The MEO blogs

Weefselbeschadiging en collageen

noreply@blogger.com (Unknown) — Sun, 19 Jan 2014 15:46:00 +0000

De moderne geneeskunde beschouwt moleculaire biologie als iets dat vastligt. Onze cellen zijn als het ware voorgeprogrammeerd bij de conceptie of kleine kinderjaren. Stel dat er mutaties plaatsvinden achteraf, dan zijn deze toevallig en hebben ze geen invloed op de genen omdat ze toch reeds vastliggen.

Het is vast iets complexer dan dat. Onze cellen veranderen in een leven, niet alleen in leeftijd maar ook van plaats.

Ideale situatie:
De ontwikkeling van een bevrucht eitje vergt enorm veel energie. Er is een constante aanvoer van zuurstof en suiker nodig om het vruchtje goed te laten groeien. Hoe verder men in het proces gaat, hoe minder energie het nodig heeft om te groeien, onderhoudswerken uit te voeren en te herstellen.
Een foetus in de buik opereren laat geen enkel litteken na. Als ze dezelfde operatie uitvoeren na de geboorte, zal collageen het litteken vormen.

Sub-optimale situatie:
Er treedt tijdens ons leven weefselbeschadiging op wat leidt tot de vorming van collageen + inflammatie.
Deze inflammatie staat in verhouding tot het tekort aan stoffen die we nodig hebben om de reparatiewerken uit te voeren.

Bijvoorbeeld als je te weinig zuurstof hebt, zal er zich melkzuur vormen + pro-inflammatoire stoffen zoals histamine en serotonine. Dit leidt op zijn beurt weer tot het verlies van proteïnen en andere stoffen.

Je zou de metabole snelheid van een lichaam dus kunnen uitdrukken als volgt: de snelheid waarbij iemand zijn cellen vernieuwt.
Stel deze is te traag:
1) dan ontstaat er een systemische inflammatie
2) dan gaat het lichaam de processen om de cellen te vervangen vertragen
3) de lege plaatsen tussen de cellen opvullen met collageen

Wat zijn mogelijke oorzaken van een metabole vertraging?

- opname van endotoxines
- verstoring van de schildklier
- teveel nitric oxide, serotonine, histamine
- stapeling van PUFA's (onverzadigde vetzuren)
- verstoring in het respiratoire systeem superoxide dismutase
- ...

Meerdere situaties zijn verantwoordelijk voor het conditioneren van het lichaam in een inflammatoire status.

Allergies And Autoimmune Disease Could Share Common Genetic Cause: BACH2 Mutations : Conditions : Medical Daily

noreply@blogger.com (Unknown) — Wed, 05 Jun 2013 06:42:00 +0000

Allergies And Autoimmune Disease Could Share Common Genetic Cause: BACH2 Mutations : Conditions : Medical Daily

Bedenkingen

noreply@blogger.com (Unknown) — Mon, 03 Jun 2013 20:08:00 +0000

De tuin is bedekt onder een laag witte sneeuw. De kleine en grote vogels vliegen aan- en af naar het extra voedsel dat voor hen aan de bomen hangt. Een doorgesneden appel, een vetbol, wat extra zaad in een bakje. Met hun opgezet pluimenpakje trotseren ze de ijzige koude. Tortelduiven, bosduiven, meesjes, roodborstjes, huismussen, heggemussen, een nieuwsgierige vink, een lijster en een paar merels wisselen om beurt. De opportunisten pikken de kruimels op die op de grond zijn gevallen. De ekster graaft in de sneeuw naar verborgen schatten. Ze zijn vinnig en levendig. Het ontbreekt hen niet aan energie ondanks de gure omstandigheden. Naast me ligt een oude kater te ronken, hij loopt op zijn laatste benen. Zijn vacht is dof en hij loopt traag en met moeite. Soms denk ik dat zijn poten pijn doen, zoals de mijne als ik te lang in de zetel lig. Hij slaapt teveel en lijdt aan diabetes. Hij is verkouden en niest regelmatig. Alsof een huisdier de kwalen van een mens kan krijgen. Onze dagen tikken traag voorbij, wachtend op, ja op wat?

Een jaar geleden zou ik nog volmondig genezing hebben geroepen maar de realiteit heeft de hoop gewurgd. Ik heb het opgegegeven. Dokters nemen geen verantwoordelijkheid voor chronisch zieken. Het systeem laat dit niet toe. Ze hebben het zelf gecreëerd. En elkeen is er slachtoffer van. Morgen bent u het misschien want ziek worden kan iedereen. Er zijn veel goede en uitstekende gezondheidsspecialisten. Het duurt jaren zware studies vooraleer je het bordje van arts aan de voorgevel mag hangen en een witte jas mag dragen. In landen met de meest moderne gezondheidszorg kunnen ze gezichtstransplantaties uitvoeren en geplette benen redden. Kromme neuzen kunnen worden rechtgezet en nieuw vel wordt gekweekt voor de zwaar verbranden. Dagelijks gebeuren er hartoperaties en worden er gebroken heupen gerepareerd. Onze ziekenhuizen zijn uitgerust met hoogtechnologische apparaten die vaak al de prijs van een dure auto kosten. Met de regelmaat van de klok komen nieuwe medicijnen uit. Dagelijks worden we overstelpt met de publicatie van onderzoeken in alle domeinen. Een specialist die ernstig genomen wil worden, moet bewijzen op tafel kunnen leggen.

Ziekenhuizen zijn zoals fabrieken, iedere patient is ongewild een nummer die een bepaalde doorlooptijd heeft en geld moet opbrengen. Omwille van het overzicht houdt men van alle patienten een dossier bij. In een ziekenhuis lukt dit al aardig omdat veelal een IT-systeem uitgewerkt is. Dit duur software pakket staat en valt met de bereidwilligheid van de arts om gegevens in te voeren en deze infote delen met een collega indien nodig. In de privé hebben niet alle artsen de luxe van een secretaresse die notities uitwerkt en grafieken bijhoudt. De communicatie met de patient loopt vaak iets gemoedelijker, de notities worden vaker op een papier bijgehouden.

En toch blijkt dit geen garantie voor een goed werkend gezondheidssysteem. Het aantal chronisch zieken tikt elk jaar onrustwekkend aan. Het aantal kankerpatienten daalt niet. Het aantal gebruikers van slaappillen stijgt. Antidepressiva en statines worden voorgeschreven als ware het snoepjes. Moderne testmethodes en behandelingen volstaan al lang niet meer. Je volgt getrouw de behandelingen die voorgeschreven worden door specialisten, protocollen en verzekeringen allerhande maar de lang verhoopte genezing blijft uit. Ondertussen eisen verzekeraars dikke verslagen van artsen die veel tijd, papier en inkt kosten. Deze instellingen en hun controle-artsen misbruiken de getallen en cijfers, zijn onredelijk en verzieken het systeem.

Onze politiek is vertegenwoordigd door artsen die meer voeling hebben met netwerking en financiële plaatjes dan met de patient. Vanuit hun positie verwacht men van kennis van zake te hebben van alle ziekten. Een onmogelijke taak dus laten ze zich adviseren door adviseurs veelal gedreven door eigenbelang al dan niet met banden met het verzekeringswezen.

Onze dokter is idealiter een mens die tijd heeft voor zijn patient en op de hoogte is van alle medische vooruitgang. Waar vind je zo’n arts?

Dit alles werd me duidelijk toen ik tijdens mijn zwangerschap in 2003 zelf geveld werd door een mysterieuze ziekte. Ze kreeg de naam stress. Vrouwen die meer verdienen dan mannen, werken volgens witte jassen per definitie te hard. Na enkele jaren was ik nog maar een schim van mezelf. De huisarts kon me niet helpen. Een spoedopname in het ziekenhuis bracht stollingsproblemen aan het licht. De hersenscan was toen ook al niet 100% zuiver. Toch bleek dit volgens de internist van dienst geen reden voor de klachten. Een jaar later beefde ik als een rietje, kon geen auto meer rijden, was letterlijk verlamd van de hoofdpijn. Mijn hart klopte standaard meer dan 120 en elke inspanning was een uitputtingsslag. Standaardtesten waren zogezegd goed. Ik had het gevoel dood te gaan en het enigste dat de artsen ervan maakten, was dat ik zou lijden aan het bulldozer syndroom. Een fluwelen omschrijving voor vrouwen die werken tot ze erbij neervallen. Tot een andere neuroloog er zich met bemoeide. Mijn hart was inmiddels goed voor een pacemaker, mijn bijnieren produceerden nog nauwelijks cortisol, alle mogelijke virussen die een mens kan hebben bleken gereactiveerd, antistoffen tegen een auto-immuunziekte verhoogden stelselmatig. Er zat niets anders op dan uitzieken want een echt behandelplan bestond er niet. Door de jaren heen werd ik onderzocht door een reeks gerespecteerde artsen en bezocht ik allerlei erkende medische onderzoekscentra. Bloed werd op mijn eigen verzoek (en kosten weliswaar) verstuurd over de hele wereld. Ondanks vele inspanningen, bleef de genezing uit. Een terugkeer naar de werkplek zat er gewoonweg niet in. De werkgever kwam eenmaal op ziekenbezoek en het ontslag volgde niet veel later. Hij was dan geen arts maar zag sneller in dan een medisch geschoolde dat ik economisch niets meer bij te dragen had aan de maatschappij en het bedrijf.

De totale bedlegerigheid was gelukkig niet meer van toepassing, mijn fiets was inmiddels weggeroest tot oud ijzer in het berghok. Elke extra inspanning – ja zelfs een stevige knuffel - zorgde voor een immuunreactie die dagenlang kon duren. Alle energie leek weggezogen uit elke cel. Alsof men was vergiftigd met een onbekend gif. De weg naar huis werd soms vergeten, simpele rekenoefeningen werden onmogelijk. Geluid, licht, geuren, gezelschap waren allemaal ondragelijk. De pijn belette je door te slapen. Jaar in jaar uit. Geen rustpauze op het einde van de dag. Geen break tijdens de weekends. De knop “ziek” draait men niet uit zoals het licht aan het einde van een werkdag.

In die jarenlange zoektocht zijn de volgende testen uitgevoerd. Lyme bleek negatief, wel zeker 5 keer uitgevoerd in evenveel labo’s. Nochtans leken 90% van de klachten op deze ziekte. Babesia, een co-infectie van Lyme was borderline positief. De virussen waaronder Epstein Barr en cytomegalovirus scoorden hoog, net als parvovirus B19, adenovirus, coxsackie B1. Bartonella henselae was hoog tussendoor. Toxoplasmose en mycoplasma’s scoorden ook positief. Chlamydia pneumonia, een intracellulaire bacterie was torenhoog. Vitamine B12 bleek ernstig verlaagd. Glutathion en omzetting van ATP naar ADP waren veel te laag. Vaso-active Intestinal Peptide veel te laag. Auto-immuunstoffen waren verhoogd. De schildklier licht afwijkend. De lijst gaat door.

De meeste dokters deden helemaal niets met de uitslag. Niets. De reacties varieerden van totale onverschilligheid tot pure razernij en alles daartussen. Deze patient kwam immers met niet-verklaarbare klachten hun kostbare tijd en deze van hun doodzieke patienten verknoeien. Alsof men dus echt ter plekke moet doodvallen van een hartaanval en geen last mocht hebben van meerdere symptomen die evenzeer echt aanvoelen?

Een kleine minderheid was empatisch, toonde begrip maar vond het allemaal “complex”. Het viel buiten hun vakgebied wel te verstaan. Welgeteld twee artsen hebben hun nek uitgestoken en wilden medicatie voorschrijven.

