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

Human C-peptide helps protect cells

noreply@blogger.com (Nicholas Dynes Gracey) — Tue, 17 Jun 2008 18:52:00 +0000

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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

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whipple triad HYPOglycemia fuel anemia

noreply@blogger.com (Nicholas Dynes Gracey) — Sun, 15 Jun 2008 18:07:00 +0000

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"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

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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

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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

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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

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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-U�?cilko H, Brzezi�?ska 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

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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.

Child TIA stroke insulin HYPOglycemia

noreply@blogger.com (Nicholas Dynes Gracey) — Tue, 10 Jun 2008 20:38:00 +0000

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Love-Diabetes.cOM: When a Child (with diabetes) Can't Remember....

Posted by Allison Love Beatty at 6/9/2008 5:28 PM and is filed under diabetes insulin drugs

In the fall of 1985, a very scary thing happened shortly after I was diagnosed with type 1 diabetes. One morning I woke up and I couldn't remember things I would normally remember. I couldn't remember the name of my neighbor's dog. I had a fanatical love for Cookie. Of course I would remember Cookie! A diabetic child would never forget such a sweet name for such an adorable dog! One more thing -- I had a pounding headache.

My mom brought me to the hospital, where my endocrinologist met us. They ran test after test and nary could an expert explain my memory loss. They confirmed I was experiencing amnesia, which turned out to be temporary because I was back to normal the next day.

How many people have experienced this same phenomenon? I surmised that this was my body reacting to the Humulin insulin I had started only a month or so before. The insulin must have been competing with my body's own attempts to generate insulin thus thwarting my blood sugar down into a dangerous hypoglycemic state. A study published in 1991 confirms that hypoglycemia results in a lesion in the left temporal lobe. I have one of those lesions now, but it wasn't discovered until 2000. Oh yeah - and my peduncle is perfectly asymmetric. What does that mean anyway?

Why weren't doctors informed of this potential reaction to insulin in 1985? A study 6 years later is a few years too late. And how many more newly diagnosed insulin-dependent diabetics experience the same thing? My parents were scared out of their mind and nobody (including specialists) had any idea what to do with me.

Love-Blocker of Adrenaline Glucagon LIFE-saver via LOVE aka beta-receptor LOVE-transmitters ... so now to help LOVE be free ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Sun, 08 Jun 2008 22:42:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
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Beta-Blockers of Adrenaline Glucagon LIFE-saver via LOVE aka beta-receptor LOVE-transmitters ... so now to help LOVE be free ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Sat, 07 Jun 2008 12:03:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
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"... There is such a thing as perfection... and our purpose for living is to find that perfection and show it forth. Each of Us is in truth an unlimited idea of freedom. Every thing that limits Us, We have to put aside ..." [Jonathan Livingston SEAGULL]

Effects of extended-release Beta-BLOCKERS i...[Lancet. 2008] - PubMed Result
http://www.ncbi.nlm.nih.gov/pubmed/18479744

Lancet. 2008 May 31;371(9627):1839-47. Epub 2008 May 12. Links

Effects of extended-release Beta-BLOCKERS ... metoprolol succinate in patients undergoing non-cardiac surgery (POISE trial): a randomised controlled trial.

McMaster University, Faculty of Health Sciences, Clinical Epidemiology and Biostatistics, Room 2C8, 1200 Main Street West, Hamilton, ON, L8N 3Z5, Canada.

philipj@mcmaster.ca

BACKGROUND: Trials of beta blockers in patients undergoing non-cardiac surgery have reported conflicting results. This randomised controlled trial, done in 190 hospitals in 23 countries, was designed to investigate the effects of perioperative beta blockers.

METHODS: We randomly assigned 8351 patients with, or at risk of, atherosclerotic disease who were undergoing non-cardiac surgery to receive extended-release metoprolol succinate (n=4174) or placebo (n=4177), by a computerised randomisation phone service.

Study treatment was started 2-4 h before surgery and continued for 30 days.

Patients, health-care providers, data collectors, and outcome adjudicators were masked to treatment allocation.

The primary endpoint was a composite of cardiovascular death, non-fatal myocardial infarction, and non-fatal cardiac arrest. Analyses were by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT00182039.

FINDINGS: All 8351 patients were included in analyses; 8331 (99.8%) patients completed the 30-day follow-up.

Fewer patients in the metoprolol group than in the placebo group reached the primary endpoint (244 [5.8%] patients in the metoprolol group vs 290 [6.9%] in the placebo group; hazard ratio 0.84, 95% CI 0.70-0.99; p=0.0399).

Fewer patients in the metoprolol group than in the placebo group had a myocardial infarction (176 [4.2%] vs 239 [5.7%] patients; 0.73, 0.60-0.89; p=0.0017).

However, there were more deaths in the metoprolol group than in the placebo group (129 [3.1%] vs 97 [2.3%] patients; 1.33, 1.03-1.74; p=0.0317). More patients in the metoprolol group than in the placebo group had a stroke (41 [1.0%] vs 19 [0.5%] patients; 2.17, 1.26-3.74; p=0.0053).

INTERPRETATION: Our results highlight the risk in assuming a perioperative beta-blocker regimen has benefit without substantial harm, and the importance and need for large randomised trials in the perioperative setting. Patients are unlikely to accept the risks associated with perioperative extended-release metoprolol.

Patient Drug Information

Metoprolol (Lopressor®, Toprol XL®, Lopressor® HCT) Metoprolol is used alone or in combination with other medications to treat high blood pressure. It also is used to prevent angina (chest 'WARNING' pain) and to treat heart attacks. Extended-release (long-acting) metoprolol also is...

» read more ...

http://articles.MERCOLA.cOM/sites/articles/archive/2008/06/07/more-drugs-that-kill-you.aspx?source=nl

More Drugs That Kill Us

People who receive blood-pressure-lowering drugs known as beta blockers shortly before, and after, having non-cardiac surgery are at higher risk of dying or having a stroke.

Surgery increases your heart's need for oxygen, and beta blockers are commonly given to help reduce blood pressure and heart rate, thereby reducing strain [AKA 'FUEL CONSUMPTION'] on the heart.

In the study of over 8,300 people, participants were randomly assigned to receive a beta blocker two to four hours before surgery, as well as for 30 days after the procedure, or a placebo.

Compared to those given a placebo, those who received beta blockers were 27 percent less likely to have a heart attack. However, they also had a 33 percent increased risk of dying, and double the risk of stroke [IE WHEN 'DISTRESSED'].

An estimated 100 million people have major non-cardiac surgery each year, so the finding could have serious consequences. Even if only 10 percent of patients undergoing non-cardiac surgery were given beta blockers, that would mean that 800,000 people died unnecessarily in the past decade.

Sources:

ABC News May 14, 2008

The Lancet May 13, 2008

Dr. Mercola's Comments:

Would you knowingly trade a slightly lower risk of heart attack for an increased risk of death and stroke?

Neither would I.

In fact, I doubt that anyone about to undergo surgery would want to take on those odds.

Of course, if you enter a hospital for surgery, you�??d be the rare exception if anyone actually explained to you the pros and cons of each pill they expected you to take. More realistically, you�??re handed some pills and down the hatch they go, for better or for worse.

Old Treatments Die Hard in Conventional Medicine

And beta blockers are a great example of that.

Beta blockers work by �??blocking�?? the normally stimulating effects of the adrenaline hormone on your heart. They also slow your heart rate and reduce your heart�??s need for oxygen when you exert yourself, which means your heart doesn�??t have to work as hard.

These drugs have been used for more than 30 years to treat high blood pressure, and they are recommended as the first line of defense in both the United States and international health guidelines.

However, it�??s being increasingly suggested that beta blockers are not a good choice for high blood pressure at all. Aside from often being ineffective, they�??re known to cause an array of serious side effects including:

Stroke
Heart attack
Type 2 diabetes
Fatigue, dizziness and weakness
Sexual dysfunction
Slow heartbeat and shortness of breath
Trouble sleeping

One review published last year in the Journal of the American College of Cardiology even concluded that �??there is a paucity of data or absence of evidence to support use of beta-blockers as �?� first-line agents [for high blood pressure].�??

And they continue:

�??Given the increased risk of stroke, their "pseudo-antihypertensive" efficacy �?� lack of effect on regression of target end organ effects �?� and numerous adverse effects, the risk benefit ratio for beta-blockers is not acceptable for this indication.�??

Despite this, they are still widely prescribed. In one six-month period in 2007 alone, more than 75 million prescriptions were written for beta blockers, according to data from IMS Health.

High Blood Pressure Can be Treated Without Drugs

The Harvard Health Letter even recently named high blood pressure as one of seven common conditions that can be managed without medication.

It�??s worth mentioning also to make sure your blood pressure really is high before you start worrying about it. Blood pressures are extremely variable, and all of the following can cause you to have a false high reading:

Emotional stress
Smoking
Coffee
Over-the-counter drugs containing caffeine
Decongestants
A cold room
A full bladder
Improper cuff size or arm position

At least two readings should be taken at each doctor visit (separated by as much time as possible), and three individual sets of readings at least one week apart should be taken before you ever consider taking a blood-pressure-lowering drug. And even then, that should only be in extreme cases.

For the vast majority of you, the following three tips will cause your high blood pressure to normalize quite quickly:

1. Limit grains and sugars in your diet. This will help to normalize your insulin leptin levels, which is essential for good blood pressure. In my experience this is one of the most common reasons why people have elevated blood pressures. High insulin levels tend to drive blood pressures up.

and 2. Exercise regularly. In some cases, you may need to work your way up to one hour a day. This will also help to get your insulin and leptin levels where they need to be.

3. Manage the stress in your life. The Emotional Freedom Technique (EFT) is a simple and inexpensive tool that can help you to do this.

Related Articles:

Placebo Lowers Blood Pressure in One-Third of Patients

Why the Treatment of Hypertension has Become Such a Deplorable Fiasco

Medicine's Dirty Little Secret

PROinsulin Cpeptide kidney healing effects aka C-Peptide effects on renal physiology and diabetes

noreply@blogger.com (Nicholas Dynes Gracey) — Sat, 07 Jun 2008 08:27:00 +0000

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C-Peptide effects on renal physiology and diabetes. [Exp Diabetes Res. 2008] - PubMed Result

Exp Diabetes Res. 2008;2008:281536. Links

PROinsulin Cpeptide kidney healing effects ...

Rebsomen L, Khammar A, Raccah D, Tsimaratos M.

UPRES EA 21-93, Laboratoire de Diabétologie, Faculté de Médecine de Marseille, Université de la Méditerranée, 13385 Marseille Cedex 05, France.

The C-peptide of proinsulin is important for the biosynthesis of insulin and has for a long time been considered to be biologically inert. Animal studies have shown that some of the renal effects of the C-peptide may in part be explained by its ability to stimulate the Na,K-ATPase activity. Precisely, the C-peptide reduces diabetes-induced glomerular hyperfiltration both in animals and humans, therefore, resulting in regression of fibrosis. The tubular function is also concerned as diabetic animals supplemented with C-peptide exhibit better renal function resulting in reduced urinary sodium waste and protein excretion together with the reduction of the diabetes-induced glomerular hyperfiltration. The tubular effectors of C-peptide were considered to be tubule transporters, but recent studies have shown that biochemical pathways involving cellular kinases and inflammatory pathways may also be important. The matter theory concerning the C-peptide effects is a metabolic one involving the effects of the C-peptide on lipidic metabolic status.This review concentrates on the most convincing data which indicate that the C-peptide is a biologically active hormone for renal physiology.

[Physiological effects of the connecting peptide] [Arch Pediatr. 2005]
Role of C-peptide in human physiology. [Am J Physiol Endocrinol Metab. 2000]
C-peptide replacement improves weight gain and renal function in diabetic rats. [Diabetes Metab. 2006]
C-peptide: a new potential in the treatment of diabetic nephropathy. [Curr Diab Rep. 2001]
C-peptide revisited--new physiological effects and therapeutic implications. [J Intern Med. 1996]
» See all Related Articles...

PROinsulin Cpeptide protects eyesight aka Proinsulin attenuates the loss of vision and delays apoptosis of photoreceptors in a mouse model of retiniti

noreply@blogger.com (Nicholas Dynes Gracey) — Sat, 07 Jun 2008 07:41:00 +0000

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Proinsulin attenuates the loss of vision and delay...[Invest Ophthalmol Vis Sci. 2008] - PubMed Result

Invest Ophthalmol Vis Sci. 2008 May 30. [Epub ahead of print]Links

Proinsulin attenuates the loss of vision and delays apoptosis of photoreceptors in a mouse model of retinitis pigmentosa.

