge on how to nourish the body in sync with its innate circadian clock – separating between a.m. foods to p.m. foods for effective removal of toxins, increased breakdown of fat for energy, increased utilization of nutrients and improved resilience to stress. The result – a leaner, stronger and healthier body.

National speaker, author and Holistic Nutritional Consultant, Tina Marie Jones, will have Ori Hofmekler show how recent studies on intermittent fasting have shown the benefits of following eating programs similar to The Warrior Diet. "Mice and rats maintained on an intermittent fasting regiment lived up to 30% longer than those fed ad libitum." and why such meal skipping diets have been shown to improve glucose regulation, reduce blood pressure and enhance cardiovascular stress adaptation, improve renal function during aging, and increase the resistance of animals to disease in experimental models of cancer and neurodegenerative disorders.

Ori Hofmekler is a modern renaissance man whose formative military experience prompted a life interest in survival science. He graduated the Bezalel Academy of Art in Jerusalem and received a degree in Human Sciences by the Hebrew University. A world renowned artist, Ori’s work has been featured in magazines worldwide and artbooks of his political satire works were published in the U.S. and Europe. As editor and chief of Mind and Muscle Power magazine, Ori introduced his diet approach to the public to immediate acclaim from readers and professionals. The Warrior Diet book was published in 2002 in the U.S., France and Italy and has been featured in newspapers, magazines and science journals. Its new revised edition was published in 2007. In 2003, Hofmekler authored the highly acclaimed Maximum Muscle Minimum Fat book, addressing the secret science behind muscle gain and fat loss. In 2006, he authored The Anti-Estrogenic Diet, dedicated to providing solutions against health shattering chemicals in the environment, food and water. In 2008 he revised Maximum Muscle Minimum Fat to a new expanded edition. Ori’s “Take No Prisoners” newsletter exposes fallacies and dirty little secrets in the areas of diet and fitness and present the true facts regarding human survival in today’s world. Available at www.WarriorDiet.com and www.DefenseNutrition.com.

"Holistic Living with Tina Marie" airs live on Tuesdays at 10 a.m. Pacific / 12 p.m. Central / 1 p.m. Eastern on The VoiceAmerica Health & Wellness Channel. To access the show, log on at http://www.modavox.com/voiceamericahealth. All shows will be available in Tina Marie's Content Library on The VoiceAmericaTM Health & Wellness Channel for on-demand and pod cast download.

The VoiceAmericaTM Network offers the latest conversations in a talk radio format, providing education, interaction, and advice on key issues live, on demand as well as through pod cast download. If interested in hosting a talk radio show on VoiceAmerica Network, or advertising/sponosorship information and other show details contact Melissa Schmitz, Health & Wellness Channel Director at 480-294-6410 or at melissa.schmitz@modavox.com.

ABOUT Tina Marie Jones: Always impassioned by health, healing and the spiritual connection to the human body, Tina Marie brings a culmination of all the teachings she has pursued over the years. From her degrees in Holistic Nutrition to her training in Spiritual Healing and Personal Counseling, she takes time to listen and connect with each client in a sacred and supportive manner. Like the gentle flow of a mountain stream, she balances her evolving career with her responsibilities as a mother & wife, PhD student, church volunteer, along with various other activities she chooses to participate in. Tina Marie is a true model of following your heart, living in balance and being in connection with the divine powers that guide our days. Tina Marie is a nutritional consultant who sees clients in her clinic and in remote offices such as Starbucks -- always a nice format to identify the unhealthy American diet. She keeps herself fit, educated and available to her family and clients. Despite the sense of humor, Tina Marie takes what she does very seriously. "We are in a war for our health", she quotes and is ready to be on the battleground for all her clients. The founder and President of Optimal Health Corporation, Optimal Health Consulting, and Optimal Health Education, Mrs. Jones is committed to the serving the health and understanding her clients through education, hands on experiential lessons, and one-on-one support.

ABOUT VoiceAmerica / Modavox: (OTC.BB MDVX), Modavox is the leading producer and distributor of online talk radio content, streaming approximately 250 hours of live programs and scheduled replays weekly on its Modavox VoiceAmerica™ Network (http://www.voiceamerica.com). Modavox, Inc. (http://www.modavox.com) is a pioneer in internet broadcasting, producing and syndicating online audio and video, and offering innovative, effective and comprehensive online tools for reaching targeted niche communities worldwide. Through its patented Modavox Central™ technology, Modavox "takes the search out of search," delivering content straight to desktops and internet-enabled devices. Through its proprietary StreamSafe™, WebcastWizard™ and Stream Syndicate™ tools, Modavox provides managed access for live and on-demand internet broadcasting and syndication, content management, online meetings, event management, enterprise communications and distance learning.