Mijn eerste huisarts begreep er niets van en weet het aan stress. Enkele jaren later en een tweede ziekenhuisopname verder werd het tijd voor een andere arts. Trillend stond ik in pyama onder mijn winterjas aan de balie van zijn huisartsenpraktijk. Onze blikken kruisten zich daar. Zijn vluchtige zorgelijke uitdrukking was de eerste menselijke blik van een arts die ik had gezien in jaren. Ik herinner me mijn onvermogen om een woord uitleg te geven. Een verslag van het ziekenhuis maakte hem wellicht meer duidelijk. Hij heeft me altijd gesteund maar gaf toe geen kaas te hebben gegeten van al die afwijkende uitslagen. Zelfs nadat hij tientallen wetenschappelijke artikelen en anti-virale protocollen onder zijn neus kreeg, gebeurde er niets. De behandeling was niet gepubliceerd in een wetenschappelijk tijdschrift, niet evidence based, was opgesteld door artsen op een ander continent, ... Het maakte niet uit dat de arts reeds 50 jaar virale infecties behandelde en gegevens van duizenden patienten had verzameld. Het moest en zou in dat wereldvermaarde boekje gepubliceerd moeten zijn. Het lijkt wel de bijbel en de dokters of hun controleurs een stel fanatieke gelovigen.

Mijn verhaal is niet uniek. Duizenden mensen, nee, miljoenen mensen liggen te creperen in hun bed. De fora van chronische zieken staan bol van de schrijnende verhalen. Regelmatig gaan er mensen aan dood, niet van ouderdom zoals het betaamt, ook niet van ziekte maar door medische verwaarlozing. En toch lijkt dit artsen niet af te schrikken. Ze zijn er immuun of ongevoelig voor geworden. Hoe kon het ooit zo ver komen?

Vele chronisch zieken worden gezond geboren. Ziekte overvalt hen veelal op een onverwacht moment en niets in het leven bereidt ons er echt op voor. We mogen wel proberen er het beste van te maken, de werkelijkheid zit iets gecompliceerder in elkaar. We doorlopen tijdens een langdurige ziekte alle mogelijke stadia van emoties die we niet voor mogelijk hielden. Alsof het overleven een nieuwe sport betreft, leren we nieuwe vaardigheden met vallen en opstaan. Gedragingen van andere mensen doen ons verbazen, maken ons blij, stellen ons teleur. Ons lichaam wordt een mysterie en mettertijd een vertrouwde plek. Niemand voelt het beter aan dan de zieke, ook niet alle geleerden van de wereld samen. We hebben hen vandaag nodig om beter te worden. Ongeacht hoe ziek een persoon ook is, zijn gevoel voor rechtvaardigheid blijft hardnekkig overeind. Hun protest neemt mondiale vormen aan.

In het begin hoop je nog dat het dat de klachten na een week wel zullen verdwijnen zoals bij een griepje. We hopen een luisterend oor te vinden bij de huisarts maar vangen vaak bot. We ontkennen de staalharde realiteit en gaan wat harder sporten tot we erbij neervallen.

Het zou interessant zijn om te begrijpen waarom zelfs de beste artsen in de val lopen van misplaatste authoriteit, machtsspelletjes, normloosheid en minachting voor de ander.

Misschien kent u er wel één? Misschien bent u er wel één? Door inzage te krijgen in de omstandigheden die ertoe leiden hoe een goed mens kan verleid worden, hoop ik dat je meer bewust wordt van je omgeving. Wist je dat er communicatietechnieken bestaan die handig gebruikt worden door mensen met kennis van zaken om je onderbewustzijn te beïnvloeden. Ook jij kan dat gebruiken om jezelf en mensen positief te beïnvloeden.

Het is geen onmogelijke opdracht om als dokter een verschil te maken. Er zijn voldoende collega’s die dagelijks bewijzen dat het ook anders kan. Het is tijd voor een nieuw tijdperk waarin we toegeven dat protocollen en handleidingen simplistisch zijn. Niet iedere mens heeft een maatje 36 en mannen dragen geen kleedjes. We moeten het verschil tussen mannen en vrouwen erkennen en onderzoeken in ziekte.

Consequences of a low body temperature and its solutions

noreply@blogger.com (Unknown) — Wed, 29 May 2013 20:14:00 +0000

http://hansacenter.com/low-body-temperature-plays-a-key-role-in-fibromyalgia-and-chronic-illness/

Excellent document!

Deficiencies in food

noreply@blogger.com (Unknown) — Fri, 22 Feb 2013 20:34:00 +0000

Trace Elements in Food: Eating to Meet Your RDAs
by Dr. Sarah Myhill, MD*
June 2, 2010http://www.prohealth.com/ME-CFS/library/showArticle.cfm?libid=15384&B1=EM060910N&slvor=10184.1007200.0.1.0.111925&eid=surpriseshan2@...

Dr. Sarah Myhill, MD, is a UK-based fatigue specialist focused on nutrition and preventive medicine.* Here she lists the daily amounts of trace minerals needed to support health; key foods we can eat to obtain these minerals; and the many physical signs that can indicate we're not getting enough of them.

_____________________________

People who traditionally live to great ages are often found living in areas watered by streams from glaciers.

Glaciers are lakes of ice which have spent the previous few thousand years crunching up rocks. Therefore the waters coming from the glaciers are very rich in minerals. This is used not just to drink but to irrigate crops and bathe in.

These people therefore had excellent levels of micronutrients. Given the right raw materials, things do not go wrong in the body and ageing is slow. For example:

- Low magnesium and selenium is a risk factor for heart disease

- Low selenium increases risk of cancer.

- Copper is necessary to make elastic tissue - deficiency causes weaknesses in arteries leading to aneurysms.

- Low chromium increases risk of diabetes.

- Good antioxidant status (vitamins A,C,E and selenium) slows the ageing process.

- Superoxide dismutase enzymes require zinc, copper and manganese to function.

- Iodine is necessary to make thyroid hormones and is highly protective against breast disease. (See "Iodine" )

- The immune system needs a huge range of minerals to work well, especially zinc, selenium, magnesium.

- Boron is highly protective against arthritis.

- Magnesium is required in at least 300 enzyme systems.

- Zinc is needed for normal brain development, a deficiency at a critical stage of development causes dyslexia.

- Any deficiency of selenium, zinc, copper, magnesium can cause infertility.

- Iron prevents anemia.

- Molybdenum is necessary to detox sulphites.

The secret of success is to copy Nature. Civilization has brought great advantages, but at the same time is responsible for escalating death rates from cancer and heart disease. I want the best of both worlds. I like my warm kitchen, fridge, cooker, computer and telly. But I want to eat and live in the environment in which primitive man thrived.

The Needed Trace Elements and Food Sources & RDA

Trace element deficiencies are common partly as a result of Western style agriculture, food processing and food choices. They can be corrected by taking the appropriate supplements, but also by eating the right foods.

RDA = recommended daily amount. This differs widely from one person to another - for example, illness increases requirements. The figure after each food [below] is how much of that food one would have to eat if the daily requirement came solely from that food.

This list illustrates the point that it is virtually impossible to eat the RDAs of vitamins and minerals living a Western lifestyle. One would have to eat large amounts of food - and take large amounts of exercise to keep a balance. This of course is what primitive man would have done! As we age and become biochemically less efficient, these amounts all increase. One also needs efficient digestion to absorb these micronutrients.

Magnesium - 350 mgs

- Kelp 2oz (57g)
- Almonds 5oz (142g)
- Cashews 5oz (142g)
- Brazil nuts 6oz (170g)
- Brown rice 14oz (397g)
- Soybeans 16oz (454g)
- Green leafy vegetables 25oz (709g)

Calcium - 800 mgsCalcium is all about vitamin D. There is plenty of calcium in food, it is the absorption that is the problem. This is dependent on vitamin D and the only real source of that is sunshine. In the winter especially we should all be taking a vitamin D supplement, at least 1,000iu a day and arguably 5,000iu! Kelp 3oz

- Almonds 8oz (227g)
- Corn tortillas 16oz (454g)
- Brazil nuts 16oz (454g)
- Tofu 14oz (397g)
- Dried figs 14oz (397g)
- Sunflower seeds 14oz (397g)

Potassium - 2,000-6,000 mg (figures for 4,000 mg)

- Kelp one teaspoonful
- Rice bran 8oz (227g)
- Nuts 10oz (283g)
- Parsnip 20oz (567g)
- Potato 20oz (567g)
- Banana 30oz (850 g) (that's a lot of bananas and represents a high glycemic load, so banana is not a good way to get potassium!)
- Leafy green vegetables 30oz (850g)

Iron
Absorption is the name of the game! Iron absorption is blocked by tea and this is the main cause of iron deficiency in UK. Another major cause of iron deficiency is hypochlorhydria [not enough stomach acid] - see Heartburn (GERD) - at last I have sussed out why this is such a common problem!"

- The richest sources of iron are in liver 8.8oz (249g) and meats.

Zinc - 15 mgs
Zinc is often low in vegetarians or people on low protein diets.

- Oysters half an ounce (14g)
- Steak/chops 9oz (255g)
- Pecans 11oz (312g)
- Brazils 12oz (340g)
- Egg yolk 12oz (340g)
- Oats

Copper - 2 mgs
Rich in nuts, split peas, liver, meat, butter. Deficiency uncommon except junk food diets.

Manganese - 5 mgs

- Pecans 5oz (142g)
- Brazils 8oz (227g)
- Oatmeal 24oz (680g)
- Rhubarb 30oz (850g)

Iodine - 75 mcgms

- Any seafoods 4oz (113g), otherwise very dependent on soil iodine levels.
- If soil levels O.K, then eggs, nuts.
- Use iodized salt.

Chromium - 200 mcgms
Chromium is poorly absorbed. It is best absorbed from yeast, black pepper, liver, cheese and wholemeal bread.

- Meat/liver 16oz (454g)
- Potato 30oz (850g)

Selenium - 200mcgms
Levels in food are very dependent on soil selenium. Since changing from Canadian to European wheat, UK selenium intakes have halved in the last 10 yearsâ€¦

- Herring 5oz (142g)
- Brazil nuts 8oz (227g)
- Any seafoods 10oz (283g)
- Milk 16oz (454g)
- Brown rice 16oz (454g)
- Meats 30oz (850g)

Molybdenum - 500mcgms

- Lentils 9oz (255g)
- Liver 10oz (283g)
- Split peas 10oz (283g)
- Green leafy vegetables 12oz (340g)
- Brown rice 20oz (567g)
- Oats 24oz (680g).

Recent research has shown that micronutrient content of food is declining, so these amounts may already be out of date!

See LifeExtension article, "Vegetables Without Vitamins."

Goodies and Baddiesâ€¦

- Use sea salt to get the trace minerals.

- Vitamin C improves absorption and tea/coffee blocks absorption. So drink fruit juice with meals, and tea/coffee between meals.

- Trace element content depends very much on soil levels.

â€¢ Organic foods will have lower water content and better trace element content than chemically fertilized foods.

- Sugar, alcohol, caffeine are *anti-nutrients*. They require trace elements for their metabolism in the body and increase daily requirements.

- Wheat bran is rich in many trace elements but contains phytic acid which blocks their absorption.

- White flour is markedly deficient in trace elements compared to wholemeal.

* * * *

Nutritional Deficiencies - Signs to Look for if You Think You May Have Them

This list has been compiled by Dr. Patrick Kingsley [a founder of The British Society of Allergy, Environmental and Nutritional Medicine] â€“ so thank you Patrick! I have added in a few of my own. The following can be pointers to mineral and vitamin deficiencies, but they do not apply in all cases.

Hands and Nails

- Cold hands - magnesium deficiency

- White spots on nails - almost any mineral deficiency but typically zinc

â€¢ Ridges on nails - poor blood supply, zinc deficiency

- Soft or brittle nails - any mineral deficiency especially magnesium

- Bitten nails - general mineral deficiency

So often, people comment that nails get tough when they start taking nutritional supplements - What everybody should be taking all the time even if nothing is wrong. Many of the raw materials for nails are the same as for bone and connective tissue - so nail health reflects bone and connective tissue health!