Corrochano S, Barhoum R, Boya P, Arroba AI, Rodriguez-Muela N, Gomez-Vicente V, Bosch F, de Pablo F, de la Villa P, de la Rosa EJ.

Cellular and Molecular Physio pathology, CIB-CSIC, Madrid, Spain.

PURPOSE: Retinitis pigmentosa (RP) is a heterogeneous group of inherited conditions that lead to blindness and for which there is no effective therapy. Apoptosis of photoreceptors is a common feature in animal models of the disease. Thus, we have studied the therapeutic potential of proinsulin, an anti-apoptotic molecule that is active during retinal development. METHODS: Transgenic mice expressing human proinsulin (hPi) in the skeletal muscle were generated in a mixed C57BL/6:SJL background and back-crossed to a C57BL/6 background. Two independent lineages of transgenic mice were established, in which hPi production in muscle was constitutive and not regulated by glucose levels. hPi levels in serum, muscle and retina were determined with a commercial ELISA kit, visual function was evaluated by electroretinogram (ERG) recording and programmed cell death was assessed by TUNEL. Immunohistochemistry was used to evaluate retinal structure preservation and oxidative damage. RESULTS: Transgenic expression of hPi in the rd10 retinal degeneration mouse model led to prolonged vision, as determined by ERG recording, in a manner that was related to the level of transgene expression. This attenuation of visual deterioration was correlated with a delay in photoreceptor apoptosis, as well as with the preservation of retinal cytoarchitecture, particularly that of the cones. CONCLUSIONS: Our results provide a new basis for possible therapies to counteract retinitis pigmentosa, as well as a new tool to dissect out the mechanisms involved in the progress of retinal neurodegeneration.

Retinal organization in the retinal degeneration 10 (rd10) mutant mouse: a morphological and ERG study. [J Comp Neurol. 2007]
Apoptotic photoreceptor cell death in mouse models of retinitis pigmentosa. [Proc Natl Acad Sci U S A. 1994]
Constitutive overexpression of human erythropoietin protects the mouse retina against induced but not inherited retinal degeneration. [J Neurosci. 2004]
Tauroursodeoxycholic acid preservation of photoreceptor structure and function in the rd10 mouse through postnatal day 30. [Invest Ophthalmol Vis Sci. 2008]
Antioxidants slow photoreceptor cell death in mouse models of retinitis pigmentosa. [J Cell Physiol. 2007]
» See all Related Articles...

Glucagon Glucagonic Fitness Glucose Cure

noreply@blogger.com (Nicholas Dynes Gracey) — Fri, 06 Jun 2008 09:57:00 +0000

Glucagon Glucagonic Fitness Glucose Cure

Glucagon is an important hormone involved in carbohydrate metabolism. Produced by the pancreas, it is released when the glucose level in the blood is low (HYPOglycemia), causing the liver to convert stored glycogen into glucose and release it into the bloodstream. The action of glucagon is thus opposite to that of insulin, which instructs the body's cells to take in glucose from the blood in times of satiation.

Production

The hormone is synthesized and secreted from alpha cells (α-cells) of the islets of Langerhans, which are located in the endocrine portion of the pancreas. In rodents, the alpha cells are located in the outer rim of the islet. Human islet structure is much less segregated, and alpha cells are distributed throughout the islet.

Regulatory mechanism

Increased secretion of glucagon is caused by:

* Decreased plasma glucose
* Increased catecholamines - norepinephrine and epinephrine
* Increased plasma amino acids (to protect from hypoglycemia if an all protein meal is consumed)
* Sympathetic nervous system
* Acetylcholine
* Cholecystokinin

Decreased secretion of glucagon (inhibition) is caused by:

* Somatostatin
* Insulin

Function

Glucagon helps maintain the level of glucose in the blood by binding to glucagon receptors on hepatocytes, causing the liver to release glucose - stored in the form of glycogen - through a process known as glycogenolysis. As these stores become depleted, glucagon then encourages the liver to synthesize additional glucose by gluconeogenesis. This glucose is released into the bloodstream. Both of these mechanisms lead to glucose release by the liver, preventing the development of hypoglycemia. Glucagon also regulates the rate of glucose production through lipolysis.

* Increased free fatty acids and ketoacids into the blood
* Increased urea production

Mechanism of action

Glucagon binds to the glucagon receptor, a G protein-coupled receptor located in the plasma membrane. The conformation change in the receptor activates G proteins, a heterotrimeric protein with α, β, and γ subunits. The subunits breakup as a result of substitution of a GDP molecule with a GTP mol, and the alpha subunit specifically activates the next enzyme in the cascade, adenylate cyclase.

Adenylate cyclase manufactures cAMP (cyclical AMP) which activates protein kinase A (cAMP-dependent protein kinase). This enzyme in turn activates phosphorylase kinase, which in turn, phosphorylates glycogen phosphorylase, converting into the active form called phosphorylase A. Phosphorylase A is the enzyme responsible for the release of glucose-1-phosphate from glycogen polymers.

Endocrinology. 1996 Aug;137(8):3193-9. Related Articles, Links: Glucagon response to HYPOglycemia is improved by insulin-independent restoration of normoglycemia in diabetic rats.

Shi ZQ, Rastogi KS, Lekas M, Efendic S, Drucker DJ, Vranic M.

Department of Physiology, Faculty of Medicine, University of Toronto, Ontario, Canada.

The aim of this study was to determine whether the impaired glucagon response to insulin-induced hypoglycemia in the diabetic rat can be improved by correction of hyperglycemia independent of insulin.; Four groups of age-matched male Sprague-Dawley rats (246 +/- 13 g BW) were studied: 1) normal controls (NC; n = 7); 2) diabetic, untreated (DU; n = 6); 3) diabetic, treated for 5-7 days using sustained release (2-3 U/day) insulin implants (DI; n = 6); and 4) diabetic, treated for 3-4 days with phlorizin (0.4 g/kg), given sc twice daily (DP; n = 7). Diabetes was induced by a single injection of streptozotocin (65 mg/kg). Basal plasma glucose was 7.4 +/- 0.3 mM in NC, but rose to 14.5 +/- 2.2 mM in DU.; Basal hyperglycemia was corrected with phlorizin and insulin treatments (5.5 +/- 0.5 and 6.7 +/- 0.8 mM, respectively). NC rats responded to insulin-induced hypoglycemia with a rapid and marked increase in glucagon (peak, 2059 +/- 311 pg/ml). The glucagon response was blunted in DU (635 +/- 180 pg/ml) and was partially improved by prolonged normalization of glycemia in DP (1335 +/- 295 pg/ml; P <>; Treatment with both insulin and phlorizin reversed the changes in the pancreatic content of both glucagon and somatostatin. Pancreatic proglucagon messenger RNA did not show significant differences among the four groups in either state. Insulin treatment in the DI group resulted in a delayed and much smaller increase in the glucagon response (740 +/- 138 pg/ml) to hypoglycemia despite normalization of glycemia.; We, therefore, conclude that in streptozotocin-diabetic rats, the impaired glucagon responsiveness to hypoglycemia is significantly improved by insulin-independent correction of hyperglycemia, suggesting the importance of normoglycemia per se in maintaining, at least in part, the glucose sensitivity of pancreatic alpha-cells.

Endocrinology. 1998 Nov;139(11):4540-6. Related Articles, Links: Insulin, but not glucose lowering corrects the hyperglucagonemia and increased proglucagon messenger ribonucleic acid levels observed in insulinopenic diabetes.

Dumonteil E, Magnan C, Ritz-Laser B, Meda P, Dussoix P, Gilbert M, Ktorza A, Philippe J.

Department of Medicine, Centre Médical Universitaire, Geneva, Switzerland.

The factors that regulate glucagon biosynthesis and proglucagon gene expression are poorly defined. We previously reported that insulin inhibits proglucagon gene expression in vitro.; In vivo, however, the effects of insulin on the regulation of the proglucagon gene have been controversial. Furthermore, whether glucose plays any role alone or in conjunction with insulin on proglucagon gene expression is unknown.; We investigated the consequences of insulinopenic diabetes on glucagon gene expression in the endocrine pancreas and intestine and whether insulin and/or glucose could correct the observed abnormalities.; We show here that in the first 3 days after induction of hyperglycemia by streptozotocin, rats have levels of plasma glucagon and proglucagon messenger RNA comparable to those of normoglycemic controls despite hyperglycemia.; With more prolonged diabetes, plasma glucagon and proglucagon messenger RNA levels increase; this increase is corrected by insulin treatment, but not by phloridzin despite normalization of the glycemia by both treatments.; Proglucagon gene expression exhibits the same regulatory response to glucose and insulin in both pancreas and ileum.; We conclude that insulin tonically inhibits proglucagon gene expression in the pancreas and ileum and that glucose plays a minor, if any, role in this regulation.

WATer Cure Saves Former Nurse Bed Free

noreply@blogger.com (Nicholas Dynes Gracey) — Fri, 06 Jun 2008 07:45:00 +0000

Energy drinks safety questioned by German agency

noreply@blogger.com (Nicholas Dynes Gracey) — Fri, 06 Jun 2008 00:51:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
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Energy drinks safety questioned by German agency

By Shane Starling

http://www.NutraIngredients-usa.com/news/ng.asp?n=85729-red-bull-federal-institute-for-risk-assessment-energy-drinks-taurine-caffeine

05-Jun-2008 - Energy drinks have the potential to cause liver damage, heart failure and even death and should carry warnings for certain population groups, according to a German body.

The Federal Institute for Risk Assessment (BfR) analysed various human trials conducted over recent years that noted cardiac dysrhythmia, seizures, kidney failure and fatalities occurred after consuming energy drinks.

It called for tighter labelling to warn consumers of potential health hazards.

BfR said it had repeatedly advocated the use of warning labels for demographic sub-groups such as children, pregnant women, lactating women and caffeine-sensitive individuals, who should refrain from using energy drinks.

It said consumers with high blood pressure and heart disease should restrict energy drink use and called for more "robust studies".

Warnings about the use of energy drinks such as Red Bull with intensive physical activity or alcoholic beverages should also be mandatory.

BfR noted the regularity with which energy drinks were mixed with alcoholic beverages meant "persons no longer realistically assess their dwindling responsiveness caused by alcohol consumption under the influence of energy drinks", a problem the energy drinks sector had never taken full responsibility for.

Such label warning were in place in countries like Finland and Canada, ingredient limitations were in place in France where taurine is banned.

Denmark and Norway had banned or recommended banning energy drinks altogether.

BfR's review took in products containing not more than 320 mg/l of caffeine, 4000 mg/l of taurine, 200 mg/l of inosite and 2400 mg/l of glucuronolactone.

Consumption hazards

It noted that as far back as 2002 a scan of German poison information and treatment centres revealed energy drink-related incidents included seizures, tachycardia (increased heart rate), cardiac dysrhythmia, rhabdomyolysis (decline of skeletal muscle cells), agitation, hypertonia (high blood pressure), respiratory disorders and psychotic conditions.

As well as citing numerous studies demonstrating the potential hazards of energy drink consumption due to different ingredients, BfR's report notes a number of case studies where energy drinks have led to adverse reactions including death in combination with alcohol and alone.

The use of energy drinks as substitutes for sports beverages was also questioned. Sports beverages supplied, "calorific energy, are consumed in larger amounts in conjunction with intensive physical activity and are, therefore, associated with the consumer conditions which are specifically contra-indicated for energy drinks."

The European Food Safety Authority (EFSA) is in the process of assessing the status of energy drinks, with an EU-wide approach a possible consequence of that assessment.

"This could encourage EU-wide data matching and lead to the emergence of new findings about consumer groups who may be particularly sensitive to energy drinks," Bfr said. "As far as exposure is concerned, it is pointed out that in a Scientific Committee on Food (SCF) expert report which is still valid, reference was made to the unit of 250 ml cans for energy drinks which had been the norm up to then whereas far larger packs are now sold internationally."

Low Blood Sugar-HYPOglycemia-What the Surgeon says...

noreply@blogger.com (Nicholas Dynes Gracey) — Wed, 04 Jun 2008 22:00:00 +0000

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A glucose meter (or glucometer) is a medical device for determining the approximate concentration of glucose in the blood. It is a key element of home blood glucose monitoring (HBGM) by people with

diabetes mellitus or with proneness to HYPOglycemia.