Forward-Looking Statements: This release contains "forward-looking statements" for purposes of the Securities and Exchange Commission's "safe harbor" provisions under the Private Securities Litigation Reform Act of 1995 and Rule 3b-6 under the Securities Exchange Act of 1934. These forward-looking statements are subject to various risks and uncertainties that could cause Modavox's actual results to differ materially from those currently anticipated, including the risk factors identified in Modavox's filings with the Securities and Exchange Commission.

Website Link: http://www.voiceamerica.com

Contact Info:

Melissa Schmitz
2617 S. 46th St., Suite 300, Phoenix, AZ 85034
Phone: 480-294-6410
Website: http://www.voiceamerica.com

Why Insulin Downregulates Glucagon HOW

noreply@blogger.com (Nicholas Dynes Gracey) — Fri, 13 Jun 2008 22:50:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
.
.
.
Symptom and Disease Prevalence in Elderly Diabetics and Nondiabetics

Page Range: 59 - 72
DOI: 10.1300/J089v05n01_06

William E. Hale MD, Ronald G. Marks PhD, Mary T. Moore MStat, Franklin E. May PhD, Ronald B. Stewart MS

Prevalence of reported symptoms and diseases and electrocardiographic changes were studied retrospectively in 2,970 ambulatory elderly participants attending a health screening program in Dunedin, Florida.

Prevalences of these conditions were compared for 179 (6.0% diabetics) and 2,791 nondiabetics.

Reports of 27 common symptoms and 34 common diseases were obtained from a standardized questionnaire completed by participants at the time of their fourth visit to the program.

After adjusting for age and sex, elderly diabetics were more likely to complain of feeling faint (p = 0.001), intermittent claudication (p = 0.0001), and the sensation of cold feet/legs on exposure to cold (p = 0.007) when compared with nondiabetics.

Diabetics reported numerous diseases more often than nondiabetics including heart failure and hypertension (p = 0.0001), gallbladder disease (p = 0.007), and gout (p = 0.001).

Insulin treated diabetics reported most symptoms and diseases with greater frequency than diabetics managing their condition by diet or oral hypoglycemics.

Abnormal EKGs were more frequently found for diabetics than nondiabetics (p = 0.008).

Left bundle branch block (p = 0.0001) and nonspecific ST-T changes (p = 0.0001) were found more frequently in diabetics.

It appears that in the elderly certain symptom complaints and/or electrocardiographic changes may be useful in alerting the physician to the possibility of diabetes.

http://www.haworthpress.com/store/Toc_views.asp?sid=VRRS3S6WG87U9NHSB0141AGL4DES5NV4&TOCName=J089v05n01_TOC&desc=Volume%3A%205%20Issue%3A%201

Diabetes Mellitus Prevalence and Treatment Outcomes in a Geriatric Nursing Home Population: A Three Year Study

Page Range: 73 - 82
DOI: 10.1300/J089v05n01_07

James W. Cooper PhD, FASCP, Janet E. Gordon BSPharm, Roy C. Parish PharmD

With prior approval of the Human Subjects Committee of the Institutional Review Board of our institution, the patient and consultant pharmacists records for a 120-bed nursing home were retrospectively reviewed for the diagnosis and treatment outcomes of diabetes mellitus (DM) over a three-year period.

A group of 41 of the 233 patients (prevalence of 17.6%) who had been in residence for 1 to 36 months was identified as having a diagnosis of DM, and both demographic and treatment data gathered on the average of 20.8 months of length of stay DM treatment.

The 233 patients were predominantly white females with an average age of 83 years, with an average length of stay of 22 months.

The DM treatment group was further subdivided into four predominant treatment groups (number): oral hypoglycemics and diet (5), insulin and diet (25), diet alone (9), and no dietary or drug treatment (2).

Seven of 41 patients crossed over between groups during the study period.

All patients were further classified by weight variance from ideal body weight (IBW) from <> 20% over their IBW and by treatment groups.

Treatment outcomes were assessed by monthly fasting blood sugars (FBSs) as hypoglycemia (FBS <> 160mg/dl) and the presence of diabetic complications of amputation, decubitus/diabetic ulcers, high blood pressure, congestive heart failure, and ischemic coronary vessel disease were noted for all patients.