Skin

- Stretch marks indicate zinc deficiency. They are common in pregnancy not because the skin is stretched but because demands for zinc are high!

- Follicular hyperkeratosis (rough skin, especially on the heels)- vitamin A deficiency

- Spontaneous hemorrhages - lack of vitamins C or K. See Vitamin K is necessary for normal bone formation and prevention of osteoporosisâ€

- Dry scaly skin with hair follicles plugged with coiled distorted hairs and a red halo - vitamin C deficiency

- Yellow palms - excessive beta carotene intake. But can be due to eating lots of colored vegetables!

- Pimply rough skin at the back of the upper arms (chicken flesh) - essential fatty acid deficiency

- Greasy red scaly skin of face and sides of nose - vitamin B2 deficiency

- Seborrheic dermatitis around nose and an acne like forehead rash - vitamin B6 deficiency

Mouth and Gums

- Pale fissured tongue - iron (Fe) deficiency

- Sore painful fissured tongue - vitamin B3 deficiency

- Sore burning tongue and lips and peeling of lips - vitamin B2 deficiency

- Swollen tongue with lateral teeth indentations - food intolerance. Also myxoedema - see Hypothyroidism.

- Painful sore tongue with a smooth appearance - folic acid deficiency

- Angular cheilosis (splits in lips) - vitamin B2 deficiency, thrush

- Gum disease and pyorrhoea â€“ CoQ-10 deficiency, folic acid deficiency.

- Bleeding gums - vitamin C deficiency.

Eyes

- Cataracts - chronium deficiency or excess free radicals

- Bags or dark rings under eyes - allergies or food intolerances

- Blue eyes and blond hair are often seen in hyperactive male children - zinc, magnesium, B6 and essential fatty acids deficiencies

- Blue eyes and premature grey hair - vitamin B12 deficiency, a feature of pernicious anemia.

Neck

- Goiter, thyroid swelling - iodine deficiency

Legs

- Tender calf muscles - magnesium deficiency

- Brisk (hyper) knee reflexes - magnesium deficiency

- Restless legs - mineral deficiency, tendency to be acidic - see"Acid-Alkali Balance"

Clinical Histories of Nutritional Relevance

The following can suggest particular deficiencies [causing or resulting] or allergies:

- Nasal polyps - salicylate sensitivity

- Catarrh, sinusitis, history of removal of tonsils and adenoids for good clinical reasons - milk intolerance

- Poor healing - zinc deficiency

- Poor dream recall - vitamin B6 deficiency

- Blood sugar swings with obvious low blood sugar episodes - chronium deficiency

- Pre-menstrual syndrome - progesterone, magnesium, zinc and essential fatty acid deficiencies

- Glandular fever - inadequate liver detoxification mechanisms

- Sensory symptoms - B12, B1, magnesium deficiencies

- Mental symptoms - B12 deficiency

- Parkinsonism/multiple sclerosis - glutathione deficiency

- Cervical dysplasia - vitamin B6 and folic acid deficiency, papilloma/wart virus. Heals well with DMSO on the end of a tampax

- Arthritis - boron and sulphur (MSM) deficiency

- Measles - vitamin A deficiency

- Persistent diarrhea leading to fatigue - magnesium and potassium deficiencies

- Many diuretics cause magnesium and potassium deficiencies

- Muscle cramps - magnesium deficiency

- Shaking hands - magnesium and vitamin B1 deficiencies

- Hypertension - magnesium deficiency

- Dysphagia (difficulty swallowing) - magnesium deficiency

- Sensitivity to light - magnesium deficiency

- Osteoporosis - don't forget to think about magnesium

- PET - magnesium deficiency

- Hair loss - thyroid, iron (Fe), biotin, zinc and essential fatty acid deficiencies (must measure serum ferritin to check iron stores)

- Frequent colds - zinc and vitamin C deficiencies

- Infertility, miscarriages and premature labor - zinc deficiency

- Poor sense of smell and taste - zinc deficiency

- Poor vision or night blindness - zinc and vitamin A deficiencies

- Dry eyes - vitamin A deficiency

- The contraceptive pill and HRT can cause an increase in copper levels, and zinc, magnesium and vitamin B6 deficiencies

- Blocked nose with red wine - molybdenum deficiency

- Bowel cancer - selenium deficiency

- Mercury amalgams in teeth - selenium and glutathione deficiencies

- Cardiomyopathies (Keshan Disease) - selenium deficiency

- Heart attacks - vitamin E deficiency (identified by the Shute brothers, â€œvitamin E pioneers.â€)

- Hair loss, dandruff, eczema, excessive ear wax production, poor wound healing, excessive thirst (especially in hyperactive children), pre-menstrual symptoms of any sort - essential fatty acid deficiency

- Carpal tunnel syndrome - vitamin B6 deficiency

- Vegans - vitamin B12, zinc and iron deficiencies

- Gastrectomy - vitamin B12 and HCL (stomach acid) deficiencies

- Diabetic peripheral neuropathy [nerve pain/numbness] - vitamin B12 deficiency

- Elderly - low everything, especially vitamin Bs and HCI deficiencies

- Persistent infections - vitamin C and zinc deficiencies.

* * * *

Different disease states may result in different deficiencies, but everybody needs the basic building blocks in order to achieve optimum health.

____

* Dr. Sarah Myhill, MD, is a UK-based fatigue specialist focused on nutrition and preventive medicine. This information is excerpted with kind permission from articles posted in the â€˜Nutrition, Vitamins, Minerals and Dietsâ€™ section of Dr. Myhillâ€™s newly redesigned educational website (www.DrMyhill.co.uk) Â® Sarah Myhill Limited, Registered in England and Wales: Reg. No. 4545198.

Note: This information has not been evaluated by the FDA. It is generic and is not meant to prevent, diagnose, treat or cure any condition, illness, or disease. Nor is it meant to take the place of the personal attention of your physician. It is very important that you make no change in your healthcare plan or health support regimen without researching and discussing it in collaboration with your professional healthcare team.

Zinc modulates your immune system

noreply@blogger.com (Unknown) — Wed, 13 Feb 2013 19:15:00 +0000

Annu Rev Nutr. 2004;24:277-98.
Reprogramming of the immune system during zinc deficiency.
Fraker PJ, King LE.
Source
Department of Biochemistry & Molecular Biology, Department of Food Science & Human Nutrition, Michigan State University, East Lansing, Michigan 48824, USA. fraker@msu.edu
Abstract
Thymic atrophy, lymphopenia, and compromised cell- and antibody-mediated responses that cause increased rates of infections of longer duration are the immunological hallmarks of zinc deficiency (ZD) in humans and higher animals. As the deficiency advances, a reprogramming of the immune system occurs, beginning with the activation of the stress axis and chronic production of glucocorticoids that accelerate apoptosis among pre-B and -T cells. This reduces lymphopoiesis and causes atrophy of the thymus. In contrast, myelopoiesis is preserved, thereby providing protection for the first line of immune defense or innate immunity. Changes in gene expression for cytokines, DNA repair enzymes, zinc transporters, signaling molecules, etc., suggest that cells of the immune system are attempting to adapt to the stress of suboptimal zinc. Better understanding of the molecular and cellular changes made in response to inadequate zinc should lead to the development of immunotherapeutic interventions.

PMID: 15189122 [PubMed - indexed for MEDLINE]

Source :
http://www.ncbi.nlm.nih.gov/pubmed/15189122

J Nutr. 2000 May;130(5S Suppl):1399S-406S.The dynamic link between the integrity of the immune system and zinc status.
Fraker PJ, King LE, Laakko T, Vollmer TL.
Source
Department of Biochemistry, Michigan State University, East Lansing, MI 48824, USA.
Abstract
The results of more than three decades of work indicate that zinc deficiency rapidly diminishes antibody- and cell-mediated responses in both humans and animals. The moderate deficiencies in zinc noted in sickle cell anemia, renal disease, chronic gastrointestinal disorders and acrodermatitis enteropathica; subjects with human immunodeficiency virus; children with diarrhea; and elderly persons can greatly alter host defense systems, leading to increases in opportunistic infections and mortality rates. Conversely, short periods of zinc supplementation substantially improve immune defense in individuals with these diseases. Mouse models demonstrate that 30 d of suboptimal intake of zinc can lead to 30-80% losses in defense capacity. Collectively, the data clearly demonstrate that immune integrity is tightly linked to zinc status. Lymphopenia and thymic atrophy, which were the early hallmarks of zinc deficiency, are now known to be due to high losses of precursor T and B cells in the bone marrow. This ultimately leads to lymphopenia or a failure to replenish the lymphocytic system. Glucocorticoid-mediated apoptosis induced by zinc deficiency causes down-regulation of lymphopoiesis. Indeed, zinc itself can modulate death processes in precursor lymphocytes. Finally, there is substantial evidence that zinc supplementation may well reduce the impact of many of the aforementioned diseases by preventing the dismantling of the immune system. The latter represents an important area for research.

PMID: 10801951 [PubMed - indexed for MEDLINE] Free full text

Source: http://www.ncbi.nlm.nih.gov/pubmed/10801951

Issues in the diagnosis and treatment of Lyme disease.

noreply@blogger.com (Unknown) — Fri, 04 Jan 2013 14:54:00 +0000

Issues in the diagnosis and treatment of Lyme disease.

Authors: Donta ST

Citation: Open Neurol J 2012; 6: 140-5.

Location: Department of Medicine (Infectious Diseases), Falmouth
Hospital, USA.

DOI: 10.2174/1874205X01206010140

Since the identification of the causative organism more than 30 years
ago, there remain questions about the diagnosis and treatment of Lyme
Disease. In this article, what is known about the disease will be
reviewed, and approaches to the successful diagnosis and treatment of
Lyme disease described. In considering the diagnosis of Lyme disease, a
major problem is the inability of documenting the existence and location
of the bacteria. After the initial transfer of the bacteria from the
Ixodes tick into the person, the spirochetes spread locally, but after
an initial bacteremic phase, the organisms can no longer be reliably
found in body fluids. The bacteria are probably present in subcutaneous
sites and intracellular loci. Currently, the use of circulating
antibodies directed against specific antigens of the Lyme borrelia are
the standard means to diagnose the disease, but specific antibodies are
not an adequate means to assess the presence or absence of the organism.
What is needed is a more Lyme-specific antigen as a more definitive
adjunct to the clinical diagnosis. As for the treatment of Lyme disease,
the earliest phase is generally easily treated. But it is the more
chronic form of the disease that is plagued with lack of information,
frequently leading to erroneous recommendations about the type and
duration of treatments. Hence, often cited recommendations about the
duration of treatment, eg four weeks is adequate treatment, have no
factual basis to support that recommendation, often leading to the
conclusion that there is another, per-haps psychosomatic reason, for the
continuing symptoms. B. burgdorferi is sensitive to various antibiotics,
including penicillins, tetracyclines, and macrolides, but there are a
number of mitigating factors that affect the clinical efficacy of these
antibiotics, and these factors are addressed. The successful treatment
of Lyme disease appears to be dependent on the use of specific
antibiotics over a sufficient period of time. Further treatment trials
would be helpful in finding the best regimens and duration periods. At
present, the diagnosis of Lyme disease is based primarily on the
clinical picture. The pathophysiology of the disease remains to be
determined, and the basis for the chronic illness in need of additional
research. Whether there is continuing infection, auto-immunity to
residual or persisting antigens, and whether a toxin or other
bacterial-associated product(s) are responsible for the symptoms and
signs remains to be delineated.