A small drop of blood obtained by pricking the skin with a lancet is placed on a disposable test strip, which the meter reads and uses to calculate the blood glucose level. The meter then displays the level in mg/dl or mmol/l.

Since approximately 1980, a primary goal of the management of type 1 diabetes has been the achievement of closer-to-normal levels of glucose in the blood for as much of the time as possible, guided by HBGM several times a day. The benefits include a reduction in the occurrence rate and severity of long-term complications from hyperglycemia as well as a reduction in the short-term, potentially life-threatening complications of HYPOglycemia.

Characteristics

A glucose meter being used in Brasília, Brazil.
Photo by Wilson Dias

There are several key characteristics of glucose meters that may differ from model to model:

Size: The average size is now approximately the size of the palm of the hand, though some are smaller or larger. They are battery-powered.

Test strips: A consumable element containing chemicals that react with glucose in the drop of blood is used for each measurement. For most models this element is a plastic test strip with a small spot impregnated with glucose oxidase and other components. Each strip can only be used once and is then discarded. Instead of strips, some models use discs that may be used for several readings.

Coding: Since test strips may vary from batch to batch, some models require the user to enter in a code that may be found on the vial of test strips, or a chip that comes with the test strip. By entering the coding or chip into the glucose meter, the meter will be calibrated to that batch of test strips. However, if this process is carried out incorrectly, the meter reading can be up to 4mmol/L inaccurate. The implications of an incorrectly coded meter can be serious for patients actively managing their diabetes. For miscoded meters, the probability of making an insulin dose error of 2 units is 50%. The probability of making an insulin dose error of 3 units is 24%, compared to 0.49% when using a no coding meter. This may place patients at increased risk of hypoglycaemia.
Bayer's No Coding Technology involves a range of meters and test strips with automatic coding.^[1]

Volume of blood sample: The size of the drop of blood needed by different models varies from 0.3 to 10 μl. (Older models required larger blood samples, usually defined as a "hanging drop" from the fingertip.) Smaller volume requirements reduce the frequency of unproductive pricks.

Alternative site testing: Smaller drop volumes have enabled "alternate site testing" �?? pricking the forearms or other less sensitive areas instead of the fingertips. Although less uncomfortable, readings obtained from forearm blood lag behind fingertip blood in reflecting rapidly changing glucose levels in the rest of the body.

Testing times: The times it takes to read a test strip may range from 3 to 60 seconds for different models.

Display: The glucose value in mg/dl or mmol/l is displayed in a small window. The preferred measurement unit varies by country: mg/dl are preferred in the US, mmol/l in Canada and Europe. To convert mmol/l of glucose to mg/dl, multiply by 18. To convert mg/dl of glucose to mmol/l, divide by 18 or multiply by 0.055. Many machines can toggle between both types of measurements and there have been a couple of published instances in which someone with diabetes has been misled into the wrong action by assuming that a reading in mmol/l was really a very low reading in mg/dl, or the converse. Recent production U.S.-marketed machines are pre-set at the factory for mg/dl and cannot be changed.

Glucose [BG] vs. Plasma glucose [PBG]: Glucose levels in plasma (one of the components of blood) are generally 10%�??15% higher than glucose measurements in whole blood (and even more after eating). This is important because home blood glucose meters measure the glucose in whole blood while most lab tests measure the glucose in plasma. Currently, there are many meters on the market that give results as "plasma equivalent," even though they are measuring whole blood glucose. The plasma equivalent is calculated from the whole blood glucose reading using an equation built into the glucose meter. This allows patients to easily compare their glucose measurements in a lab test and at home. It is important for you and your healthcare provider to know whether your meter gives its results as "whole blood equivalent" or "plasma equivalent."

Clock/memory: All meters now include a clock that is set for date and time, and a memory for past test results. The memory is an important aspect of diabetes care, as it enables the person with diabetes to keep a record of management and look for trends and patterns in blood glucose levels over days. Most memory chips can display an average of recent glucose readings.

Data transfer: Many meters now have more sophisticated data handling capabilities. Many can be downloaded by a cable or infrared to a computer that has diabetes management software to display the test results. Some meters allow entry of additional data throughout the day, such as insulin dose, amounts of carbohydrates eaten, or exercise. A number of meters have been combined with other devices, such as insulin injection devices, PDAs, and even Game Boys.^[1] A radio link to an insulin pump allows automatic transfer of glucose readings to a calculator that assists the wearer in deciding on an appropriate insulin dose. One model also measures beta-hydroxybutyrate in the blood to detect ketoacidosis (ketosis).

Hospital glucose meters: Special glucose meters for multi-patient hospital use are now used. These provide more elaborate quality control records, and the data handling capabilities are designed to transfer glucoses into electronic medical records and the laboratory computer systems for billing purposes.

Cost

The cost of home blood glucose monitoring is substantial due to the cost of the test strips. In 2006, the consumer cost of each glucose strip ranged from about $0.35 to $1.00. Manufacturers often provide meters at no cost to induce use of the profitable test strips. Type 1 diabetics test as often as 10 to 12 times a day due to the dynamics of insulin adjustment, whereas type 2 test less frequently, especially when insulin is not part of treatment.

Some batches of counterfeit test strips for some meters have been identified, and these have been shown to produce inaccurate results^[2]. They should not be used and should be reported to the supposed manufacturer.

Accuracy

Accuracy of glucose meters is a common topic of clinical concern. Nearly all of the meters have similar accuracy (±10-15%) when used optimally. However, a variety of factors can affect the accuracy of a test. Factors affecting accuracy of various meters have included calibration of meter, ambient temperature, pressure use to wipe off strip, size of blood sample, high levels of certain drugs in blood, hematocrit, dirt on meter, humidity, and aging of test strips. Models vary in their susceptibility to these factors, and in their ability to prevent or warn of inaccurate results with error messages. The Clarke error grid is a common way of analyzing and displaying accuracy of readings related to management consequences. More recently an improved version of the Clarke error grid has come into use - this is known as the Consensus Error Grid.

History

The earliest glucose meter was the Ames Reflectance Meter by Anton H. Clemens. It was used in American hospitals in the 70's. It was about 10 inches long. It needed connection to an electrical outlet for the power. A moving needle indicated the blood glucose after about a minute.

Home glucose monitoring was demonstrated to improve glycemic control of type 1 diabetes in the late 1970s, and the first meters were marketed for home use around 1980. The two models initially dominant in North America in the 1980s were the Glucometer whose trademark is owned by Bayer [3] and the Accu-Chek meter (by Roche). Consequently, these brand names have become synonymous with the generic product to many health care professionals.

Test strips that changed color and could be read "visually", without a meter, were also widely used in the 1980s. They had the added advantage that they could be cut with scissors longitudinally to save money. As meter accuracy and insurance coverage improved, they lost popularity and are no longer marketed.

At least in North America, hospitals resisted adoption of meter glucose measurements for inpatient diabetes care for over a decade. Managers of laboratories argued that the superior accuracy of a laboratory glucose measurement outweighed the advantage of immediate availability and made meter glucose measurements unacceptable for inpatient diabetes management. Patients with diabetes and their endocrinologists eventually persuaded acceptance.

Home glucose testing was adopted for type 2 diabetes more slowly than for type 1, and a large proportion of people with type 2 diabetes have never been instructed in home glucose testing.

Future

Development of noninvasive devices may enable continuous monitoring. Research is being done on noninvasive methods for measuring blood glucose, such as using electric currents and ultrasound.

There is one noninvasive glucose meter that has been approved by the FDA: The GlucoWatch G2 Biographer is designed to be worn on the wrist, and it uses electric fields to draw out body fluid for testing. The device does not replace conventional blood glucose monitoring. One limitation is that the GlucoWatch system is not able to cope with perspiration at the measurement site. The sweat must be allowed to dry before measurement can resume. Due to these limitations and others, the product is no longer on the market.

The market introduction of noninvasive blood glucose measurement by spectroscopic measurement methods, in the field of near-infrared (NIR), by extracorporal measuring devices, failed so far because at the present time, the devices measure tissue sugar, in body tissues, and not the blood sugar in blood fluid. To determine blood glucose, the measuring beam of infrared light, for example, has to penetrate the tissue for measurement of blood glucose.[4]

It is speculated that within the next decade, meters may be replaced with continuous glucose sensors for many people with diabetes. This will likely decrease complications found in people with diabetes by limiting problems associated with hyperglycemia and hypoglycemia.

There are currently 2 CGMS (continuous glucose monitoring system) available. The first is Medtronic's Minimed Paradigm RTS with a sub-cutaneous probe attached to a small transmitter (roughly the size of a quarter) that sends interstitial glucose levels to a small pager sized receiver every 5 minutes. As well, the DexCom STS System is available (2Q 2006). It is a hypodermic probe with a small transmitter. The receiver is about the size of a cell phone and can operate up to five feet from the transmitter. Aside from a two hour calibration period, monitoring is logged at five-minute intervals for up to 72 hours. High and low glucose alarms are user-settable.

There is currently an effort to develop an integrated treatment system with a glucose meter, insulin pump and wristop controller, as well as an effort to integrate the glucose meter and a cell phone. These glucose meter/cellular phone combinations are under testing and currently cost $149.00 USD retail. Testing strips are proprietary and available only through the manufacturer (no insurance availability.) These "Glugophones" are currently offered in three forms: as a dongle for the iPhone, an addon pack for LG model UX5000, VX5200, and LX350 cell phones, as well as an addon pack for the Motorola Razr cell phone. This limits providers to AT&T for the iPhone and Verizon for the others.

Technology

Many glucose meters employ the oxidation of glucose to gluconolactone catalyzed by glucose oxidase. Others use a similar reaction catalysed instead by another enzyme, Glucose Dehydrogenase (GHD). This has the advantage of sensitivity over glucose oxidase, but is more susceptible to interfering reactions with other substances.

The first-generation devices relied on the same colorimetric reaction that is still used nowadays in glucose test strips for urine. Besides glucose oxidase, the test kit contains a benzidine derivative, which is oxidized to a blue polymer by the hydrogen peroxide formed in the oxidation reaction. The disadvantage of this method was that the test strip had to be developed after a precise interval (the blood had to be washed away), and the meter needed to be calibrated frequently.

Most glucometers today use an electrochemical method. Test strips contain a capillary that sucks up a reproducible amount of blood and an enzyme electrode containing glucose oxidase. The enzyme is reoxidized with an excess of ferrocyanide ion. The total charge passing through the electrode is measured and is proportional to the concentration of glucose in the blood. The coulometric method is a technique used to define a reaction where the amount of charge measured over a fixed time is measured. The amperometric method is used by some meters that allows the reaction to go to completion and where the total charge transfer is measured. The coulometric method allows for a fixed test time, whereas test times with a meter using the amperometric techique can vary.

Meter use for HYPOglycemia

Although the apparent value of immediate measurement of blood glucose might seem to be higher for HYPOglycemia than hyperglycemia, meters have been less useful. The primary problems are precision and ratio of false positive and negative results. An imprecision of ±15% is less of a problem for high glucose levels than low. There is little difference in the management of a glucose of 200 mg/dl compared with 260 (i.e., a "true" glucose of 230±15%), but a ±15% error margin at a low glucose concentration brings greater ambiguity with regards to glucose management.

The imprecision is compounded by the relative likelihoods of false positives and negatives in populations with diabetes and those without. People with type 1 diabetes usually have glucose levels above normal, often ranging from 40 to 500 mg/dl (2.2 to 28 mmol/l), and when a meter reading of 50 or 70 (2.8 or 3.9 mmol/l) is accompanied by their usual hypoglycemic symptoms, there is little uncertainty about the reading representing a "true positive" and little harm done if it is a "false positive."

In contrast, people who do not have diabetes but periodically have hypoglycemic symptoms will have a much higher rate of false positives to true, and a meter is not accurate enough to base a diagnosis of hypoglycemia upon. A meter can occasionally be useful in the monitoring of severe types of hypoglycemia (e.g., congenital hyperinsulinism), to ensure that the average glucoses when fasting remain above 70 mg/dl (3.9 mmol/l).

YouTube Videos of Blood Glucose Meters

External links used as references

References

^ Healthcare Professionals -- Products and Services. Bayer Healthcare. Retrieved on 2008-01-30.