Diabetic complications and FBSs outside the acceptable FBS treatment range of 100-160mg/dl were predominantly in the insulin plus diet treatment group.

Statistical treatment of the variables of weight and FBSs found that hyperglycemic episodes were more common (27 of 30 episodes) in the overweight insulin group who did not comply with ADA diet nor lose weight.

Hypoglycemic reactions were most common in the underweight insulin group (17 of 24 episodes).

Hospitalization and death rates were compared for both DM and non-DM patients over the study period.

While there was no statistically significant difference in the percentage death rate (24.4 vs. 25.5) or percentage of patients hospitalized (60.9 vs. 60.1) there was significant difference in the rate of hospitalization per DM patient (2.84) vs. non-DM patients (1.82) who required hospitalization during their length of stay or study period.

http://www.haworthpress.com/store/Toc_views.asp?sid=VRRS3S6WG87U9NHSB0141AGL4DES5NV4&TOCName=J089v05n01_TOC&desc=Volume%3A%205%20Issue%3A%201

HYPOglucose-induced autonomic failure in IDDM is specific for stimulus of HYPOglycemia and is not attributable to prior autonomic activation ... HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Thu, 12 Jun 2008 08:12:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
.
.
.
Diabetes. 1994 Jun;43(6):809-18.

Links

NeuroGlycoPenia - induced autonomic failure in IDDM is specific for stimulus of HYPOglycemia and is not attributable to prior autonomic activation.

Rattarasarn C, Dagogo-Jack S, Zachwieja JJ, Cryer PE.

Division of Endocrinology, Diabetes, and Metabolism, Washington University School of Medicine, St. Louis, Missouri 63110.

It has been HYPOthesized, first, that recent antecedent HYPOglycemia causes reduced autonomic responses to subsequent HYPOglycemia in patients with well-controlled insulin-dependent diabetes mellitus (IDDM) and that the reduced responses are specific for the stimulus of hypoglycemia while the responses to other stimuli are unaltered and, second, that reduced autonomic responses, specifically sympathochromaffin, so-induced are not simply the result of prior activation of the system.

To test the first HYPO-thesis, eight patients with IDDM, selected for HbA1c levels. HYPO-glucose-associated autonomic failure can be induced in patients with well-controlled IDDM and is specific for the stimulus of HYPOglycemia and, second, that this is not simply the result of prior activation of the system.

Related Articles ...

HYPOglycemia-associated autonomic failure in insulin-dependent diabetes mellitus. Recent antecedent HYPOglycemia reduces autonomic responses to, symptoms of, and defense against subsequent HYPOglycemia. [J Clin Invest. 1993]

Exaggerated epinephrine response to HYPOglucose in a physically fit, well-controlled IDDM subject. [Diabetes Res Clin Pract. 1994]

Mechanism of awareness of hypoglycemia. Perception of neurogenic (predominantly cholinergic) rather than neuroglycopenic symptoms. [Diabetes. 1993]

Contribution of autonomic neuropathy to reduced plasma adrenaline responses to hypoglycemia in IDDM: evidence for a nonselective defect. [Diabetes. 1997]

Reversal of hypoglycemia unawareness, but not defective glucose counterregulation, in IDDM. [Diabetes. 1994]

1: Related Articles,
Links

Cryer PE.
HYPOglycemia in diabetes: pathophysiological mechanisms and diurnal variation.
Prog Brain Res. 2006;153:361-5. Review.
PMID: 16876586 [PubMed]

2: Related Articles,
Links

Goldberg PA, Weiss R, McCrimmon RJ, Hintz EV, Dziura JD, Sherwin RS.
Antecedent HYPERcortisolemia is not primarily responsible for generating HYPOglycemia-associated autonomic failure.
Diabetes. 2006 Apr;55(4):1121-6.
PMID: 16567537 [PubMed]

3: Related Articles,
Links

Jacobson L, Ansari T, Potts J, McGuinness OP.
Glucocorticoid-deficient corticotropin-releasing hormone knockout mice maintain glucose requirements but not autonomic responses during repeated HYPOglucose.
Am J Physiol Endocrinol Metab. 2006 Jul;291(1):E15-22. Epub 2006 Jan 31.
PMID: 16449297 [PubMed]

4: Related Articles,
Links

Mishriki YY.
HYPOglucose-induced neurogenic-type pulmonary edema: an underrecognized association.
Endocr Pract. 2004 Sep-Oct;10(5):429-31.
PMID: 15760791 [PubMed]