10.2174/1874205X01206010140

Happy New Year Doctor!

noreply@blogger.com (Unknown) — Mon, 31 Dec 2012 10:56:00 +0000

Rest in peace my dear friend

noreply@blogger.com (Unknown) — Sat, 29 Dec 2012 20:41:00 +0000

In Memoriam - Denise de Hoop (Niessie)

Denise de Hoop

08.10.1967 - 28.12.2012

Je hebt een moedige maar oneerlijke
strijd gestreden. Wij zullen nu jouw
strijd voor ME voortzetten.
Niessie, je zal altijd in ons hart blijven.

Rouwbericht
'Ik had nog niet dood gehoeven.' 28.12.12 (volgt).
Een jaar uit het leven van een ME-patiënt. Dagboekfragmenten. 26.11.12
De dood of de Gladiolen. De ziekte ME: ont- of erkenning. 19.11.12
Gebombardeerd tot martelares van ME-patiënten. 15.07.11
Diagnose kanker gemist bij ME-patiënte door psychosomatisch stigma. 02.07.11

In Memoriam

Denise de Hoop
(Niessie)

8 oktober 1967 – 28 december 2012

Vanmorgen bereikte ons het bericht dat Denise
om 7.37 uur overleden is in het hospice van Hoorn.

Zij heeft zich de laatste jaren met heel haar energie en
kracht ingezet om de ernst van ME aan iedereen over
te brengen. En ook het in gebreke blijven van een aantal
artsen en behandelaars, mede door de stigmatisering
die nog steeds op ME als psychosomatische aandoening
rust in Nederland.

Nog geen drie weken geleden moest zij zelfs nog knokken
voor een plek in het hospice, omdat medici haar niet terminaal
genoeg vonden.

Vandaag verschijnt in het Noord-Hollands Dagblad een deze week
afgenomen interview met haar, waarvan de openingszinnen
luiden:

“Ik had nog niet dood gehoeven. Als ik kom te overlijden, vraag ik de mensen om de petitie voor erkenning van ME te tekenen. De artsen hebben mijn tumor te laat ontdekt, doordat ze mij als ME-patiënt niet serieus namen”.

Denises blog op me.net, zal de kern worden van een boek waaraan enkele mensen nu al werken. Het was haar bekend dat dat in de maak is, zodat zij wist dat haar strijd wordt voortgezet.

Wij wensen haar man en beide dochters alle kracht om het grote gemis in hun leven te vullen met de mooie en dierbare herinneringen aan een bewonderenswaardige en diep liefhebbende
vrouw, moeder en vriendin.

Bovenstaande in memoriam werd opgesteld door de ME/cvs Vereniging [PDF], waarvoor dank.

How to get rid of neurotoxines?

noreply@blogger.com (Unknown) — Fri, 21 Dec 2012 12:28:00 +0000

http://www.lyme-symptoms.com/LymeNeurotoxins.html

Neurotoxins
of the Borrelia burgdorferi Bacteria What is Neurotoxins:

A neurotoxin is a poison that acts specifically on nerve cells. Neurotoxins are attracted to the nervous system, are then absorbed by nerve endings and then travel inside the neuron to the cell body. There they disrupt vital functions of the nerve cell.

Sources of Neurotoxins:

Neurotoxins are caused by heavy metals, Aspartame, MSG, Sodium Nitrite in processed meats, alcohol, Fluoride, Aluminum Zirconium, paints, cocaine, statins,food additives,viruses, fungi, molds, mycoplasma, enteroviruses, Chlamydia pneumonia, Candida,parasites and protozoans (in the case of Babsiosis)and bacteria (as in the Lyme Bb bacteria) ..to name only a few of the 1178 chemicals officially listed as neurotoxins and the various bacteria's.

Neurotoxin Poison released by the Bb Bacteria :

The Borrelia burgdorferi bacteria, in their life process (living and dying) release nerve poisons/toxins/biotoxins (similar to Clostridium botulinum) and are believed to be the cause, both directly and indirectly, of most, if not all, the symptoms of Lyme disease. These toxins are dumped into the intersitial fluid and circulated throughout the body, until they can either be eliminated by the body or get lodged in areas of weakened tissues or fat cells- all the while causing problems with the nerves and distorting the messages of the nerves to any or all areas of the body.

Role of Chronic Bacterial and Viral Infections

noreply@blogger.com (Unknown) — Thu, 20 Dec 2012 16:55:00 +0000

Role of Chronic Bacterial and Viral Infections in Neurodegenerative, Neurobehavioural, Psychiatric, Autoimmune and Fatiguing Illnesses: Part 2

Garth L. Nicolson and Jörg Haier

Cite this article as: BJMP 2010;3(1):301
Download PDF

ABSTRACT
Chronically ill patients with neurodegenerative and neurobehavioural and psychiatric diseases commonly have systemic and central nervous system bacterial and viral infections. In addition, other chronic illnesses where neurological manifestations are routinely found, such as fatiguing and autoimmune diseases, Lyme disease and Gulf War illnesses, also show systemic bacterial and viral infections that could be important in disease inception, progression or increasing the types/severities of signs and symptoms. Evidence of Mycoplasma species, Chlamydia pneumoniae, Borrelia burgdorferi, human herpesvirus-1, -6 and -7 and other bacterial and viral infections revealed high infection rates in the above illnesses that were not found in controls. Although the specific roles of chronic infections in various diseases and their pathogeneses have not been carefully determined, the data suggest that chronic bacterial and/or viral infections are common features of progressive chronic diseases.

Introduction

In the first part of this review we considered neurodegenerative and neurobehavioural diseases and the findings that these diseases commonly are associated with systemic and central nervous system bacterial and viral infections.¹ In this second part we continue with psychiatric diseases, autoimmune diseases, fatiguing illnesses, and other chronic diseases where chronic infections play an important role.

Psychiatric diseases

Borrelia-associated psychiatric disorders

In addition to neurologic and rheumatologic symptoms Borrelia burgdorferi has been associated with several psychiatric manifestations^{2, 3} (see also below). Such infections can invade the central nervous system and may cause or mimic psychiatric disorders or cause a co-morbid condition. A broad range of psychiatric conditions have been associated with Lyme disease, including paranoia, dementia, schizophrenia, bipolar disorder, panic attacks, major depression, anorexia nervosa and obsessive-compulsive disorder.^4-7 For example, depressive states among patients with late Lyme disease are fairly common, ranging from 26% to 66%.³ It is not known whether B. burgdorferi contributes to overall psychiatric morbidity, but undiagnosed chronic Lyme disease caused by this spirochete is considered a differential diagnosis in patients with certain psychiatric symptoms such as depressive symptoms, lack of concentration and fatigue.

The neuropsychiatric sequelae of chronic Lyme disease remains unclear. Studies were performed, some on large numbers of patients, to investigate whether a correlation exists between chronic Lyme disease (defined by seropositivity) and psychiatric disorders.^8-11 Interestingly, different results were reported on the association between B. burgdorferi infection and psychiatric morbidity.^8-11 For example, Hájek et al.⁸ compared the prevalence of antibodies to B. burgdorferi in groups of psychiatric patients and healthy subjects. Among the matched pairs, 33% of the psychiatric patients and 19% of the healthy comparison subjects were seropositive. In contrast, Grabe et al.¹¹ did not find an association between Borrelia seropositivity and mental and physical complaints. In 926 consecutive psychiatric patients that were screened for antibodies and compared with 884 simultaneously recruited healthy subjects, seropositive psychiatric patients were found to be significantly younger than seronegative ones, and this was not found in the healthy controls.¹⁰ However, none of the psychiatric diagnostic categories used in this study exhibited a stronger association with seropositivity.¹⁰ These findings suggest a potential association between B. burgdorferi infection and psychiatric morbidity, but fail to identify any specific clinical 'signature' of the infection. This might be due to the very low incidence in an endemic region (0.2%, CI 95% 0.0% to 1.1%) as demonstrated in 517 patients hospitalized for psychiatric diseases.⁹

In addition to serological data, clinical evidence for the association of psychiatric symptoms and post-Lyme disease has also been investigated. If mental and physical complaints in patients were assessed with the von Zerssen's complaint scale using multivariate analyses, the data revealed that definitions of seropositivity were not associated with increased mental or physical complaints.¹¹ In contrast, if the SF-36 was used to determine Quality of Life (QOL) in post-Lyme patients, the average SF-36 physical component summary (40±9, range 29-44) and mental component summary (39±14, range 23-46) of the QOL assessment were worse than the general USA population, and they could be significantly improved by anti-Lyme antibiotics (46% versus 18%, p=0.007).⁵ Barr et al.¹² examined the relation between complaints of memory disturbance and measures of mood and memory functioning in 55 patients with serological evidence of late-stage Lyme borreliosis. There was a significant correlation between subjective memory ratings and self-reported depression (p<0 .001=".001" 30="30" a="a" affect="affect" and="and" battery="battery" but="but" checklist="checklist" chronic="chronic" disturbance="disturbance" in="in" indicating="indicating" interview="interview" lyme="lyme" memory="memory" negative="negative" neuropsychological="neuropsychological" not="not" objective="objective" of="of" patients.="patients." patients="patients" performance="performance" positive="positive" post-lyme="post-lyme" psychiatric="psychiatric" schedule="schedule" span="span" structured="structured" symptom="symptom" tests="tests" the="the" using="using" with="with">, participants did not appear to have an elevated incidence of psychiatric disorders or psychiatric history.¹³ Their mood, however, was characterized by lowered levels of positive affect and typical levels of negative affect that were similar to affect patterns in individuals with chronic fatigue syndrome (CFS). Similarly, Hasset et al.^{4, 7} reported on 240 consecutive post-Lyme patients who were screened for clinical psychiatric disorders, such as depression and anxiety. After adjusting for age and sex, these disorders were more common in symptomatic patients than in the comparison group (Odds Ratio=3.54, CI 95% 1.97-6.55, p<0 .001=".001" both="both" but="but" comparable="comparable" disorders="disorders" groups.="groups." in="in" personality="personality" span="span" were="were">

Although psychiatric co-morbidity and other psychological factors are prominent in post-Lyme patients, it remains uncertain whether these symptoms can be directly attributed to the chronic course of Borrelia infections or to other chronic illness-related factors.

Schizophrenia

...

Neuropsychiatric Movement Disorders

... As mentioned above, streptococcal infections are likely to play a pivotal role in these syndromes.³⁵

The pathogenic mechanism may be secondary to an activation of the immune system, resulting in an autoimmune response. This will be discussed in the next section.

Autoimmune Diseases

Infections are associated with various autoimmune conditions.^38-40 Autoimmunity can occur when infections like cell-wall-deficient bacteria are released from cells containing parts of cell membranes that are then seen as part of a bacterial antigen complex, or bacteria can synthesize mimicry antigens (glycolipids, glycoproteins or polysaccharides) that are similar enough in structure (molecular mimicry) to stimulate autoimmune responses against similar host antigens. Alternatively, viral infections can weaken or kill cells and thus release cellular antigens, which can stimulate autoimmune responses, or they can incorporate molecules like gangliosides into their structures.

In addition to molecular mimicry, autoimmunity involves several other complex relationships within the host, including inflammatory cytokines, Toll-like receptor signalling, stress or shock proteins, nitric oxide and other stress-related free radicals, among other changes that together result in autoimmune disease.^{38, 39}

Guillain-Barré syndrome

...

Viruses have also been found to be associated with GB.⁴⁰ Examples are: CMV,⁴⁷ HIV,⁴⁸ herpes simplex virus,⁴⁹ West Nile virus,⁵⁰ and HHV-6.⁵¹

Paediatric autoimmune neuropsychiatric disorders associated with Streptococci ('PANDAS')

Streptococcal infections in children are usually benign and self-limited. In a small percentage of children, however, prominent neurologic and/or psychiatric sequelae can occur. Post-streptococcal basal ganglia dysfunction has been reported with various manifestations, all of which fall into a relatively well-defined symptom complex or syndrome called paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS).⁵²

...