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HYPOglycemia (HYPOglycaemia in British English) is the medical term for a pathologic glucose (sugar) in the blood. The term hypoglycemia literally means "under-sweet blood" (Gr. hypo-, glykys, haima). Hypoglycemia can produce a variety of symptoms and effects but the principal problems arise from an inadequate supply of glucose as fuel to the brain, resulting in impairment of function (neuroglycopenia). Derangements of function can range from vaguely "feeling bad" to coma and (rarely) permanent brain damage or death. Hypoglycemia can arise from many causes and can occur at any age. state produced by a lower than normal level of

The most common forms of moderate and severe hypoglycemia occur as a complication of treatment of diabetes mellitus with insulin or certain oral medications. Hypoglycemia is usually treated by the ingestion or administration of dextrose, or foods digestible to glucose.

Endocrinologists (specialists in hormones, including those which regulate glucose metabolism) typically consider the following criteria (referred to as Whipple's triad) as proving that individual's symptoms can be attributed to hypoglycemia:

Symptoms known to be caused by hypoglycemia
Low glucose at the time the symptoms occur
Reversal or improvement of symptoms or problems when the glucose is restored to normal

However, not everyone has accepted these suggested diagnostic criteria, and even the level of glucose low enough to define HYPOglycemia has been a source of controversy in several contexts. For many purposes, plasma glucose levels below 70 mg/dl or 3.9 mmol/L are considered HYPOglycemic; these issues are detailed below ...

Defining hypoglycemia

No single glucose value alone serves to define the medical condition termed hypoglycemia for all people and purposes. Throughout the 24 hour cycles of eating, digestion, and fasting, blood plasma glucose levels are generally maintained within a range of 70-140 mg/dL (3.9-7.8 mmol/L) for healthy humans.^[1] Although 60 or 70 mg/dL (3.3 or 3.9 mmol/L) is commonly cited as the lower limit of normal glucose, different values (typically below 40, 50, 60, or 70 mg/dL) have been defined as low for different populations, clinical purposes, or circumstances.

The precise level of glucose considered low enough to define hypoglycemia is dependent on (1) the measurement method, (2) the age of the person, (3) presence or absence of effects, and (4) the purpose of the definition. While there is no disagreement as to the normal range of blood sugar, debate continues as to what degree of hypoglycemia warrants medical evaluation or treatment, or can cause harm.^[2]^[3]^[4]

This article expresses glucose in milligrams per deciliter (mg/dL or mg/100 mL) as is customary in the United States, while millimoles per litre (mmol/L or mM) are the SI (International System) units used in most of the rest of the world. Glucose concentrations expressed as mg/dL can be converted to mmol/L by dividing by 18.0 g/mol (the molar mass of glucose). For example, a glucose concentration of 90 mg/dL is 5.0 mmol/L or 5.0 mM.

Measurement method

Blood glucose levels discussed in this article are venous plasma or serum levels measured by standard, automated glucose oxidase methods used in medical laboratories. For clinical purposes, plasma and serum levels are similar enough to be interchangeable. Arterial plasma or serum levels are slightly higher than venous levels, and capillary levels are typically in between.^[5] This difference between arterial and venous levels is small in the fasting state but is amplified and can be greater than 10% in the postprandial state.^[6] On the other hand, whole blood glucose levels (e.g., by fingerprick meters) are about 10%-15% lower than venous plasma levels.^[5] Furthermore, available fingerstick glucose meters are only warranted to be accurate to within 15% of a simultaneous laboratory value under optimal conditions, and home use in the investigation of hypoglycemia is fraught with misleading low numbers.^[7]^[8] In other words, a meter glucose reading of 39 mg/dL could be properly obtained from a person whose laboratory serum glucose was 53 mg/dL; even wider variations can occur with "real world" home use.

Ironically, most meters sold are routinely tested for accuracy at the high-end of the scale, sometimes up to 800 mg/dL, despite the fact that there is little immediate danger from hyperglycemia, whereas there is very real immediate danger from HYPOglycemia, making accuracy at the low-end extremely critical.

Two other factors significantly affect glucose measurement: hematocrit and delay after phlebotomy. The disparity between venous and whole blood concentrations is greater when the hematocrit is high,^[6] as in newborn infants, or adults with polycythemia. High neonatal hematocrits are particularly likely to confound glucose measurement by meter. Second, unless the specimen is drawn into a fluoride tube or processed immediately to separate the serum or plasma from the cells, the measurable glucose will be gradually lowered by in vitro metabolism of the glucose at a rate of approximately 7 mg/dL/hr, or even more in the presence of leukocytosis.^[9]^[10]^[6]

Age differences

Surveys of healthy children and adults show that plasma glucoses below 60 mg/dL (3.3 mM) or above 100 mg/dL (5.6 mM) are found in less than 5% of samples after an overnight fast.^[11] In infants and young children up to 10% have been found to be below 60 mg/dL after an overnight fast.^{[citation needed]} As the duration of fasting is extended, plasma glucose levels can fall further, even in healthy people. In other words, many healthy people can occasionally have glucose levels in the hypoglycemic range without symptoms or disease.

The normal range of newborn blood sugars continues to be debated. Surveys and experience have revealed blood sugars often below 40 mg/dL (2.2 mM), rarely below 30 mg/dL (1.7 mM),^{[citation needed]} in apparently healthy full-term infants on the first day after birth. It has been proposed that newborn brains are able to use alternate fuels when glucose levels are low more readily than adults. Experts continue to debate the significance and risk of such levels, though the trend has been to recommend maintenance of glucose levels above 60-70 mg/dL after the first day after birth. In ill, undersized, or premature newborns, low blood sugars are even more common, but there is a consensus that sugars should be maintained at least above 50 mg/dL^{[citation needed]} (2.8 mM) in such circumstances. Some experts advocate 70 mg/dL^{[citation needed]} as a therapeutic target, especially in circumstances such as hyperinsulinism where alternate fuels may be less available.

Presence or absence of effects

Research in healthy adults shows that mental efficiency declines slightly but measurably as blood glucose falls below 65 mg/dL (3.6 mM) in many people. Hormonal defense mechanisms (adrenaline and glucagon) are activated as it drops below a threshold level (about 55 mg/dL for most people), producing the typical symptoms of shakiness and dysphoria. On the other hand, obvious impairment does not often occur until the glucose falls below 40 mg/dL, and up to 10% of the population may occasionally have glucose levels below 65 in the morning without apparent effects. Brain effects of hypoglycemia, termed neuroglycopenia, determine whether a given low glucose is a "problem" for that person, and hence some people tend to use the term HYPOglycemia only when a moderately low glucose is accompanied by symptoms.

Even this criterion is complicated by the facts that A) hypoglycemic symptoms are vague and can be produced by other conditions; B) people with persistently or recurrently low glucose levels can lose their threshold symptoms so that severe neuroglycopenic impairment can occur without much warning; and C) many measurement methods (especially glucose meters) are imprecise at low levels.

Diabetic hypoglycemia represents a special case with respect to the relationship of measured glucose and hypoglycemic symptoms for several reasons. Although home glucose meter readings are sometimes misleading, the probability that a low reading accompanied by symptoms represents real hypoglycemia is higher in a person who takes insulin. Second, the hypoglycemia has a greater chance of progressing to more serious impairment if not treated, compared to most other forms of hypoglycemia that occur in adults. Third, because glucose levels are above normal most of the time in people with diabetes, hypoglycemic symptoms may occur at higher thresholds than in people who are normoglycemic most of the time. For all of these reasons, people with diabetes usually use higher meter glucose thresholds to determine hypoglycemia.

Purpose of definition

For all of the reasons explained in the above paragraphs, deciding whether a blood glucose in the borderline range of 45-75 mg/dL (2.5-4.2 mM) represents clinically problematic hypoglycemia is not always simple. This leads people to use different "cutoff levels" of glucose in different contexts and for different purposes.

Pathophysiology

Like most animal tissues, brain metabolism depends primarily on glucose for fuel in most circumstances. A limited amount of glucose can be derived from glycogen stored in astrocytes, but it is consumed within minutes. For most practical purposes, the brain is dependent on a continual supply of glucose diffusing from the blood into the interstitial tissue within the central nervous system and into the neurons themselves.

Therefore, if the amount of glucose supplied by the blood falls, the brain is one of the first organs affected. In most people, subtle reduction of mental efficiency can be observed when the glucose falls below 65 mg/dl (3.6 mM). Impairment of action and judgement usually becomes obvious below 40 mg/dl (2.2 mM). Seizures may occur as the glucose falls further. As blood glucose levels fall below 10 mg/dl (0.55 mM), most neurons become electrically silent and nonfunctional, resulting in coma. These brain effects are collectively referred to as neuroglycopenia.

The importance of an adequate supply of glucose to the brain is apparent from the number of nervous, hormonal and metabolic responses to a falling glucose level. Most of these are defensive or adaptive, tending to raise the blood sugar via glycogenolysis and gluconeogenesis or provide alternative fuels. If the blood sugar level falls too low the liver converts a storage of glycogen into glucose and releases it into the bloodstream, to prevent the person going in to a diabetic coma, for a short period of time.

Brief or mild hypoglycemia produces no lasting effects on the brain, though it can temporarily alter brain responses to additional hypoglycemia. Prolonged, severe hypoglycemia can produce lasting damage of a wide range. This can include impairment of cognitive function, motor control, or even consciousness. The likelihood of permanent brain damage from any given instance of severe hypoglycemia is difficult to estimate, and depends on a multitude of factors such as age, recent blood and brain glucose experience, concurrent problems such as hypoxia, and availability of alternative fuels. The vast majority of symptomatic hypoglycemic episodes result in no detectable permanent harm.^[12]

Signs and symptoms

Hypoglycemic symptoms and manifestations can be divided into those produced by the counterregulatory hormones (epinephrine/adrenaline and glucagon) triggered by the falling glucose, and the neuroglycopenic effects produced by the reduced brain sugar.

Adrenergic manifestations

Shakiness, anxiety, nervousness, tremor
Palpitations, tachycardia
Sweating, feeling of warmth
Pallor, coldness, clamminess
Dilated pupils
Feeling of numbness "pins and needles" in the fingers

Glucagon manifestations

NeuroGlycoPenic manifestations ...

Abnormal mentation, impaired judgement
Nonspecific dysphoria, anxiety, moodiness, depression, crying
Negativism, irritability, belligerence, combativeness, rage
Personality change, emotional lability
Fatigue, weakness, apathy, lethargy, daydreaming, sleep
Confusion, amnesia, dizziness, delirium
Staring, "glassy" look, blurred vision, double vision
Automatic behavior, also known as automatism
Difficulty speaking, slurred speech
Ataxia, incoordination, sometimes mistaken for "drunkenness"
Focal or general motor deficit, paralysis, hemiparesis
Paresthesia, headache
Stupor, coma, abnormal breathing
Generalized or focal seizures

Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms, if symptoms even occur. Specific manifestations may vary by age and by severity of the hypoglycemia. In young children, vomiting can sometimes accompany morning hypoglycemia with ketosis. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person may be similar from episode to episode, but are not necessarily so and may be influenced by the speed at which glucose levels are dropping, and previous incidence.

In newborns, HYPOglycemia can produce irritability, jitters, myoclonic jerks, cyanosis, respiratory distress, apneic episodes, sweating, hypothermia, somnolence, hypotonia, refusal to feed, and seizures or "spells". HYPOglycemia can resemble asphyxia, hypocalcemia, sepsis, or heart failure.

In both young and old patients, the brain may habituate to low glucose levels, with a reduction of noticeable symptoms despite NeuroGlycoPenic impairment. In insulin-dependent diabetic patients this phenomenon is termed HYPOglycemia unawareness and is a significant clinical problem when improved glycemic control is attempted. Another aspect of this phenomenon occurs in type I glycogenosis, when chronic hypoglycemia before diagnosis may be better tolerated than acute hypoglycemia after treatment is underway.

Nearly always, hypoglycemia severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurological damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe HYPOglycemia.

Determining the cause

Hundreds of conditions can cause hypoglycemia. Common causes by age are listed below. While many aspects of the medical history and physical examination may be informative, the two best guides to the cause of unexplained hypoglycemia are usually

the circumstances
a critical sample of blood obtained at the time of hypoglycemia, before it is reversed.

The circumstances of hypoglycemia provide most of the clues to diagnosis

Circumstances include the age of the patient, time of day, time since last meal, previous episodes, nutritional status, physical and mental development, drugs or toxins (especially insulin or other diabetes drugs), diseases of other organ systems, family history, and response to treatment. When hypoglycemia occurs repeatedly, a record or "diary" of the spells over several months, noting the circumstances of each spell (time of day, relation to last meal, nature of last meal, response to carbohydrate, and so forth) may be useful in recognizing the nature and cause of the hypoglycemia.