5: Related Articles,
Links

Davis SN, Shavers C, Davis B, Costa F.
Prevention of an increase in plasma cortisol during HYPOglucose preserves subsequent counterregulatory responses.
J Clin Invest. 1997 Jul 15;100(2):429-38.
PMID: 9218521 [PubMed]

6: Related Articles,
Links

Cryer PE.
HYPOglucose-induced autonomic failure in insulin-dependent diabetes mellitus.
Proc Assoc Am Physicians. 1995 Apr;107(1):67-70. Review.
PMID: 8630745 [PubMed]

7: Related Articles,
Links

Havel PJ, Akpan JO, Curry DL, Stern JS, Gingerich RL, Ahren B.
Autonomic control of pancreatic polypeptide and glucagon secretion during neuroglucopenia and hypoglycemia in mice.
Am J Physiol. 1993 Jul;265(1 Pt 2):R246-54.
PMID: 8102036 [PubMed]

8: Related Articles,
Links

Katsura M.
[Mechanism of the blunted glucagon response to insulin-induced HYPOglucose in Diabetics]
Nippon Naibunpi Gakkai Zasshi. 1986 Nov 20;62(11):1276-88. Japanese.
PMID: 3542595 [PubMed]

9: Related Articles,
Links

Koyama Y, Galassetti P, Coker RH, Pencek RR, Lacy DB, Davis SN, Wasserman DH.
Prior exercise and the response to insulin-induced HYPOglycemia in the dog.
Am J Physiol Endocrinol Metab. 2002 May;282(5):E1128-38.

PMID: 11934679 [PubMed]

10: Related Articles,
Links

Horm Metab Res. 1979 Oct;11(10):561-6.

Effect of thyroxine treatment on metabolic responses to a single insulin injection.
Kaciuba-Uścilko H, Brzezińska Z.

Metabolic responses to a single i.v. injection of cristalline insulin (0.2 i.u./kg b.w.) were compared in control and T4-treated dogs both at rest and after prolonged physical exercise. The post-insulin decrease in blood glucose was significantly correlated with the pre-insulin BG concentration. Thus, the insulin-induced fall of BG was greatest in T4-treated dogs at rest, in which significantly higher BG levels were found in comparison with controls, and smallest in the same dogs after exercise, i.e. at the lowest initial BG concentrations. The post-insulin hypoglycaemia caused marked increases in the plasma FFA level in control dogs, both at rest and after physical effort, and in T4-treated dogs at rest. They were accompanied by elevations in the plasma adrenaline levels. In T4-treated dogs given insulin after exercise decreases both in the plasma FFA and A concentrations were found. In the majority of the control and T4-treated dogs insulin injected at rest caused an increase in blood LA levels, being more pronounced in the latter. Insulin injected after physical exercise did not change blood LA level in T4 treated dogs, and it caused its decrease in the control animals. The results of these investigations show that both T4-treatment and physical exercise, performed prior to insulin injection, modify the metabolic response to insulin and post-insulin HYPOglucose.

Links
PMID: 11934679 [PubMed]

Patient Drug Information

Glucagon (GlucaGen Diagnostic Kit®) Glucagon is a hormone produced in the pancreas. Glucagon is used to raise very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs.

» read more ...

www.HYPO-thesis.cOM

Glucose Monitoring Errors HYPOglycemia

noreply@blogger.com (Nicholas Dynes Gracey) — Wed, 11 Jun 2008 19:27:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
.
.
.
Avoiding Glucose Monitoring Errors in Patients Receiving Other Sugars (February 2006) This story originally aired in February 2006.

... some of the most important safety issues that continue to pose a public health problem.

FDA issued a reminder about the potential for falsely elevated glucose readings in patients who are also receiving products that contain other sugars. These products include oral xylose, parenterals that contain maltose or galactose, and peritoneal dialysis solutions that contain icodextrin.

Several patients have died because of this problem. Their glucose readings were very high, so they were given aggressive insulin treatment. The glucose readings were falsely high, however, and too much insulin was administered.

The patients suffered HYPOglycemic shock or irreversible brain damage and died. In these cases, the glucose meter was reading the patient's actual blood glucose level, plus the maltose that was contained in the IV immune globulin he was receiving.

The readings were falsely elevated because the glucose monitoring device couldn't distinguish between glucose and other sugars.

All glucose meters don't suffer from this problem. There are several kinds of enzymatic glucose monitoring methods that are used, and only one of those has this problem.