Fatiguing illnesses

Chronic fatigue syndrome/myalgic encephalomyelitis

Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a fatiguing illness characterised by unexplained, persistent long-term disabling fatigue plus additional signs and symptoms, including neurophysiological symptoms.⁶⁵ Brain imaging studies have shown that CFS/ME patients are dysfunctional in their ventral anterior cingulate cortex, and they also have other brain MRI abnormalities.^{66, 67} In addition, CFS/ME patients also have immunological and inflammation abnormalities, such as alternations in natural killer cell function^{68, 69}and cytokine profiles.^{70, 71} In addition, the hypothalamo-pituitary-adrenal axis, which plays a major role in stress responses, appears to be altered in CFS/ME.⁷²

Most, if not all, CFS/ME patients have multiple chronic bacterial and viral infections.^73-80 For example, when patients were examined for evidence of multiple, systemic bacterial and viral infections, the Odds Ratio for this was found to be 18 (CI 95% 8.5-37.9, p< 0.001).⁷⁵ In this study CFS/ME patients had a high prevalence of one of four Mycoplasma species (Odds Ratio=13.8, CI 95% 5.8-32.9, p< 0.001) and often showed evidence of co-infections with different Mycoplasma species, C. pneumoniae (Odds Ratio=8.6, CI 95% 1.0-71.1, p< 0.01) and HHV-6 (Odds Ratio=4.5, CI 95% 2.0-10.2, p< 0.001).⁷⁵ In a separate study the presence of these infections was also related to the number and severity of signs and symptoms in CFS/ME patients, including neurological symptoms.⁷⁷ Similarly, Vojdani et al.⁷⁶ found Mycoplasma species in a majority of CFS/ME patients, but this has not been seen in all studies.⁸¹ Interestingly, when European CFS/ME patients were examined for various Mycoplasma species, the most common species found was M. hominis,⁸² whereas in North America the most common species found was M. pneumoniae,^{75, 77} indicating possible regional differences in the types of infections in CFS/ME patients. In addition to Mycoplasma species, CFS/ME patients are also often infected with B. burgdorferi,⁸⁰and as mentioned above, C. pneumoniae.^{75, 77, 83}

Other infections are also found in CFS/ME patients, such as viral infections: CMV,⁸⁴ parvovirus B19,⁷⁸enterovirus⁷⁹ and HHV-6.^{75, 77, 85-88} For example, Ablashi et al.⁸⁸ found that 54% of CFS/ME patients had antibodies against HHV-6 early protein, compared to 8% of controls. Similarly, Patnaik et al.⁸⁶ found that 77% of CFS/ME patients were positive for HHV-6 early antigen IgG or IgM antibodies, whereas only 12% of control subjects had IgG or IgM antibodies to HHV-6 early antigen. Recently a new retrovirus, XMRV, was found in mononuclear blood cells of 67% of 101 chronic fatigue syndrome patients compared to only 3.7% of healthy controls. Cell culture experiments determined that the patient-derived virus was infectious and could possibly be transmitted.⁸⁹

Gulf War illnesses

GWI is a syndrome similar to CFS/ME.⁹⁰ In most GWI patients the variable incubation time, ranging from months to years after presumed exposure, the cyclic nature of the relapsing fevers and the other chronic signs and symptoms, and their subsequent appearance in immediate family members, are consistent with an infectious process.^{90, 91} GWI patients were exposed to a variety of toxic materials including chemicals, radiochemicals and biologicals so not all patients are likely to have infections as their main clinical problem. Neurological symptoms are common in GWI cases.⁹⁰ Baumzweiger and Grove⁹² have described GWI as neuro-immune disorder that involves the central, peripheral and autonomic nervous systems as well as the immune system. They attribute a major source of the illness to brainstem damage and central, peripheral and cranial nerve dysfunction from demyelination. They found GWI patients have muscle spasms, memory and attention deficits, ataxia and increased muscle tone.⁹²

Bacterial infections were a common finding in many GWI patients.⁹⁰ Mycoplasmal infections were found in about one-half of GWI patients, and more than 80% of these cases were PCR positive for M. fermentans.^{90, 91, 93-95} In studies of over 1,500 U.S. and British veterans with GWI, approximately 45% of GWI patients have PCR evidence of such infections, compared to 6% in the non-deployed, healthy population. Other infections found in GWI cases at much lower incidence were Y. pestis, Coxiella burnetii and Brucella species.⁹⁰

When we examined the immediate family members of veterans with GWI who became sick only after the veteran returned to the home, we found that >53% had positive tests for mycoplasmal infections and showed symptoms of CFS/ME. Among the CFS/ME-symptomatic family members, most (>80%) had the same Mycoplasma fermentans infection as the GWI patients compared to the few non-symptomatic family members who had similar infections (Odds Ratio=16.9, CI 95% 6.0-47.6, p<0 .001=".001" sup="sup">91

In contrast, in the few non-symptomatic family members that tested Mycoplasma-positive, the Mycoplasma species were often different from the species found in the Gulf War Illness patients (M. fermentans).The most sensible conclusion is that veterans came home with M. fermentans infections and then transmitted these infections to immediate family members.⁹¹

Some other infectious diseases with neurological aspects

Lyme Disease

Lyme disease is caused by a tick bite and the entry of the spiral-shaped spirochete B. burgdorferi as well as other co-infections.⁹⁶ Lyme disease is the most common tick-borne disease in North America. After incubation for a few days to a month, the Borrelia spirochete and co-infections migrate through the subcutaneous tissues into the lymph and blood where they can travel to near and distant host sites, including the central nervous system.^{3, 97-99} Transplacental transmission of B. burgdorferi and co-infections can occur in pregnant animals, including humans, and blood-borne transmission to humans by blood transfusion is likely but unproven. The tick-borne co-infections associated with Lyme disease can and usually do appear clinically at the same time, complicating clinical dignoses.¹⁰⁰

Lyme disease signs and symptoms eventually overlap with the signs and symptoms of other chronic illnesses, and patients are often diagnosed with illnesses like CFS/ME, chronic arthritis or a neurological disease.^80, ^97-100About one-third of cases with Lyme disease start with the appearance of a round, red, bulls-eye skin rash (erythema migrans) at the site of the tick bite, usually within 3-30 days.¹⁰⁰ Within days to weeks mild flu-like symptoms can occur that include shaking chills, intermittent fevers and local lymph node swelling. After this localised phase, which can last weeks to months, the infection can spread to other sites resulting in disseminated disease. In the disseminated (late) phase patients present with malaise, fatigue, fever and chills, headaches, stiff neck, facial nerve palsies (Bell’s palsy) and muscle and joint pain, and other signs and symptoms.^100-104

The disseminated (late) phase of Lyme disease is a chronic, persistent disease with ophthalmic, cardiac, musculoskeletal, central nervous system and internal organ invasion. When it involves the central and peripheral nervous systems, it is often termed neuroborreliosis.^{100, 104} At this late stage, arthritis, neurological impairment with memory and cognitive loss, cardiac problems (such as myocarditis, endocarditis causing palpitations, pain, bradycardia, hypertension) and severe chronic fatigue are usually apparent.^{80, 100-102} The signs and symptoms of the chronic (late) phase of the disease usually overlap with other chronic conditions, such as CFS/ME, chronic arthritis, as well as neurodegenerative diseases, causing confusion in the diagnosis and treatment of the chronic phase in patients with Lyme Disease.^{80, 97, 100, 105} Patients with late stage neuroborreliosis exhibit neuropathologic and neuropsychiatric disease similar to some of the neurodegenerative diseases discussed in previous sections.¹

Diagnostic laboratory testing for Lyme disease at various clinical stages is not fool-proof, and experts often use a checklist of signs and symptoms and potential exposures, along with multiple laboratory tests to diagnose Lyme disease.¹⁰⁴ The laboratory tests include serology, Western blot analysis of B.burgdorferi associated bands, PCR analysis of blood and the nonspecific decrease in CD-57 natural killer cells. Unfortunately, similar to other intracellular bacteria, Borrelia spirochetes are not always released into the blood circulation or other body fluids, making the very sensitive PCR method less than reliable for diagnosing Lyme Borrelia with blood samples. Lebech and Hansen¹⁰⁶ found that only 40% of cerebrospinal fluid samples from patients with Lyme neuroborreliosis were positive for B. burgdorferi by PCR.

Co-infections in Lyme disease are important but, in general, have not received the attention that B. burgdorferi attracts. Some of the Lyme Disease co-infections on their own, such as M. fermentans, have been shown to produce signs and symptoms comparable to B. burgdorferi infections.^{80, 102}

The most common co-infections found in Lyme disease are species of Mycoplasma, mostly M. fermentans, present in a majority of cases.^{80, 103, 107} In some cases multiple mycoplasmal infections are present in patients with Lyme disease,⁸⁰ while other common co-infections include Ehrlichia species, Bartonella species and Babesia species. Such co-infections are present in 10-40% of cases.^{103, 104, 108-112} Ehrlichia and Bartonella species are usually found along with Mycoplasma species in Lyme disease.^{94, 98, 108-111}Bartonella species, such as B. henselae,¹¹¹ which also causes cat-scratch disease,¹¹³ are often found in neurological cases of Lyme disease.^{100, 111}

Protozoan co-infections have been found with B. burgdorferi, such as intracellular Babesia species.^{100, 108, 109, 112, 114} The combination of Borrelia, Mycoplasma and Babesia infections can be lethal in some patients, and ~7% of patients can have disseminated intravascular coagulation, acute respiratory distress syndrome and heart failure.¹⁰⁹

Brucellosis

^...

Final comments to part 2

The progression, and in some cases, the inception of many chronic diseases are probably elicited by various bacterial and viral infections.^{1, 39, 40, 119} Even if infections are not directly involved in the pathogenesis of these diseases, patients with chronic conditions are at risk of a variety of opportunistic infections that could result in co-morbid conditions or promote disease progression. Infections can complicate diagnosis and treatment, and patients with late-stage disease with complex neurological manifestations, such as meningitis, encephalitis, peripheral neuropathy, psychiatric conditions, or with other signs and symptoms could have infections that are not recognized or treated.

Patients with chronic diseases are particularly difficult to treat using single modality approaches, and this is particularly true for patients who also have multiple chronic infections.^{103, 109} The multi-focal nature of chronic diseases and the fact that often treatments are given to suppress signs and symptoms, rather than treat causes of the disease or its progression, have resulted in incomplete or ineffective treatments. On the other hand, even if the causes of chronic diseases are known, by the time therapeutic intervention is undertaken, it may be entirely too late to use approaches that should work on the disease if chronic infections were not present. Moreover, if complex, chronic infections are ignored or left untreated, recovery may be difficult, if not impossible to achieve.

At the moment the evidence that particular or specific types of infections are responsible for the inception or pathogenesis of chronic diseases is inconclusive.¹¹⁹ One of the problems that arises in trying to prove this hypothesis is that not all patients appear to have similar chronic infections. Some individuals can harbour chronic infections without any observable signs or symptoms. Although the incidence of chronic infections of the types discussed in this review in symptom-free individuals is generally very low, usually only a few percent,^{74-76, 120} that does not prove that they are important in pathogenesis. Since patients with chronic diseases have been identified that do not have easily diagnosed chronic infections, most researchers have concluded that infections are not involved in the pathogenesis of chronic diseases. Unfortunately, the tools available to find chronic infections are not optimal, and many patients are likely go undiagnosed with chronic infections for purely technical reasons.^1, ^119-121

In the history of medicine animal models of disease have provided useful information that could not be obtained through clinical studies alone. Indeed, the field of chronic diseases could benefit from the greater use of relevant animal models. We suggest that to be useful, the pathogenesis of the animal models of disease must be similar to the pathogenesis of human disease and the animal models must have a similar response to therapy as humans. Thus such models are only relevant if they closely mimic human disease and its response to treatment. For example, the infection of non-human primates with neuropathologic microorganisms, such as Mycoplasma fermentans, resulted in brain infections and fatal diseases with clinically typical neurological signs and symptoms.¹²² These primates also respond to therapies that have been used successfully to treat humans.^93, ¹²³ Thus this particular model may be useful if it can be reproucibly infected with specific microorganisms and later develop neurological signs and symptoms that closely mimic chronic human neurological diseases. Future efforts to determine the relationship between specific infections and the pathogenesis of various chronic diseases may well depend on the further development of relevant animal models.