An especially important aspect is whether the patient is seriously ill with another problem. Severe disease of nearly all major organ systems can cause hypoglycemia as a secondary problem. Hospitalized patients, especially in intensive care units or those prevented from eating, can suffer hypoglycemia from a variety of circumstances related to the care of their primary disease. Hypoglycemia in these circumstances is often multifactorial or even iatrogenic. Once identified, these types of hypoglycemia are readily reversed and prevented, and the underlying disease becomes the primary problem.

Apart from determining nutritional status and identifying whether there is likely to be an underlying disease more serious than hypoglycemia, the physical examination of the patient is only occasionally helpful. Macrosomia in infancy usually indicates hyperinsulinism. A few syndromes and metabolic diseases may be recognizable by clues such as hepatomegaly or micropenis.

Response to treatment, especially the amount of carbohydrate needed to reverse or prevent recurrence of HYPOglycemia, may provide important clues as well. When 15-30 grams of sugar or starch are given by mouth, a low blood glucose will usually rise by 18-36 mg/dl (1-2 mmol/l) within 5-10 minutes, relieving HYPOglycemia symptoms within 10 minutes^{[citation needed]}. It may take longer to recover from severe hypoglycemia with unconsciousness or seizure even after restoration of normal blood glucose. When a person has not been unconscious, failure of carbohydrate to reverse the symptoms in 10-15 minutes increases the likelihood that hypoglycemia was not the cause of the symptoms. When severe hypoglycemia has persisted in a hospitalized patient, the amount of glucose required to maintain satisfactory blood glucose levels becomes an important clue to the underlying etiology. Glucose requirements above 10 mg/kg/minute in infants, or 6 mg/kg/minute in children and adults are strong evidence for hyperinsulinism. In this context this is referred to as the glucose infusion rate (GIR). Finally, the blood glucose response to glucagon given when the glucose is low can also help distinguish among various types of hypoglycemia. A rise of blood glucose by more than 30 mg/dl (1.70 mmol/l) suggests insulin excess as the probable cause of the hypoglycemia.

In less obvious cases, a "critical sample" may provide the diagnosis

In the majority of children and adults with recurrent, unexplained hypoglycemia, the diagnosis may be determined by obtaining a sample of blood during hypoglycemia. If this critical sample is obtained at the time of HYPOglycemia, before it is reversed, it can provide information that would otherwise require a several-thousand-dollar hospital admission and unpleasant starvation testing. Perhaps the most common inadequacy of emergency department care in cases of unexplained HYPOglycemia is the failure to obtain at least a basic sample before giving glucose to reverse it.

Part of the value of the critical sample may simply be the proof that the symptoms are indeed due to hypoglycemia. More often, measurement of certain hormones and metabolites at the time of hypoglycemia indicates which organs and body systems are responding appropriately and which are functioning abnormally. For example, when the blood glucose is low, hormones which raise the glucose should be rising and insulin secretion should be completely suppressed.

The following is a brief list of hormones and metabolites which may be measured in a critical sample. Not all tests are checked on every patient. A "basic version" would include insulin, cortisol, and electrolytes, with C-peptide and drug screen for adults and growth hormone in children. The value of additional specific tests depends on the most likely diagnoses for an individual patient, based on the circumstances described above. Many of these levels change within minutes, especially if glucose is given, and there is no value in measuring them after the hypoglycemia is reversed. Others, especially those lower in the list, remain abnormal even after hypoglycemia is reversed, and can be usefully measured even if a critical specimen is missed. Although interpretation in difficult cases is beyond the scope of this article, for most of the tests, the primary significance is briefly noted.

Glucose: needed to document actual hypoglycemia
Insulin: any detectable amount is abnormal during hypoglycemia, but physician must know assay characteristics
Cortisol: should be high during hypoglycemia if pituitary and adrenals are functioning normally
Growth hormone: should rise after hypoglycemia if pituitary is functioning normally
Electrolytes and total carbon dioxide: electrolyte abnormalities may suggest renal or adrenal disease; mild acidosis is normal with starvation hypoglycemia; usually no acidosis with hyperinsulinism
Liver enzymes: elevation suggests liver disease
Ketones: should be high during fasting and hypoglycemia; low levels suggest hyperinsulinism or fatty acid oxidation disorder
Beta-hydroxybutyrate: should be high during fasting and hypoglycemia; low levels suggest hyperinsulinism or fatty acid oxidation disorder
Free fatty acids: should be high during fasting and hypoglycemia; low levels suggest hyperinsulinism; high with low ketones suggests fatty acid oxidation disorder
Lactic acid: high levels suggest sepsis or an inborn error of gluconeogenesis such as glycogen storage disease
Ammonia: if elevated suggests hyperinsulinism due to glutamate dehydrogenase deficiency, Reye syndrome, or certain types of liver failure
C-peptide: should be low or undetectable; if elevated suggests hyperinsulinism; low c-peptide with high insulin suggests exogenous (injected) insulin
Proinsulin: detectable levels suggest hyperinsulinism; levels disproportionate to a detectable insulin level suggest insulinoma
Ethanol: suggests alcohol intoxication
Toxicology screen: can detect many drugs causing hypoglycemia, especially for sulfonylureas
Insulin antibodies: if positive suggests repeated insulin injection or antibody-mediated hypoglycemia
Urine organic acids: elevated in various characteristic patterns in several types of organic aciduria
Carnitine, free and total: low in certain disorders of fatty acid metabolism and certain types of drug toxicity and pancreatic disease
Thyroxine and TSH: low T4 without elevated TSH suggests hypopituitarism or malnutrition
Acylglycine: elevation suggests a disorder of fatty acid oxidation
Epinephrine: should be elevated during hypoglycemia
Glucagon: should be elevated during hypoglycemia, except in the case of type 1 diabetes mellitus where irreparable damage is done to the cells which produce this counterregulatory hormone.
IGF-1: low levels suggest hypopituitarism or chronic malnutrition
IGF-2: low levels suggest hypopituitarism; high levels suggest non-pancreatic tumor hypoglycemia
ACTH: should be elevated during hypoglycemia; unusually high ACTH with low cortisol suggests Addison's disease
Alanine or other plasma amino acids: abnormal patterns may suggest certain inborn errors of amino acid metabolism or gluconeogenesis
Somatostatin should be elevated during hypoglycemia as it acts to inhibit insulin production and increase blood glucose level

Further diagnostic steps

When suspected hypoglycemia recurs and a critical specimen has not been obtained, the diagnostic evaluation may take several paths. However good nutrition and prompt intake is essential.

When general health is good, the symptoms are not severe, and the person can fast normally through the night, experimentation with diet (extra snacks with fat or protein, reduced sugar) may be enough to solve the problem. If it is uncertain whether "spells" are indeed due to hypoglycemia, some physicians will recommend use of a home glucose meter to test at the time of the spells to confirm that glucoses are low. This approach may be most useful when spells are fairly frequent or the patient is confident that he or she can provoke a spell. The principal drawback of this approach is the high rate of false positive or equivocal levels due to the imprecision of the currently available meters: both physician and patient need an accurate understanding of what a meter can and cannot do to avoid frustrating and inconclusive results.

In cases of recurrent hypoglycemia with severe symptoms, the best method of excluding dangerous conditions is often a diagnostic fast. This is usually conducted in the hospital, and the duration depends on the age of the patient and response to the fast. A healthy adult can usually maintain a glucose level above 50 mg/dl (2.8 mM) for 72 hours, a child for 36 hours, and an infant for 24 hours. The purpose of the fast is to determine whether the person can maintain his or her blood glucose as long as normal, and can respond to fasting with the appropriate metabolic changes. At the end of the fast the insulin should be nearly undetectable and ketosis should be fully established. The patient's blood glucose levels are monitored and a critical specimen is obtained if the glucose falls. Despite its unpleasantness and expense, a diagnostic fast may be the only effective way to confirm or refute a number of serious forms of hypoglycemia, especially those involving excessive insulin.

A traditional method for investigating suspected hypoglycemia is the oral glucose tolerance test, especially when prolonged to 3, 4, or 5 hours. Although quite popular in the United States in the 1960s, repeated research studies have demonstrated that many healthy people will have glucose levels below 70 or 60 during a prolonged test, and that many types of significant hypoglycemia may go undetected with it. This combination of poor sensitivity and specificity has resulted in its abandonment for this purpose by physicians experienced in disorders of glucose metabolism.

Causes

There are several ways to classify hypoglycemia. The following is a list of the more common causes and factors which may contribute to hypoglycemia grouped by age, followed by some causes that are relatively age-independent. See causes of hypoglycemia for a more complete list grouped by etiology.

HYPOglycemia in newborn infants

Hypoglycemia is a common problem in critically ill or extremely low birthweight infants. If not due to maternal hyperglycemia, in most cases it is multifactorial, transient and easily supported. In a minority of cases hypoglycemia turns out to be due to significant hyperinsulinism, hypopituitarism or an inborn error of metabolism and presents more of a management challenge.

Transient neonatal hypoglycemia
- Prematurity, intrauterine growth retardation, perinatal asphyxia
- Maternal hyperglycemia due to diabetes or iatrogenic glucose administration
- Sepsis
- Prolonged fasting (e.g., due to inadequate breast milk or condition interfering with feeding)
Congenital hypopituitarism
Congenital hyperinsulinism, several types, both transient and persistent
Inborn errors of carbohydrate metabolism such as glycogen storage disease

HYPOglycemia in young children

Single episodes of hypoglycemia may occur due to gastroenteritis or fasting, but recurrent episodes nearly always indicate either an inborn error of metabolism, congenital hypopituitarism, or congenital hyperinsulinism. A list of common causes:

Prolonged fasting
- Diarrheal illness in young children, especially rotavirus gastroenteritis
Idiopathic ketotic hypoglycemia
Isolated growth hormone deficiency, hypopituitarism
Insulin excess
- Hyperinsulinism due to several congenital disorders of insulin secretion
- Insulin injected for type 1 diabetes
Gastric dumping syndrome (after gastrointestinal surgery)
Other congenital metabolic diseases; some of the common include
- Maple syrup urine disease and other organic acidurias
- Type 1 glycogen storage disease
- Disorders of fatty acid oxidation
- Medium chain acylCoA dehydrogenase deficiency (MCAD)
Accidental ingestions
- Sulfonylureas, propranolol and others
- Ethanol (mouthwash, "leftover morning-after-the-party drinks")

HYPOglycemia in older children and young adults

by far the most common cause of severe hypoglycemia in this age range is insulin injected for type 1 diabetes. Circumstances should provide clues fairly quickly for the new diseases causing severe hypoglycemia. All of the congenital metabolic defects, congenital forms of hyperinsulinism, and congenital hypopituitarism are likely to have already been diagnosed or are unlikely to start causing new hypoglycemia at this age. Body mass is large enough to make starvation hypoglycemia and idiopathic ketotic hypoglycemia quite uncommon. Recurrent mild hypoglycemia may fit a reactive hypoglycemia pattern, but this is also the peak age for idiopathic postprandial syndrome, and recurrent "spells" in this age group can be traced to orthostatic hypotension or hyperventilation as often as demonstrable hypoglycemia.

Insulin-induced hypoglycemia
- Insulin injected for type 1 diabetes
- Factitious insulin injection (Munchausen syndrome)
- Insulin-secreting pancreatic tumor
- Reactive hypoglycemia and idiopathic postprandial syndrome
Addison's disease
Sepsis

HYPOglycemia in older adults

The incidence of hypoglycemia due to complex drug interactions, especially involving oral hypoglycemic agents and insulin for diabetes rises with age. Though much rarer, the incidence of insulin-producing tumors also rises with advancing age. Most tumors causing hypoglycemia by mechanisms other than insulin excess occur in adults.

Insulin-induced hypoglycemia
- Insulin injected for diabetes
- Factitious insulin injection (Munchausen syndrome)
- Excessive effects of oral diabetes drugs, beta-blockers, or drug interactions
- Insulin-secreting pancreatic tumor
- Alimentary (rapid jejunal emptying with exaggerated insulin response)
  - After gastrectomy dumping syndrome or bowel bypass surgery or resection
- Reactive hypoglycemia and idiopathic postprandial syndrome
Tumor hypoglycemia, Doege-Potter syndrome
Acquired adrenal insufficiency
Acquired hypopituitarism
Immunopathologic hypoglycemia ^[13]

Treatment and prevention

Management of hypoglycemia involves immediately raising the blood sugar to normal, determining the cause, and taking measures to hopefully prevent future episodes.