This problem occurs only with the monitoring method that uses an enzyme called GDH-PQQ. This method is employed in some glucose monitoring devices used by diabetics at home and in point-of-care settings.

The other methods currently used in glucose monitoring systems are called GDH-NAD, GDH-FAD, glucose oxidase, and glucose hexokinase, and they are capable of distinguishing between glucose and other sugars.

The test method used in glucose meters is identified in the package insert that comes with the glucose test strips. The package insert is also available from the manufacturer. The most important thing to remember is not to use the GDH-PQQ method if the patient recently received other sugars.

That includes oral xylose for a D-Xylose absorption test, or an IV solution containing maltose or galactose, or a peritoneal dialysis solution containing icodextrin.

Furthermore, the manufacturers of thiazolidinedione drugs have strengthened warnings about the risks of heart failure with these medications, which are use to treat type 2 diabetes. They are sold as Avandia (rosiglitazone maleate), Avandaryl (rosiglitazone maleate and glimepiride), and Avandamet (rosiglitazone maleate and metformin hydrochloride), which all contain rosiglitazone, and Actos (pioglitazone hydrochloride), Duetact (pioglitazone hydrochloride and glimepride) and Actoplus met, which all contain pioglitazone.

The drug labels already had information about heart failure risk, but now there is a new boxed warning that re-emphasizes that these drugs may cause or worsen heart failure in certain patients, and stresses the importance of carefully monitoring patients for signs of heart failure.

The labeling recommends that after starting thiazolidinedione therapy or increasing the dose, patients should be observed carefully for the signs and symptoms of heart failure, including excessive, rapid weight gain, shortness of breath, and edema.

If any of these signs and symptoms develop and heart failure is confirmed, practitioners should start appropriate management of the heart failure and consider stopping or reducing the dose of the drug.

The boxed warning also notes that these drugs are not recommended for patients with symptomatic heart failure, and are specifically contraindicated in patients with NYHA Class III or IV heart failure.

Nick Gracey WATerian BSc(Hons) Medical BioChemistry, Birmingham University, Adrenaline LIFE2345.©OM

A Spoon Full Of Honey 'CPR' rubbed inside a mouth ... A fainting COMA needs FUEL to recover from a sudden drop / fall of blood fuel [glucose]

ARMAGH

ANTRIM

DERRY

DOWN

DONEGAL

FERMANAGH

MONAGHAN

TYRONE

CONNACHT

LEITRIM

MAYO

ROSCOMMON

LEINSTER

DUBLIN

KILKENNY

LAOIS

LOUTH

OFFALY

WEXFORD

WICKLOW

MUNSTER

CLARE

CLARE

KERRY

LIMERICK

WATERFORD

TSG = Transient Supernormal Glycemia ... Why ZERO symptoms following 100% blockage occlusion of coronary artery [0:32 to 0:55 mins] ...HOW ?

Acute HYPERglycemia [TRANSIENT SUPERNORMAL GLYCEMIA (TSG)] induces a HEALTHY IMMUNE response in young HUMANS withOUT ... 'GM-INSULIN-TREATED diabetes' ...

Related Articles

History of wound care AND HYPERGLYCEMIA LIKE HEALING VIA HONEY [AND SUGAR WORKS JUST AS WELL] ...

Ancient medical practice

Honey [AKA CONCENTRATED HYDRATED LIQUID SUGAR] ...

19th century

Wound-site dressing

1950s onward

References

Sources

External links

SOD = SuperOxide Dismutase

Hepatic effects of a fructose diet in the stroke-prone spontaneously HYPERtensive rat.

Related Articles

SuperOxide Dismutase

Contents

Reaction

Types

General

Human

Biochemistry

Physiology

Role in disease

Delivery systems

Cosmetic uses

References

See also

External links

TSG-type1-CURE

Mechanisms involved in the beta-cell mass increase induced by chronic sucrose feeding to normal rats.

Related Articles

Function

Pathology

Research

See also

References

External links

Type3 diabetes

Adiposity, HYPERinsulinemia, diabetes and Alzheimer's disease: an epidemiological perspective.

Related Articles

Adiposity and Alzheimer's disease.

Related Articles

Gluca-gone

Effect of near physiologic insulin therapy on HYPOglycemia counter-regulation in type-1 diabetes.

Related Articles

Effect of experimentally induced HYPOglycemia and different insulin levels on feelings of hunger in type 1 Diabetic Patients.

Related Articles

Knight Bill

Arguments for and against

Literature you may find helpful

12.45 p.m.