Competing Interests
None declared
Author Details
GARTH L. NICOLSON, Department of Molecular Pathology, The Institute for Molecular Medicine, Huntington Beach, California 92647, USA JORG HAIER, Department of General and Visceral Surgery, University Hospital, Münster 48149, Germany
CORRESSPONDENCE: PROF. GARTH L. NICOLSON, Office of the President, The Institute for Molecular Medicine, P.O. Box 9355, S. Laguna Beach, California, 92652 USA. Website: www.immed.org
Email: gnicolson@immed.org

References

Controversial Illness is Real and Treatable

noreply@blogger.com (Unknown) — Fri, 14 Dec 2012 08:30:00 +0000

Research Shows Controversial Illness is Real and Treatable

CHARLESTON, S.C., July 27 /PRNewswire/ -- Today, Policyholders of America (POA) released a consensus statement written by treating physicians and researchers in the field on the mechanism and treatment of illness found in people sickened by exposure to water-damaged buildings. This illness has been the subject of heated debate that has resulted in harsh allegations being lobbed at patients by experts hired by industry to cast doubt on the legitimacy of the illness. Today however, so-called "Sick Building Syndrome" is now unveiled to be very real; it's a chronic inflammatory illness that is easily identified with available lab testing and treatable using FDA-approved medications. The research paper is the first in the field written by physicians with experience treating the illness. Thorough and rigorous, the paper references governmental agency opinions, current published literature and an extensive review of patient data that has made this subject a political and legal hot potato obstructing patient care.

Nearly six months ago, a distinguished and credentialed panel of medical doctors and researchers, all from outside of POA's membership, were assembled and charged with developing a consensus statement on the diagnosis and treatment of a growing public health problem across America: illness acquired from water-damaged buildings. The consensus statement was then peer-reviewed by other medical doctors and researchers. The research paper is being released to help physicians and their patients understand the mechanisms, symptoms, diagnosis and treatment protocols available for sickened patients.

After reviewing hundreds of peer reviewed studies, analyzing hard data from research conducted on thousands of patients, and incorporating published results of treatment of thousands of patients, the authors embarked on this massive assignment with eyes wide open -- knowing that if the resulting research did not lessen liability of the powerful stakeholders involved, industry would likely attempt to discredit the findings.

With the research now concluded, the mysterious illness now has a name: Chronic Inflammatory Response Syndrome or "CIRS", and when the cause of the illness can be directly linked to a water-damaged building, or ("WDB"), it is called "CIRS-WDB".

Says Co-Author, Ritchie Shoemaker , MD, of Pocomoke, Maryland, "This statement builds consensus by debunking false ideas about illness from water-damaged buildings and establishes the basis by which practicing physicians can assess the complex illnesses these patients experience. We don't have to guess what might be wrong when we have the labs to prove what is abnormal. Patients don't have to suffer any longer after being given incorrect diagnoses such as allergy, stress or depression."

Co-authors included Laura Mark MD from Williamsburg, Virginia; Scott McMahon MD from Roswell, New Mexico; Jack Thrasher PhD of Oakland, California and Carl Grimes HHS, CIEC, President of the Indoor Air Quality Association, from Denver, Colorado.

The 161-page research paper can be found, in its entirety, at: http://www.policyholdersofamerica.org/doc/CIRS_PEER_REVIEWED_PAPER.pdf

A layperson's summary of the research paper follows:

CIRS-WDB is a multisystem, multi-symptom illness acquired following exposure to the interior environment of WDB. It exists as a recognizable syndrome that is identifiable and treatable;
CIRS-WDB is identified as immunologic in origin, with differential inflammatory responses seen according to (i) genetic susceptibility and (ii) unique aspects of host innate immune responses.
CIRS-WDB consistently involves loss of normal control of inflammation and the resulting "inflammation gone wild."
Treatment of human illness that is acquired following exposure to the interior environment of WDB involves a series of steps, each correcting the physiologic problems one by one.
CIRS-WDB can be readily identified by current methods of clinical diagnoses. This process of diagnosis is supported by (i) identification of unique subsets ("clusters") of symptoms found in epidemiologic cohorts of affected patients; (ii) identification of unique groupings of biomarkers, such as genetic markers, neuropeptides, inflammatory markers, and autoimmune findings.
Patients with CIRS-WDB are often given incorrect diagnoses such as depression, stress, allergy, fibromyalgia, Post Traumatic Stress Disorder, and somatization. Those conditions, when actually present, will not improve with therapies employed in CIRS-WDB.
CIRS-WDB is acquired primarily from inhalation of microbial products that are contaminants found in the complex mixture of WDB.
Re-exposure of previously affected patients will bring about immunological host responses that are enhanced in their rapidity of onset and magnitude, such that these patients are "sicker, quicker."

Melinda Ballard , POA's president said, "About 25% of our members have experienced health effects after exposure to toxigenic mold and other organisms in their homes and of those, the vast majority put on the treatment protocol outlined in this paper have reported back to us that their symptoms have either subsided or vanished altogether. While our experience with these members is purely anecdotal, this research paper is not; the findings are irrefutable. Most importantly, the rigorous science in the paper offers hope to so many who are in desperate need of an effective and inexpensive treatment.

POA is a nonprofit educational organization that, at no charge, helps policyholders receive adequate payment when a property insurance claim is filed. Since it was founded in 2001, more than 2.5 million people have joined, an unfortunate reflection on the manner in which claims are often handled by insurance companies. Its web address is: www.policyholdersofamerica.org. POA is a member of ACHEMMIC (the Action Committee on the Health Effects of Mold, Microbes and Indoor Contaminants), a group of scientists, researchers, physicians, indoor air quality experts, environmental engineers, industrial hygienists, structural engineers, teachers and advocates working to advance the understanding of the health effects of mold, microbes and indoor contaminants. ACHEMMIC's website is www.achemmic.com.

MEDIA ONLY CONTACT:
Melinda Ballard
Policyholders of America
(843) 367-4574

SOURCE Policyholders of America

RELATED LINKS
http://www.policyholdersofamerica.org

PR Newswire (http://s.tt/1bJ00)

Zwarte schimmel veroorzaakt meningitis

noreply@blogger.com (Unknown) — Wed, 12 Dec 2012 09:27:00 +0000

http://www.toxicmoldfoundation.com/fungus-caused-meningitis.html

Fungus Caused Meningitis? Black Mold

A black mold entering the spines of hundreds of people who received contaminated vaccines for back pain has marked uncharted medical territory.
This fungus, classified as being difficult to diagnose, has never seemingly caused meningitis, until now. It requires at least three months of a treatment that can cause hallucinations. Not only is it unknown when is it safe to stop treating, but there is also no good way to know how to monitor those who fear the fungus, which may be festering silently inside their bodies.
The fungus’ brown-black color signals an armor that helped the mold sneak past the immune defenses of healthy people.
“I don’t think there is a precedent for this kind of thing,” said Dr. Arjun Srinivasan of the Centers for Disease Control and Prevention (CDC). “This is definitely new territory for us.”

Dat noemen ze struisvogelpolitiek. Vraag het maar eens aan de vele mensen die lijden aan Sick Building Syndrome en excruciating headaches hadden vooraleer ze doodziek werden.

Yuppie flu, stress, ... we kennen het al wel.

http://www.policyholdersofamerica.org/doc/CIRS_PEER_REVIEWED_PAPER.pdf
Hier het bewijs dat ze het al lang weten.

Vervuild medicijn in VS te vroeg verdeeld

Door: Redactie
24/10/12 - 04u44 Bron: ad.nl © ap.

Het vervuilde geneesmiddel dat tot nu toe aan 23 Amerikanen het leven heeft gekost, is gedistribueerd voordat de producent de testresultaten binnen had over de veiligheid van het medicijn. Dat hebben de gezondheidsautoriteiten in de staat Massachusetts bekendgemaakt.

Inspecteurs troffen onder meer schimmel aan, een lekkende boiler, sterk vervuilde vloermatten en een slordige sterilisatieprocedure.

Tijdens een inspectie van de New England Compounding Center (NECC) in de plaats Framingham zijn de afgelopen week gebreken geconstateerd die erop lijken te duiden dat de producent de hygiënevoorschriften niet heeft nageleefd. Zo troffen inspecteurs tijdens hun onderzoek van de fabriek onder meer schimmel aan. Ook stuitten ze op sterk vervuilde vloermatten en een lekkende boiler. De manier waarop het bedrijf zijn apparatuur steriliseert, wordt bovendien omschreven als slordig.

308 besmettingen
Het aantal besmettingen ten gevolge van de uitbraak van hersenvliesontsteking (meningitis) is intussen opgelopen tot 308. De uitbraak is zeer waarschijnlijk veroorzaakt door een geneesmiddel dat bij NECC werd vervaardigd, een steroïdencocktail die wordt gebruikt als pijnbestrijder.

Black mold works antiviral

noreply@blogger.com (Unknown) — Wed, 12 Dec 2012 08:12:00 +0000

Have you ever wondered why never catch a cold anymore since you have ME or CFS?

Maybe you suffer from mold intoxication. Some people simply cannot eliminate the neurotoxines released by mold. Some bacteria like Lyme, bartonella and babesia produce the same symptoms. Blue green algue, ciguaterae, chlamydia pneumonia, ... yessss same effect.

Sick building syndrome is not a new concept but a severely underestimated factor in ME. Why do doctors don't ever ask you if you have a leaky roof at your work or house, have musty tiles in the bathroom, HVAC at work, did you work as an airhostess, ... Maybe it is like opening a jar of worms because fixing mold is very expensive.
If it is at your work, change! If it is your house, move! If none of it is possible, think about it again!

Never ever try to remove the mold yourself. Never! You can die from it. Period. Google a professional. Check with your insurance company what can be done.

Minagawa K, Kouzuki S, Yoshimoto J, Kawamura Y, Tani H, Iwata T, Terui Y, Nakai H, Yagi S, Hattori N, Fujiwara T, Kamigauchi T. Stachyflin and acetylstachyflin, novel anti-influenza A virus substances, produced by Stachybotrys (black mold) sp. RF-7260. I. Isolation, structure elucidation and biological activities. J Antibiot (Tokyo). 2002 Feb;55(2):155-64. PMID: 12002997

Two novel compounds, stachyflin and acetylstachyflin, have been isolated by solid-state fermentation of Stachybotrys sp. RF-7260.

Stachyflin showed antiviral activity against influenza A virus (H1N1) in vitro with an IC50 value of 0.003 microM. Acetylstachyflin was about 77-fold less active than stachyflin.

*

Mari Nakatani, Masahiko Nakamura, Akiyuki Suzuki, Munenori Inoue, and Tadashi Katoh. A New Strategy toward the Total Synthesis of Stachyflin, A Potent Anti-Influenza A Virus Agent: Concise Route to the Tetracyclic Core Structure. Org. Lett., 2002, 4 (25), pp 44834486. PMID: 12465918

A new strategy directed toward the total synthesis of stachyflin, a potent and novel anti-influenza A virus agent isolated from a microorganism, has been presented through the enantioselective synthesis of the tetracyclic core structure. The synthetic method features a BF3Et2O-induced domino epoxide-opening/rearrangement/cyclization reaction as the key step.