Reversing acute hypoglycemia

The blood glucose can be raised to normal within minutes by taking (or receiving) 10-20 grams of carbohydrate. It can be taken as food or drink if the person is conscious and able to swallow. This amount of carbohydrate is contained in about 3-4 ounces (100-120 ml) of orange, apple, or grape juice although fruit juices contain a higher proportion of fructose which is more slowly metabolized than pure dextrose, alternatively, about 4-5 ounces (120-150 ml) of regular (non-diet) soda may also work, as will about one slice of bread, about 4 crackers, or about 1 serving of most starchy foods. Starch is quickly digested to glucose (unless the person is taking acarbose), but adding fat or protein retards digestion. Symptoms should begin to improve within 5 minutes, though full recovery may take 10-20 minutes. Overfeeding does not speed recovery and if the person has diabetes will simply produce hyperglycemia afterwards.

If a person is suffering such severe effects of hypoglycemia that they cannot (due to combativeness) or should not (due to seizures or unconsciousness) be given anything by mouth, medical personal such as EMTs and Paramedics, or in-hospital personel can establish an IV and give intravenous Dextrose, concentrations varying depending on age (Infants are given 2cc/kg Dextrose 10%, Children Dextrose 25%, and Adults Dextrose 50%). Care must be taken in giving these solutions because they can be very necrotic if the IV is infiltrated. If an IV cannot be established, the patient can be given 1 to 2 milligrams of Glucagon in an intramuscular injection. More treatment information can be found in the article diabetic hypoglycemia.

One situation where starch may be less effective than glucose or sucrose is when a person is taking acarbose. Since acarbose and other alpha-glucosidase inhibitors prevents starch and other sugars from being broken down into monosaccharides that can be absorbed by the body, patients taking these medications should consume monosaccharide-containing foods such as glucose tablets, honey, or juice to reverse hypoglycemia.

Prevention

The most effective means of preventing further episodes of hypoglycemia depends on the cause.

The risk of further episodes of diabetic hypoglycemia can often (but not always) be reduced by lowering the dose of insulin or other medications, or by more meticulous attention to blood sugar balance during unusual hours, higher levels of exercise, or alcohol intake.

Many of the inborn errors of metabolism require avoidance or shortening of fasting intervals, or extra carbohydrates. For the more severe disorders, such as type 1 glycogen storage disease, this may be supplied in the form of cornstarch every few hours or by continuous gastric infusion.

Several treatments are used for hyperinsulinemic hypoglycemia, depending on the exact form and severity. Some forms of congenital hyperinsulinism respond to diazoxide or octreotide. Surgical removal of the overactive part of the pancreas is curative with minimal risk when hyperinsulinism is focal or due to a benign insulin-producing tumor of the pancreas. When congenital hyperinsulinism is diffuse and refractory to medications, near-total pancreatectomy may be the treatment of last resort, but in this condition is less consistently effective and fraught with more complications.

Hypoglycemia due to hormone deficiencies such as hypopituitarism or adrenal insufficiency usually ceases when the appropriate hormone is replaced.

Hypoglycemia due to dumping syndrome and other post-surgical conditions is best dealt with by altering diet. Including fat and protein with carbohydrates may slow digestion and reduce early insulin secretion. Some forms of this respond to treatment with a glucosidase inhibitor, which slows starch digestion.

Reactive hypoglycemia with demonstrably low blood glucose levels is most often a predictable nuisance which can be avoided by consuming fat and protein with carbohydrates, by adding morning or afternoon snacks, and reducing alcohol intake.

Idiopathic postprandial syndrome without demonstrably low glucose levels at the time of symptoms can be more of a management challenge. Many people find improvement by changing eating patterns (smaller meals, avoiding excessive sugar, mixed meals rather than carbohydrates by themselves), reducing intake of stimulants such as caffeine, or by making lifestyle changes to reduce stress. See the following section of this article.

HYPOglycemia as American folk medicine

Hypoglycemia is also a term of contemporary American folk medicine which refers to a recurrent state of symptoms of altered mood and subjective cognitive efficiency, sometimes accompanied by adrenergic symptoms, but not necessarily by measured low blood glucose. Symptoms are primarily those of altered mood, behavior, and mental efficiency. This condition is usually treated by dietary changes which range from simple to elaborate. Advising people on management of this condition is a significant "sub-industry" of alternative medicine. More information about this form of "hypoglycemia", with far more elaborate dietary recommendations, is available on the internet and in health food stores. Most of these websites and books describe a conflation of reactive hypoglycemia and idiopathic postprandial syndrome but do not recognize a distinction. The value of most of their recommendations is unproven from a controlled, empirical scientific perspective.

References

^ Philip E. Cryer (1997). Hypoglycemia: pathophysiology, diagnosis, and treatment. Oxford [Oxfordshire]: Oxford University Press. ISBN 0-19-511325-X.
^ Koh TH, Eyre JA, Aynsley-Green A (1988). "Neonatal hypoglycaemia--the controversy regarding definition". Arch. Dis. Child. 63 (11): 1386-8. PMID 3202648.
^ Cornblath M, Schwartz R, Aynsley-Green A, Lloyd JK (1990). "Hypoglycemia in infancy: the need for a rational definition. A Ciba Foundation discussion meeting". Pediatrics 85 (5): 834-7. PMID 2330247.
^ Cornblath M, Hawdon JM, Williams AF, Aynsley-Green A, Ward-Platt MP, Schwartz R, Kalhan SC (2000). "Controversies regarding definition of neonatal hypoglycemia: suggested operational thresholds". Pediatrics 105 (5): 1141-5. doi:10.1542/peds.105.5.1141. PMID 10790476.
^ ^a ^b Tustison WA, Bowen AJ, Crampton JH (1966). "Clinical interpretation of plasma glucose values". Diabetes 15 (11): 775-7. PMID 5924610.
^ ^a ^b ^c [edited by] John Bernard Henry (1979). Clinical diagnosis and management by laboratory methods. Philadelphia: Saunders. ISBN 0-7216-4639-5.
^ Clarke WL, Cox D, Gonder-Frederick LA, Carter W, Pohl SL (1987). "Evaluating clinical accuracy of systems for self-monitoring of blood glucose". Diabetes Care 10 (5): 622-8. doi:10.2337/diacare.10.5.622. PMID 3677983.
^ Gama R, Anderson NR, Marks V (2000). "'Glucose meter hypoglycaemia': often a non-disease". Ann. Clin. Biochem. 37 ( Pt 5): 731-2. PMID 11026531.
^ de Pasqua A, Mattock MB, Phillips R, Keen H (1984). "Errors in blood glucose determination". Lancet 2 (8412): 1165. PMID 6150231.
^ Horwitz DL (1989). "Factitious and artifactual hypoglycemia". Endocrinol. Metab. Clin. North Am. 18 (1): 203-10. PMID 2645127.
^ Samuel Meites, editor-in-chief; contributing editors, Gregory J. Buffone... [et al.] (1989). Pediatric clinical chemistry: reference (normal) values. Washington, D.C: AACC Press. ISBN 0-915274-47-7.
^ edited by Allen I. Arieff, Robert C. Griggs (1992). Metabolic brain dysfunction in systemic disorders. Boston: Little, Brown. ISBN 0-316-05067-9.
^ The Hypoglycemic states - Hypoglycemia. The Hypoglycemic states. Armenian Medical Network (2007).

External links

The National Diabetes Information Clearinghouse

[hide] v �?� d �?� e Endocrine pathology: endocrine diseases (E00-35, 240-259)

Thyroid	Hypothyroidism (Iodine deficiency, Cretinism, Congenital hypothyroidism, Goitre, Myxedema) - Hyperthyroidism (Graves disease, Toxic multinodular goitre, Teratoma with thyroid tissue or Struma ovarii) - Thyroiditis (De Quervain's thyroiditis, Hashimoto's thyroiditis, Riedel's thyroiditis) - Euthyroid sick syndrome

Pancreas	Diabetes mellitus (type 1, type 2, coma, angiopathy, ketoacidosis, nephropathy, neuropathy, retinopathy) - Hypoglycemia - Hyperinsulinism - Zollinger-Ellison syndrome - insulin receptor (Rabson-Mendenhall syndrome)

Parathyroid	Hypoparathyroidism (Pseudohypoparathyroidism) - Hyperparathyroidism (Primary, Secondary, Tertiary)

Pituitary	Hyperpituitarism (Acromegaly, Hyperprolactinaemia, SIADH) - Hypopituitarism (Simmonds' disease/Sheehan's syndrome, Kallmann syndrome, Growth hormone deficiency, Diabetes insipidus) - Adiposogenital dystrophy - Empty sella syndrome - Pituitary apoplexy

Adrenal	Cushing's syndrome (Nelson's syndrome, Pseudo-Cushing's syndrome) - CAH (Lipoid, 3β, 11β, 17α, 21α) - Hyperaldosteronism (Conn syndrome, Bartter syndrome) - Adrenal insufficiency (Addison's disease) - Hypoaldosteronism

Gonads	ovarian dysfunction (Polycystic ovary syndrome, Premature ovarian failure) - testicular dysfunction (5-alpha-reductase deficiency) - testosterone biosynthesis (17-beta-hydroxysteroid dehydrogenase deficiency) - general (Hypogonadism, Delayed puberty, Precocious puberty)

Other	Androgen insensitivity syndrome - Autoimmune polyendocrine syndrome - Carcinoid syndrome - Gigantism - Short stature (Laron syndrome, Psychogenic dwarfism) - Multiple endocrine neoplasia (1, 2) - Progeria - Woodhouse-Sakati syndrome

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

Categories: Medical emergencies | Metabolic disorders

WATerCure, WATer Cure

noreply@blogger.com (Nicholas Dynes Gracey) — Wed, 04 Jun 2008 18:34:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
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Victims of circumstance in HYPOglycemia unawareness - The Diabetes Blog

noreply@blogger.com (Nicholas Dynes Gracey) — Wed, 04 Jun 2008 16:17:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
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Victims of circumstance in hypoglycemic unawareness - The Diabetes Blog:

"Victims of circumstance in hypoglycemic unawareness...

First Posted Jun 6th 2007 9:50PM by Allison Love Beatty
Filed under: Type 1, Type 2, Childhood, Adult Onset, Lifestyle, Drugs, Research, Opinion, Support
http://www.thediabetesblog.com/2007/06/06/victims-of-circumstance-in-hypoglycemic-unawareness/

Lately the news has seen a lot of devastating diabetic events due to hypoglycemic unawareness. Hypoglycemic unawareness is commonly defined as an inability to recognize the symptoms (sweating, tremor, hunger, anxiety, and palpitations) of decreased blood sugar or a failure of the warning signs to occur before development of neuroglycopenia, which means a shortage of glucose in the brain. Curiously, this term was not coined for diabetes until 10 years after the introduction of genetically modified human synthetic insulin and insulin analogues.

I hate to say it but diabetes is a crapshoot. You never know what you are going to get, but you can sure try your best to keep your eye on the ball. Removing the inherent dangers of hypoglycemic unawareness would make me a happier diabetic, and improve the lives of all those I care about (diabetics like myself). The answer might lie in the only type of treatment available nowadays, insulin analogues. Diabetics who do not take any form of drug to control blood sugar do NOT have hypoglycemic unawareness.

It's called human but it is nothing"

...

http://www.thediabetesblog.com/2007/06/06/victims-of-circumstance-in-hypoglycemic-unawareness/#c5614998

Hi Love & Brent;

potentially 'OVERdosing' or potentially 'UNDERdosing' insulin or GM insulin ... (A) Which is SAFER; (B) Why does the human body sometimes appear to have an 'allergy' to human insulin; and (C) What is the optimum 'self-help' strategy for achieving an indefinite "Honeymoon Period" and/or maybe a "2nd Honeymoon Period" aka 'beta-islet cell regeneration'?