*

Minagawa K, Kouzuki S, Tani H, Ishii K, Tanimoto T, Terui Y, Kamigauchi T.. Novel stachyflin derivatives from Stachybotrys sp. RF-7260. Fermentation, isolation, structure elucidation and biological activities. J Antibiot (Tokyo). 2002 Mar;55(3):239-48. PMID: 12014438

Stachybotrys sp. RF-7260 was found to produce stachyflins, novel anti-influenza virus agents, under solid-state fermentation conditions. Feeding DL-lysine to a culture of Stachybotrys sp. RF-7260 induced the formation of the novel compounds, SQ-02-S-L2 and -L1, and feeding DL-valine the formation of SQ-02-S-VI and -V2. The structures of these metabolites were determined by detailed 2D NMR analyses in comparison with acetylstachyflin. SQ-02-S-L2 and -L1 have the lysine moiety and SQ-02-S-V1 has the valine moiety. SQ-02-S-V2 has an amidine moiety instead of the lactam moiety in acetylstachyflin. SQ-02-S-L2, -L1 and -V1, substituted on the lactam amide hydrogen, displayed only a low level of the antiviral activity. However, deacetyl SQ-02-S-V2 showed potent antiviral activity similar to stachyflin.

*

Tani N, Dohi Y, Onji Y, Yonemasu K. Antiviral activity of trichothecene mycotoxins (deoxynivalenol, fusarenon-X, and nivalenol) against herpes simplex virus types 1 and 2. Microbiol Immunol. 1995;39(8):635-7. PMID: 7494505

The effect of trichothecene mycotoxins, deoxynivalenol (DON), fusarenon-X (FX) and nivalenol (NIV), on plaque formation of herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) in HEp-2 cells was examined.

The 50% effective concentrations (EC50) of DON, FX, and NIV for HSV-1 plaque formation were 160, 56, and 120 ng/ml, respectively. Those for HSV-2 plaque formation were 94, 26, and 50 ng/ml, respectively. These three mycotoxins showed about 2-fold higher selectivity to HSV-2 than to HSV-1. Plaque formation of HSV-1 was not inhibited with trichothecenes at concentrations completely inhibiting plaque formation when cells were treated during virus adsorption period or 15 hr before infection.

These results indicate that trichothecenes affect replication of HSV-1 after virus adsorption, but not before or during virus adsorption to the host cells.

*

Sawadjoon S, Kittakoop P, Isaka M, Kirtikara K, Madla S, Thebtaranonth Y. Antiviral and antiplasmodial spirodihydrobenzofuran terpenes from the fungus Stachybotrys nephrospora. Planta Med. 2004 Nov;70(11):1085-7. PMID: 15549667

Two known spirodihydrobenzofuran terpenes (1 and 2) were isolated from a mycelium extract of the fungus Stachybotrys nephrospora BCC 3900. Compound 1 (Mer-NF5003F or stachybotrydial) exhibited potent antiviral activity (the IC50 value of 4.32 microg/mL) comparable to the standard drug, acyclovir, while compound 2 was inactive against the HSV-1 virus. Both 1 and 2 possessed antiplasmodial activity (IC50 values of 0.85 and 0.15 microg/mL for 1 and 2, respectively), and were not toxic towards the Vero cell line. A regiospecific conversion of the dialdehyde 1 to the lactone 2 proceeded simply under acidic conditions.

noreply@blogger.com (Unknown) — Tue, 11 Dec 2012 20:12:00 +0000

Signs and Symptoms of Autonomic Dysfunction

Some of the listed symptoms are always present while others occur
when a person with Autonomic Dysfunction has been standing or sitting too long:

-Dizziness

-Lightheadedness

-Vertigo (room spinning or the sensation of spinning)

-Feeling faint (pre-syncope)

-Fainting (syncope)

-Chest pain or pressure

-Excessive fatigue

-Rapid heart rate (tachycardia)

-Stomach pain

-Intestinal cramping

-Nausea

-Vomiting

-Retching

-Exercise Intolerance: becoming short of breath on mild exertion,

having chest pain or palpitations on mild exertion. Having excessive

heart rate during or immediately after exercise. Leg cramps or

numbness of arms and legs during or after mild exercise.

-Visible pooling in arms and legs: Deep purple-red color in fingers

and toes.

-White appearance of fingers. Some present with white patches of skin

on arms and legs.

-Extremely cold hands and feet.

-Numbness of hands and feet.

-Muscle weakness

-Muscle and joint pain

-Tremors or mild shaking of hands

-Frequent headaches or migraine headaches

-Irritability due to decreased blood flow to the brain

-Feeling anxious/Having panic attacks due to increased production of

adrenaline

-Mood changes

-Forgetfullness

-Inability to concentrate or remember (frequently referred to

as "brain fog")

-Inability to tolerate changes in temperature

-Decreased sweating or excessive sweating

-Abnormal deep tendon reflexes may or may not be present.

-Basic neurological exam is normal.

-Intelligence normal when receiving adequate cerebral perfusion.

Less frequently recognized signs and symptoms:

-Insomnia

-Disruption of sleep/wake cycle usually consisting of increased

energy late in the evening and lowest energy level in the morning

irregardless of amount or quality of sleep.

-Central sleep apnea

-Need to sleep 12-14 hours in order to complete simple activities of

daily living.

-Anoxic or convulsive seizures that are not epileptic.

-Frequent need to urinate at night.

-Upon standing feels head is "heavy". This resolves with lying down

or with walking around.

-Decrease in (or absence of) lubricating tears in the eye.

-Sensitivity to bright, florescent light and bright sunlight. Many patients report feeling pre-syncopal in large grocery stores and

department stores that use excessive florescent lighting. Flashing

lights and multi-colored lighting can also produce symptoms.

-Visual distortion: Television screens and computer screens can

appear distorted, especially post-syncopal or pre-syncopal episode.

Flat screens are recommended.

-Distorted depth perception resulting in a feeling of unsteadiness.

Often appears to be "clumsy" or excessively cautious when climbing

stairs, reaching for an object, etc.

-Other visual disturbances include a graying out or blacking out of

the visual field; either partially or completely.

-Decreased awareness of what is in the peripheral visual field. This

often causes the patient to startle because they did not perceive

anyone or anything next to them.

-Frequent "bumping into things". Attributed to a combination of

visual and depth perception deficits.

-Noise sensitivity. Loud or beating sounds can cause pre-syncopal

episodes. Difficulty filtering out sounds. Easily distracted by

sounds.

-Sensitivity to odors, even pleasant smelling chemicals such as

perfume. Odors such as cleaning products, gasoline, strong foods,

etc. may cause extreme nausea, retching, vomiting, dizziness and

headache.

Decrease production of saliva or excessive production of saliva.

-Severe constipation and decreased gut motility.

-Weight gain irregardless of diet modifications.

-Overall slowing of metabolism is common. -Increased metabolism (rare)

-Excessive gut motility leading to chronic diarrhea and weight loss.

(less common)

-Sensitivity to touch. Mild pat on the arm or squeeze of the hand can

cause excruciating pain especially right after an episode or if the

patient has not had enough sleep.

-Decrease sensitivity to pain/touch in certain areas. If standing or

sitting too long causes hands and feet to turn cold and blue, patient

will have decreased sensation in these areas due to poor blood flow.

-Taste and appetite changes. Fruits and other acidic foods may taste

extremely acidic. Foods may taste differently if patient is tired,

stressed, or post-syncopal episode.

-Hair loss due to decreased blood supply to hair folicles.

-Speech disturbances: Inability to finish an expressed thought, loss

of train of thought, "spoonerisms", especially if up and about for 2

hours or more without lying flat and resting.

-Comprehension difficulties. Inability to follow a conversation. May

hear words but is unable to understand their context in the sentence.

Cannot focus on more than one activity at a time. May not realize

they are being addressed. Losses conversation focus when topic is

changed. Is easily distracted from the conversation focus by any

environmental stimuli.

-Memory recall deficits in long and short term memory. Improves with

lying down and resting.

-Abdominal migraines. Severe stomach pain triggered by large meal or

by sitting or standing too long. Usually resolves if patient lies

quietly.

-Drifting to the right or left when walking. Most commonly patients

report drifting to the left. Many patients report always fainting to

the left as well. Appears to be unrelated to hand-dominance, but

further research is needed.

-Tend to have mild symptoms of Ehlers-Danlos, but do not necessarily

test positive for the disease. This includes hypermobile joints,

double joints, and soft, velvet-like skin that has little or no

texture.

-Often has another auto-immune disorder.

-Family History of auto-immune disorder or symptoms that resemble

autonomic dysfunction.

-Appears to have more viral illnesses than general population. Often

diagnosed with Chronic Fatigue Immune Dysfunction Syndrome.

I did not compile this list, credit goes to the owners of:

http://www.dysautonomia-eduinfo.org/index.html

Why do you need trace elements?

noreply@blogger.com (Unknown) — Wed, 05 Dec 2012 08:50:00 +0000

COPPER: cytochrome oxidase, ceruloplasmin, dopamine beta-hydroxylase, tyrosinase, cytosolic SOD

ZINC: carbonic anhydrase, cytosolic SOD, carboxypeptidase

MOLYBDENUM: xanthine oxidase

SELENIUM: glutathione peroxidase, (antioxidant)

COBALT: vitamin B12, heme synthesis and synthesis and maintenance of myelin

MANGANESE: pyruvate carboxylase, mitochondrial SOD

Wat is SOD?
Wikipedia: Als gevolg van de biologische oxidatieve reacties, kan ook superoxide-ion als bijproduct in cellen ontstaan. Dit is een zeer reactief deeltje, en het wordt dan ook zo snel mogelijk, voor het schade kan aanrichten, door een enzym, (superoxide dismutase), opgeruimd. Superoxide wordt in verband gebracht met allerlei ziekten en het verouderingsproces. Superoxide dismutase dat superoxide laat reageren tot zuurstof en waterstofperoxide, is voor zover bekend het snelste enzym.

What is SOD?
Wikipedia: SOD is an extremely efficient enzyme; it catalyzes the neutralization of superoxide nearly as fast as the two can diffuse together spontaneously in solution. Other proteins, which can be both oxidized and reduced by superoxide, have weak SOD-like activity (e.g. hemoglobin).
While the action of superoxide in the pathogenesis of some conditions is strong, for instance, mice and rats overexpressing CuZnSOD or MnSOD are more resistant to strokes and heart attacks ...

Chronic immune activation

noreply@blogger.com (Unknown) — Tue, 04 Dec 2012 13:59:00 +0000

http://imdtheory.blogspot.be/

Abstract: The conclusion of this paper is that non-communicable diseases such as the psychiatric disorders, neurological diseases, autoimmune diseases and other diseases associated with immune system upregulation but not deemed to be autoimmune, such as cardiovascular disease, cancer, type 2 diabetes, porphyria and many others, all arise as a consequence of chronic, aberrant activation of an immune system response which is driven by the transcription factor, nuclear factor kappa beta (NF-kB).

One of the principal functions of the NF-kB immune response is to control intracellular pathogens which establish latency within cells. To achieve this, reactive oxygen species (ROS), such as hydroxyl radical, which are destructive to these pathogens, are generated inside cells. In addition, the cell membrane receptors which are used by these pathogens to gain entry into cells are reduced in number, desensitised, or blocked by antibodies, causing these cells to become hypofunctional. To compensate for this, receptors on other cells may become hyperfunctional.

...