(1) re Love's blog & Brent's comment #3 relating to that blog...
www.thediabetesblog.com/2007/06/06/victims-of-circumstance-in-hypoglycemic-unawareness
... "To put a chink in your �??good control�?? theory, I present my own case�??with attendant feelings. For more than 30 years, I used natural (animal) insulins to manage my disease. The �??feelings�?? I had were sweats, tremors, hunger�??and those �??feelings�?? triggered an urgent need for food. Before bG monitors were even a gleam in the diabusiness eye, my �??feelings�?? held me in good stead . . . never an episode of unconsciousness, never the need for outside intervention. A1c�??s�??which are the metric for assessing �??good control�??�??were assessed infrequently, but my 5.5 readings should indicate I was not out of control. Quite frankly, I must state that while I did not enjoy these �??feelings,�?? I was certainly appreciative that the �??feelings�?? kept me out of danger and in control. Jump ahead to my interlude with �??the latest, the greatest, rDNA Human insulin�??it�??s better�?? (so my doctor assured me). �??Feelings�?? disappeared. While my monitor (upon which I became more and more dependent) told me my bG was low . . . my �??feelings�?? did not. This interlude was short-lived, fortunately. Despite best efforts at achieving control with this peaky, unpredictable insulin, my A1c�??s began to climb. Then I took a shot at pump therapy and Humalog/Novalog analogs. NO FEELINGS. bG monitoring became increasingly frequent. When my A1c reached 7.2 . . . I decided that as long as animal insulin was available and importable, I was better served using these products."

(2) re Love's blog & Scott's comment #1 relating to that blog...
www.thediabetesblog.com/2007/04/03/the-honeymoon-period
... "But I think he has one undeniable truth, and that is the law of small numbers, namely that by minimizing the amount of insulin required, the patient also reduces the possibility for errors, and if errors occur, they are likely to be less severe ... but the basic idea is the same: insulin is not an easy medicine to use, therefore the idea of reducing our need for it is probably a goal that is worthy of pursuit."

(3) re Love's blog & Scott's comment #3 relating to that blog...
www.thediabetesblog.com/2007/06/17/the-rising-prices-of-insulin
... "However, the biggest question was why are we treating patients with "human" insulin when type 1 diabetes is known to be the result of a human allergy to "human" insulin?"

AND another interesting question...

What about treating Patients with the absolute MINIMUM amount of GM insulin ... when type 1 diabetes is known to be the result of a human allergy to "human" insulin?

AND because Scott's question has inspired this question which in my opinion is one of the most fundamental questions ever to be asked about type 1 diabetes ... please allow my asking similar related questions, yet again, so We can really focus on quickly finding the right answers...

What about treating Patients [and especially newly diagnosed Patients still in their "Honeymoon Period"] with the ABSOLUTE minimum amount of GM insulin & carbohydrates ... when type 1 diabetes so often and so certainly appears to be an ALLERGY to 'excess' GM insulin [... or is it a transient ALLERGY to carbohydrates related to the inherent capacity of carbohydrates to induce high > low bs patterns even in 'normal' People?].

Brent's experience appears to be a raised level of normal and/or raised mean glycaemia marked by raised HbA1c ... irrespective of which Brent reports more insulin-induced HYPOglycaemia events with GM insulin than with animal derived insulin. For Brent, who has had experience of both animal derived insulin & GM insulin, it is the latter that appears to be more 'efficient' at removing glucose availability, from Brent's brain, even though his mean blood sugar level apparently remains high enough to raise his HbA1c measurements. If Brent adopted the absolute minimum GM insulin dose to prevent 'ketoACIDosis' [ie with a focus upon adopting GM insulin primarily for maintaining his pH above 7.1] ... then GM insulin-induced HYPOglycaemia events may be reduced? AND then Brent and other type 1 & type 2 Diabetics [in a similar position] could focus much more of their energy upon 'HbA1c control' by means of, focus upon, dietary control of carbohydrate ingestion.

Here's some related possibilities which may favour protection and/or recovery of pancreatic beta-cells by reducing GM insulin 'OVERdosing' at all times and especially during the "Honeymoon Period" ...

There is a 'middle ground' of SAFELY reducing insulin by SAFELY skipping meals / snacks rather than simply 'skipping GM insulin'...

Careful study of scientific literature provides scientific EVIDENCE that the substantial DAILY danger from insulin is from insulin OVERdosing [or does that usually 'flow from' carbohydrate OVERdosing?].

www.thediabetesblog.com/2007/04/19/no-food-no-problem
Every Diabetic has the right to substantially lower GM insulin dosage, on any given DAY basis [to their preferred 'skip meals' dosage] and/or skip meals and reduce their body fat % by that SAFE means [aka 'water fasting']. It is perfectly SAFE for a type 1 diabetic or type 2 diabetic to skip meals or eat just 1 healthy meal per day. Every Diabetic has the right to eat just 1 meal a day and to know that it is a FACT that is scientifically proven to be SAFE to lower GM insulin dosage in order to SAFELY skip meals and/or safely water fast...
http://www.thediabetesblog.com/2007/04/19/no-food-no-problem

HYPOglycaemia IS the most substantial of any 'Diabetic DISEASE' ...

How may the human body 'protecting itself from HYPOglycaemia' be related to the onset of type 1 diabetes and/or a reduction in a potentially indefinite "Honeymoon Period"?

PRE 'Diabetic Growing Children' aka 'Juvenile Onset Diabetics' are particularly venerable to HYPOglycaemia [related to 'fuelling' growth requirements] and it is reasonable to suppose that their bodies [including their immune system] may 'work overtime' to prevent HYPOglycaemia [possibly resulting from 'excess pancreatic (endogenous) insulin' and/or immediately upon treatment 'excess (exogenous) GM insulin'] which is often associated with eating carbohydrates... 'Too Much And Or Too Often' ... often associated with distress stimulated release of glucagon [which protects against HYPOglycaemia following insulin surges following prolonged stress (aka distress) including eating carbohydrates and/or GM insulin treatment ... 'Too Much And Or Too Often'].

Glucose = emergency fuel = very positive for emergency refuelling [as long as that emergency is other than HYPOglycaemia].

A "spike" or transient super glycaemia [TSG] is a healthy natural response to stress including eating excessively [as long as that stress is other than HYPOglycaemia].

D3HydroxyButyricAcid [D3HBA] is the body's normal fuel = very positive in normal situations including being free from emergencies [and protects from HYPOglycaemia]. D3HBA can be increased by skipping meals and/or substantially reducing the carbohydrate %percentage% of any given meal.

"insulin resistance" & "impaired glucose tolerance" by way of insulin receptors protects the intracellular contents of every cell [having an insulin receptor] from sudden rises / spikes of glucose. [HbA1c measures bs outside the cells NOT inside the cells]...

... However ... sudden rises in blood sugar following periods of HYPOglycaemia can have VERY negative effects IF the excess glucose [contained within the 'inside' of the bloodstream] can get out of the bloodstream and into the 'inside' of the cells ... too suddenly ... as outlined by this ORIGINAL research ...
http://www.jci.org/cgi/content/full/117/4/910
AND the commentary upon the abovementioned original research is also worth a read ...
www.medindia.net/news/view_news_main.asp?x=19870

"insulin receptors" can resist sudden surges of glucose into the cells and so help to prevent HYPOglycaemia ...

There is increasing evidence that 'tightly controlled numbers', 'low bs' and associated transient HYPOglycaemia should be of far far greater concern than transient 'bs spikes' / transient HYPERglycaemia ... Please read this ORIGINAL research to see why TSG is perfectly healthy ...
http://care.diabetesjournals.org/cgi/content/full/29/7/1486?ijkey=94e3c9770f5c4db2a7b913326420344c278b4260

Until PROOF exists to the contrary ... The FMCSA 140-200mg/dl blood sugar level recommendation should be every Diabetic's target range c/o basal GM insulin or any other DRUG:-
www.thediabetesblog.com/2007/03/29/my-friend-jeff-the-trucker

Any bs lower than the FMCSA recommendation should be entirely via dietary control ie If 'high' bs is a concern for those blessed with 'insulin resistant receptors' (why?) ... increasingly reduce the amount of carbohydrates swallowed. AKA a LOW [sub15 %] carbohydrate Diet eg Dr Joel Fuhrman's [cure Type2 & reduce Type1 GM dose by half]; or Dr Richard K Bernstein's [probably cure Type2 & reduce Type1 GM dose by half]; or Dr Robert Atkins' [possibly cure Type2 & reduce Type1 GM dose by half].

Carbohydrates = glucose [lots of it]

Peanut allergy = 1 peanut = potentially fatal.

'Carbohydrate allergy' [aka 'insulin allergy'] = glucose = diabetes [alive and GM insulin kicking].

There is already evidence that lowering insulin levels can be protective eg...
www.docguide.com/news/content.nsf/news/852571020057CCF6852572F4006A7661
and there is increasing evidence that every Diabetic's primary concern should be that insulin levels can & should be lowered by focussing upon encouraging "KETOSIS" and controlling 'ketoACIDosis' rather than chasing questionable 'HYPOglycaemia UNawareness levels' of low blood sugar [bs] eg...
www.blackwell-synergy.com/doi/abs/10.1111/j.1399-5448.2007.00240.x

When have Diabetics ever considered how much easier an ultra low carbohydrate [sub15 %] diet is as compared to a zero nut diet?

Carbophiles may reasonably be described as craving eating emergency fuel to repetitively create emergency stimulation via 'repetitive HYPOglycaemia' ...
www.obesityresearch.org/cgi/content/abstract/3/suppl_4/477S

Why have breakfast? Why have snacks? Why have lunch? Why have snacks? What do You think 'body fat' is for? Why do You think every Human Being's LIVER produces "KETONES" [especially 'D3HBA'] when blood sugar [bs] AND insulin levels are 'healthily low'? 1 meal a day is enough for Anyone Who can chew...
www.thediabetesblog.com/2007/04/19/no-food-no-problem

"Say NO to Carbophilia"

AND WHEN YOU HAVE YOUR '3 COURSE MEAL' ...
PLEASE REMEMBER WHERE THE 'SWEET' COMES?

Warm thanks, Nick Dynes Gracey, BSc(Hons) Medical Biochemistry, Birmingham University, UK, WATerian c/o www.TheDiabetesBlog.com @ 19:23hrs MON.25.JUN.2007.

ps... Diabetes Is Caused By Food And Or Drug Administration Too Much And Or Too Often.

First Posted at 3:53PM on Jun 25th 2007 by Nicholas Dynes Gracey

Virtual Book Tour Secrets Authors Tip #7 - Alex Mandossian

noreply@blogger.com (Nicholas Dynes Gracey) — Wed, 04 Jun 2008 14:27:00 +0000

http://www.VirtualBookTourSecrets.com - Alex Mandossian shares his Virtual Book Tour Secrets Tip #7.

Book Authors, Info Marketers, Publishers and Entrepreneurial CEO's visit http://www.VirtualBookTourSecrets.com

NeuroGlycoPenia cramp attack Wean spasm seizure stimulating Glucagon release...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Tue, 03 Jun 2008 19:57:00 +0000

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NeuroGlycoPenia is a medical term that refers to a shortage of glucose (glycopenia) in the brain, usually due to hypoglycemia. Glycopenia affects the function of neurons, and alters brain function and behavior. Prolonged neuroglycopenia can result in permanent damage to the brain.

Signs and symptoms of neuroglycopenia

Abnormal mentation, impaired judgement
Nonspecific dysphoria, anxiety, moodiness, depression, crying, fear of dying, suicidal thoughts
Negativism, irritability, belligerence, combativeness, rage
Personality change, emotional lability
Fatigue, weakness, apathy, lethargy, daydreaming, sleep
Confusion, amnesia, dizziness, delirium
Staring, "glassy" look, blurred vision, double vision
Automatic behavior
Difficulty speaking, slurred speech
Ataxia, incoordination, sometimes mistaken for "drunkenness"
Focal or general motor deficit, paralysis, hemiparesis
Paresthesia, headache
Stupor, coma, abnormal breathing
Generalized or focal seizures

Not all of the above manifestations occur in every case of hypoglycemia. There is no consistent order to the appearance of the symptoms. Specific manifestations vary by age and by the severity of the hypoglycemia. In older children and adults, moderately severe hypoglycemia can resemble mania, mental illness, drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. The symptoms of a single person do tend to be similar from episode to episode.

In the large majority of cases, hypoglycemia severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain. Cases of death or permanent neurologic damage occurring with a single episode have usually involved prolonged, untreated unconsciousness, interference with breathing, severe concurrent disease, or some other type of vulnerability. Nevertheless, brain damage or death has occasionally resulted from severe hypoglycemia (e.g., Sunny von Bülow).

Compensatory responses to neuroglycopenia

Most neurons have the ability to use other fuels besides glucose (e.g., lactic acid, ketones). Our knowledge of the "switchover" process is incomplete. The most severe neuroglycopenic symptoms occur with hypoglycemia caused by excess insulin because insulin reduces the availability of other fuels by suppressing ketogenesis and gluconeogenesis.

A few types of specialized neurons, especially in the hypothalamus, act as glucose sensors, responding to changing levels of glucose by increasing or decreasing their firing rates. They can elicit a variety of hormonal, autonomic, and behavioral responses to neuroglycopenia. The hormonal and autonomic responses include release of counterregulatory hormones. There is some evidence that the autonomic nervous system can alter liver glucose metabolism independently of the counterregulatory hormones.

Adjustment of efficiency of transfer of glucose from blood across the blood-brain barrier into the central nervous system represents a third form of compensation which occurs more gradually. Levels of glucose within the central nervous system are normally lower than the blood, regulated by an incompletely understood transfer process. Chronic hypoglycemia or hyperglycemia seems to result in an increase or decrease in efficiency of transfer to maintain CNS levels of glucose within an optimal range.

In both young and old patients, the brain may habituate to low glucose levels, with a reduction of noticeable symptoms, sometimes despite neuroglycopenic impairment. In insulin-dependent diabetic patients this phenomenon is termed hypoglycemia unawareness and is a significant clinical problem when improved glycemic control is attempted. Another aspect of this phenomenon occurs in type I glycogenosis, when chronic hypoglycemia before diagnosis may be better tolerated than acute hypoglycemia after treatment is underway.

Neuroglycopenia without hypoglycemia

A rare metabolic disease of the blood-brain glucose transport system has been described in which severe neuroglycopenic effects occurred despite normal blood glucose levels. Low levels of glucose were discovered in the cerebrospinal fluid (CSF), a condition referred to as hypoglycorrhacia.

Perhaps a much more common example of the same phenomenon occurs in the people with poorly controlled type 1 diabetes who develop symptoms of HYPOglycemia at levels of blood glucose which are 'normal' for most People.

Glucagon Deficiency Attacked Again ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Tue, 03 Jun 2008 00:03:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
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http://www.ncbi.nlm.nih.GOV/pubmed/8452077
'... Patients younger than 70 years of age had a success rate of 16.2 percent ... versus 12.4 percent for patients older than 70 years ...'

= Over 70 years of age Patients 'treated' by HealthCare services CPR = approx 87 deaths every 100 times CPR is adopted ... usually without any glucagon or glucose which apparently results in the patient's brain / heart being starved to death by the distress of the CPR procedure.

= Under 70 years of age Patients 'treated' by HealthCare services CPR = approx 83 deaths every 100 times CPR is adopted ... usually without any glucagon or glucose which apparently results in the patient's brain / heart being starved to death by the distress of the CPR procedure.

http://www.ChestJournal.org/cgi/content/full/130/2/419
'... only 2.7% of Patients understood thatthe success rate of CPR was less than 10% in sick Patients. A minority of Patients(34%) had discussed CPR with their Physician; 37% did not wantto discuss their preferences with their Doctor. Patients whofelt that end-of-life issues were relevant to them were 5.5times more likely to want a discussion with the physician regardingresuscitation ... The preferred role in decision making was variable,but most Patients (59.7%) and Family Members (81.6%) preferredsome degree of shared decision making that included the FamilyMember. There were no significant differences between cancerand medical Patients in their preferred decisional role ...'

http://www.InteliHealth.com/IH/ihtIH/E/9273/35323/372221.html?d=dmtHMSContent
'... chest compressions alone may be as effective ...'

Medical Myths

CPR: Less Effective Than You Might Think

March 2001
Last reviewed on January 31, 2008

By Robert H. Shmerling, M.D.
Beth Israel Deaconess Medical Center

Imagine your typical TV drama. A child, playing in the park, hovering too close to the pond, falls in. His parents, distracted for a few moments, soon notice that their child is missing. Frantic, they call her name and look everywhere, and it dawns on them. Perhaps she fell in. When they finally locate their daughter and pull her out, she is no longer breathing and has no signs of a pulse. Instinct would tell the viewer that someone would come to the rescue and use CPR to save the day. The child would sputter, wake up, and be returned, shaken but otherwise unharmed, to her parent's arms.

CPR (cardiopulmonary resuscitation) is a method of trying to restore circulation and breathing for a person who has no pulse or is not breathing. You may have the impression from television shows or movies that CPR is a highly effective emergency treatment for anyone who has collapsed.

It surprises many to learn that the dramatic CPR results they often see are a myth. Unfortunately, CPR is often ineffective, and only in certain circumstances is its success rate anything other than dismal. This is not to say it should be abandoned in dire situations, but in general, the expectations of loved ones or those performing CPR are often higher than the situation warrants.

CPR can and does work, but CPR lacks the magical quality people often associate with it. As I've said in other columns, medical myths often have some truth behind them: A drowning victim [AND/OR PATIENTS SUFFERING MASSIVE BLOOD LOSS] should promptly receive CPR, and good outcomes may follow as depicted in the typical TV drama. However, the success rate of CPR varies widely, based on many factors, including:

The cause of cardiac or respiratory arrest
The underlying health of the victim
The time elapsed between the arrest and CPR
The technique used by the person performing CPR

For example, when a person has stopped breathing because of low body temperature (such as someone rescued after falling through ice into a cold lake) or another readily reversible condition, the success rate is higher. On the other hand, when an elderly person has stopped breathing because of heart problems or pneumonia, especially when other medical problems are present, CPR has a very low success rate.

There are new developments in CPR, including a study showing that for untrained bystanders receiving directions by emergency dispatchers, chest compressions alone may be as effective as compressions with artificial respiration (breathing into the person's mouth to provide oxygen). New guidelines, released in November 2005, suggest more frequent and more rapid chest compressions for most people requiring CPR. In addition, battery-powered defibrillators (that shock the victim's dangerously abnormal heart rhythm back to a safer, more stable rhythm) are becoming smaller, easier to use and increasingly available. These developments may increase the effectiveness of emergency rescues.

As opposed to many medical myths, researchers have reliable data concerning the success rates of CPR (without the use of automatic defibrillators) in a variety of settings:

2% to 30% effectiveness when administered outside of the hospital
6% to 15% for hospitalized patients
Less than 5% for elderly victims with multiple medical problems

In June 1996, the New England Journal of Medicine published a study about the success rates of CPR as shown on the television medical shows "ER," "Chicago Hope" and "Rescue 911." According to the shows, CPR successfully revived the victim 75% of the time, more than double the most conservative real-life estimates. In addition, while most CPR is actually performed on sick, older individuals with cardiac disease, most of these shows' patients were young and victims of trauma or a near-drowning �?? conditions with the highest success rates.

Finally, the patients on these shows either died or fully recovered. In real life, many of those who are revived by CPR wind up severely debilitated. One reason may be that, as noted by a study published in the January 2005 issue of the Journal of the American Medical Association, CPR is frequently not administered adequately, even when provided by trained ambulance personnel. Improved technique (including more frequent and rapid compressions, as recommended in the new guidelines) and use of automatic defibrillators could dramatically improve success rates.

The low success rate of CPR may be an example of how a medical myth is perpetuated by the media because it is more appealing than the truth. Unfortunately, sugar-coating the concept of CPR leads to unrealistic expectations when a loved one requires CPR or is ill, and heroic measures are under consideration. A better understanding of when CPR may be effective and when it is highly unlikely to help will better serve everyone in the unfortunate event of catastrophic illness or injury. If you learn to administer CPR, you may save someone's life, so learning the proper technique is worth the effort. However, you should not expect the results you see on television.

Robert H. Shmerling, M.D. is associate physician at Beth Israel Deaconess Medical Center and associate professor at Harvard Medical School. He has been a practicing rheumatologist for over 20 years at Beth Israel Deaconess Medical Center. He is an active teacher in the Internal Medicine Residency Program, serving as the Robinson Firm Chief. He is also a teacher in the Rheumatology Fellowship Program.

To Love Or Not To Love That Is A Choice ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Sun, 01 Jun 2008 19:05:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
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http://www.YouTube.cOM/user/adampants2007

adampants2007

Style: Stand-Up

Joined: October 18, 2007

Last Login: 13 hours ago

Videos Watched: 2,733

Subscribers: 385

Channel Views: 13,007

What is the difference between the "mind/ego" and "spirit"? If, perhaps, your spirit shines through your being at a time, someone may say, "your eyes are youthful and sparkling". The "ego" will then look in a mirror and SEE...OBSERVE...the sparkle in the eyes. The insane ego LIKES how it feels in that moment. In an attempt to feel more of it, it attempts "replication". The person/ego will then TRY...ATTEMPT...to MAKE their eyes sparkle with "behavior". Perhaps they will try to "widen" their eyelids...try to induce the sparkle. It is at this point that the "ego" blocks the access of your spirit to you and the sparkle goes away.

Influences: The essence of life itself.
Similar To: What Christ was talking about that religion HIDES from you.

It is VERY simple. Do the cells in your body attack each other when they are healthy? Do they hurt each other in any way? We are just a few scales up from cells. We are all cells to something larger. I believe life is a dream. Is that so bad? Would you want the cells in your body to be aware that they are just sitting there being cells? No. Wouldn't you want your cells to be able to dream? I think they might. I think we are larger cells dreaming.

Basically the truth is this. "Radiating" energy is NO different than "doing" anything else. If you send "energy" that is no different than giving a "hug". But, that is NOT "love". It can be the "result" of love. There is only ONE way to love....love.

It requires no more effort than that. So VERY simple that it has eluded almost EVERYONE. All of your cells in your body are unique systems, right? WHAT is animating them? YOU. YOU are EVERY cell in your body. If you know the scalar nature of this reality, there is only one truth. YOU are ME. If that is true, HOW can you "send" me love? Just LOVE ME.

Picture two people in your mind, standing there looking at each other. Now, picture these two being in love with each other. Picture them loving and expressing love to each other. WHO "really" did that? You have two characters in your mind "interacting" with love. But that love was an INTENT. It was YOUR intention. In your mind, you had two people "expressing" your intention.

The beauty of life is that YOU are a CREATION and also the CREATOR. As a creation, you get to express the intent of the creator (the larger part of you) and also be able to "create", so you can observe the manifestation of YOUR intent.

I love you.

:)

Country: United States
Website: www.YouTube.cOM/user/adampants2007

Temperature Control Patterns c/o God and/or LOVE ...HOW ?

noreply@blogger.com (Nicholas Dynes Gracey) — Sat, 31 May 2008 22:33:00 +0000

"Every Day And In Every Way I Am Getting Better And Better" ...
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Nick Gracey WATerian BSc(Hons) Medical BioChemistry, Birmingham University, Adrenaline LIFE2345.©OM

Human C-peptide helps protect cells

Human C-peptide antagonises high glucose-induced endothelial dysfunction through the nuclear factor-kappaB pathway.

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By Shane Starling

Low Blood Sugar-HYPOglycemia-What the Surgeon says...

Characteristics

Cost

Accuracy

History

Future

Technology

Meter use for HYPOglycemia

YouTube Videos of Blood Glucose Meters

External links used as references

References

Defining hypoglycemia

Measurement method

Age differences

Presence or absence of effects

Purpose of definition

Pathophysiology

Signs and symptoms

Adrenergic manifestations

Glucagon manifestations

NeuroGlycoPenic manifestations ...

Determining the cause

The circumstances of hypoglycemia provide most of the clues to diagnosis

In less obvious cases, a "critical sample" may provide the diagnosis

Further diagnostic steps

Causes

HYPOglycemia in newborn infants

HYPOglycemia in young children

HYPOglycemia in older children and young adults

HYPOglycemia in older adults

Treatment and prevention

Reversing acute hypoglycemia

Prevention

HYPOglycemia as American folk medicine

References

See also

External links

WATerCure, WATer Cure

Victims of circumstance in HYPOglycemia unawareness - The Diabetes Blog

Virtual Book Tour Secrets Authors Tip #7 - Alex Mandossian

NeuroGlycoPenia cramp attack Wean spasm seizure stimulating Glucagon release...HOW ?

Signs and symptoms of neuroglycopenia

Compensatory responses to neuroglycopenia

Neuroglycopenia without hypoglycemia

Glucagon Deficiency Attacked Again ...HOW ?

CPR: Less Effective Than You Might Think

To Love Or Not To Love That Is A Choice ...HOW ?

Temperature Control Patterns c/o God and/or LOVE ...HOW ?