Many of the diseases which are known to be associated with a chronically activated NF-kB driven immune response are also associated with an above average incidence of infection with specific pathogens. I have compiled a list of those pathogens which appear to be most important. They are herpes simplex virus-1, herpes simplex virus-2, human herpes virus-6, cytomegalovirus (herpes family), Epstein-Barr virus (herpes family), varicella zoster (herpes family), mycobacteria, Borna virus, enteroviruses, hepatitis C virus, human papilloma virus, Borrelia bacterium, Toxoplasma gondii protozoon, human endogenous retroviruses, mycoplasma pneumoniae bacterium, Chlamydia pneumoniae bacterium, Helicobacter pylori bacterium, JC virus, Candida albicans fungus and intestinal worms.

This list reveals a crucially important fact. Except for Candida and worms, all these infectious organisms are obligate intracellular parasites which are known to establish latency within cells and can persist in a dormant state for years without causing illness.

...

Enzymes are frequently seen to be autoantigens in autoimmune diseases and are attacked by antibodies generated by B-cells. About a third of enzymes utilise a metal co-factor, very often iron, which may produce ROS, including hydroxyl radicals. However, virtually all of the enzyme autoantigens I have studied are metalloenzymes which use transition metal ions as a co-factor. The only exception I am aware of is glutamic acid decarboxylase, which utilises pyridoxal phosphate (vitamin B6) as a co-factor and is often an autoantigen in type 1 diabetes. This means that it is the metal or a product of the chemical reactivity of the metal which is attracting the attention of the immune system. The products may be ROS or alterations to the enzymes, co-factors or substrates caused by reactions with ROS. Examples of metalloenzyme autoantigens in autoimmune diseases include thyroid peroxidase (iron in heme) in thyroiditis, tyrosinase (copper) in vitiligo, transglutaminase (manganese) in coeliac disease and cytochrome P450 (iron in heme) in Addison’s disease. The cytochrome P450 superfamily of enzymes are frequent targets of the immune system, with CYPc21 and CYPc17 both antigens in Addison’s disease, CYPc17 and CYPscc in premature menopause, CYPc17 in gonadal failure, CYP1a2 and CYP2a6 in autoimmune polyglandular syndrome type1 and CYP1a2 in halothane hepatitis.

Het document is een pareltje, klik door naar de originele blog!
The original blog is a gem, please click to the original blog!

http://imdtheory.blogspot.be/

Crossreaction between bartonella and chlamydia

noreply@blogger.com (Unknown) — Sun, 25 Nov 2012 14:20:00 +0000

J Clin Microbiol. 1997 Sep;35(9):2283-7.

Serological cross-reactions between Bartonella and Chlamydia species: implications for diagnosis.

Maurin M, Eb F, Etienne J, Raoult D.

Source

Unité des Rickettsies, CNRS UPRESA 6020, Université de la Méditerranée, Faculté de Médecine, Marseille, France.

Abstract

Diagnosis of Chlamydia or Bartonella infections continues to rely mainly on serology. However, serological cross-reactions between members of these genera have recently been described. Sera from eight patients originally diagnosed as having Chlamydia pneumoniae endocarditis reacted with both Chlamydia sp. and Bartonella quintana antigens (microimmunofluorescence technique). Adsorption of sera with B. quintana or C. pneumoniae antigens removed anti-C. pneumoniae antibodies, whereas adsorption with C. pneumoniae antigens did not change antibody titers to B. quintana. Western blot analysis confirmed the presence of cross-reacting antigens and showed antibody patterns in all sera to be compatible with a Bartonella infection. These patients were therefore probably suffering from Bartonella-induced rather than Chlamydia-induced endocarditis. In contrast, sera from 10 patients presumed to be suffering from C. pneumoniae pneumonia did not display anti-B. quintana antibodies, although cross-reacting antigens were revealed by Western blotting. This work highlights the possibility that cases of infective Bartonella endocarditis are erroneously diagnosed as chlamydial infections.

http://www.ncbi.nlm.nih.gov/pubmed/9276403

Severe lactic acidosis reversed by thiamine within 24 hours

noreply@blogger.com (Unknown) — Sat, 24 Nov 2012 19:44:00 +0000

http://ccforum.com/content/15/6/457

Severe lactic acidosis reversed by thiamine within 24 hours

Karin Amrein^*, Werner Ribitsch, Ronald Otto, Harald C Worm and Rudolf E Stauber

* Corresponding author: Karin Amrein karin.amrein@yahoo.de

Author Affiliations

Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, A-8036 Graz, Austria

For all author emails, please log on.

Critical Care 2011, 15:457 doi:10.1186/cc10495

The electronic version of this article is the complete one and can be found online at: http://ccforum.com/content/15/6/457

Published:

1 December 2011

Letter

Thiamine is a water-soluble vitamin that plays a pivotal role in carbohydrate metabolism. In acute deficiency, pyruvate accumulates and is metabolized to lactate, and chronic deficiency may cause polyneuropathy and Wernicke encephalopathy. Classic symptoms include mental status change, ophthalmoplegia, and ataxia but are present in only a few patients [1]. Critically ill patients are prone to thiamine deficiency because of preexistent malnutrition, increased consumption in high-carbohydrate nutrition, and accelerated clearance in renal replacement. In retrospective [2] and prospective [3,4] studies, a substantial prevalence of thiamine deficiency has been described in both adult (10% to 20%) and pediatric (28%) patients. Thiamine deficiency may become clinically evident in any type of malnutrition that outlasts thiamine body stores (2 to 3 weeks), including alcoholism, bariatric surgery, or hyperemesis gravidarum, and results in high morbidity and mortality if untreated [1].

We report the case of a 56-year-old man with profound lactic acidosis that resolved rapidly after thiamine infusion. He was admitted because of a decreased level of consciousness (Glasgow Coma Scale score of 6). Vital signs, including blood pressure, heart rate, and oxygen saturation, were normal. Besides reporting regular alcohol consumption, relatives reported recent progressive weakness and 5-kg weight loss. Laboratory findings on admission were remarkable for moderate hypoglycemia and metabolic acidosis - pH of 6.87, base excess of -29.5, partial pressure of carbon dioxide (pCO₂) of 14 mm Hg - with a high anion gap (37 mmol/L) that was attributed to severe hyperlactatemia (21 mmol/L). After intravenous glucose administration, the patient was transferred to the intensive care unit, where he received sodium bicarbonate and 1,500 mL of lactate-free isotonic crystalloids. Within the next few hours, lactate levels increased further while pH slowly improved. Clinically, thiamine deficiency was suspected after other causes of hyperlactatemia, such as hypoxia and hepatic failure, were excluded. After administration of 300 mg of intravenous thiamine, hyperlactatemia normalized rapidly (Figure 1). Unfortunately, the patient suffered persistent neurocognitive deficits.

Figure 1. Lactate levels during the first 24 hours. IV, intravenous.

Thiamine deficiency may cause unspecific neurologic symptoms. Glucose administration or feeding may aggravate depletion. Thiamine deficiency is an underdiagnosed cause of lactic acidosis, although treatment is safe, inexpensive, and readily available. Current guidelines on parenteral nutrition recommend a daily intravenous dose of 100 to 300 mg of thiamine during the first 3 days in the intensive care unit when deficiency is a possibility (grade B) [5]. In conclusion, although its clinical significance has been known for decades, thiamine deficiency remains an under-recognized condition. Intensivists should have an increased awareness of this problem and a low threshold to infuse high-dose thiamine. Future prospective studies to define the optimal dose and duration of treatment are warranted.

Competing interests

The authors declare that they have no competing interests and that the data presented have not been published previously, except in abstract form.

Acknowledgements

We thank Steven Amrein for critical review of the manuscript.

References

Sechi G, Serra A: Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management.
Lancet Neurol 2007, 6:442-455. PubMed Abstract | Publisher Full Text
Cruickshank AM, Telfer AB, Shenkin A: Thiamine deficiency in the critically ill.
Intensive Care Med 1988, 14:384-387. PubMed Abstract | Publisher Full Text
Lima LF, Leite HP, Taddei JA: Low blood thiamine concentrations in children upon admission to the intensive care unit: risk factors and prognostic significance.
Am J Clin Nutr 2011, 93:57-61. PubMed Abstract | Publisher Full Text
Donnino MW, Carney E, Cocchi MN, Barbash I, Chase M, Joyce N, Chou PP, Ngo L: Thiamine deficiency in critically ill patients with sepsis.
J Crit Care 2010, 25:576-581. PubMed Abstract | Publisher Full Text
Singer P, Berger MM, Van den Berghe G, Biolo G, Calder P, Forbes A, Griffiths R, Kreyman G, Leverve X, Pichard C, ESPEN: ESPEN Guidelines on Parenteral Nutrition: intensive care.
Clin Nutr 2009, 28:387-400. PubMed Abstract | Publisher Full Text

http://ccforum.com/content/15/6/457

Chronic latent (!) viruses cause disease

noreply@blogger.com (Unknown) — Sun, 18 Nov 2012 20:45:00 +0000

Latent Viruses Cause Disease; CBCD Explains

Many scientists believe that latent viruses can only cause disease if reactivated. This is simply untrue.

Rochester, New York (PRWEB) June 13, 2012

The Center for the Biology of Chronic Disease (CBCD) has learned that Medpagetoday.com has published a story regarding the reactivation of latent viruses. The story focuses on the ability of the latent Epstein Barr virus (EBV) to reactivate and begin replicating itself…which in turn can spark inflammation in Multiple Sclerosis.
Many scientists believe that latent viruses can only cause disease if reactivated. Reactivation means that the virus begins to produce all of its proteins and make copies of itself on a large scale. In contrast, Dr. Polansky’s discovery says that viruses can cause disease while still latent, that is, without being reactivated.
The Theory of Microcompetition, as put forward by Dr. Hanan Polansky in his highly acclaimed “Purple Book” entitled “Microcompetition with Foreign DNA and the Origin of Chronic Disease,” explains how latent viruses can cause many major diseases. One of these viruses is the Epstein Barr virus, and one of these diseases is cancer.
Why is this important? Because most people who have an EBV infection do not know it. They harbor a latent infection that shows no symptoms, which are associated with reactivation. These people should be careful. They are at risk of developing cancer even if they don’t see the usual EBV symptoms.
Latent viruses replicate on a small scale even when they are not reactivated. This is something overlooked by many in the medical field today. As stated by Dr. Hanan Polansky, the latent EBV virus microcompetes with human genes for limited genetic resources, and as a result, can drive the human genes to malfunction, and cause disease.
Some scientists wrongly believe that if a virus is latent, then it is harmless. A latent virus is not dead. It continues to express some of its proteins and therefore to microcompete with human genes.
Consider the paper entitled “Human Cytomegalovirus Persistence” published February 13, 2012 in the journal, Cellular Microbiology. [1]
“Both the chronic and latent states of infection contribute to HCMV persistence and to the high HCMV seroprevalence worldwide. The chronic infection is poorly defined molecularly, but clinically manifests as low-level virus shedding over extended periods of time and often in the absence of symptoms.”
A virus is still shedding copies of itself during the latent phase, meaning it still replicates, and still microcompetes.
The same paper goes on to say: “Transcripts and proteins encoded from a region encompassing the major immediate early region are detected in hematopoietic cells following infection in vitro as well as in latently infected individuals.” (Kondo et al., 1996; Landini et al., 2000).
What does it all mean? Latent viruses such as the Epstein Barr virus continue to replicate, and therefore can cause disease even without reactivation, or while still latent.
Listen to Dr. Polansky describing his discovery during a recent interview by clicking on the following link.
http://dl.dropbox.com/u/41576890/02.06.12%20HHH%20Polansky%20Interview%20.mp3
“The key to your health is to reduce the level of latent viruses in your body to harmless levels.” – Dr. Hanan Polansky
So how does one reduce latent EBV?
It’s not easy. There are two traditional ways to attack the latent EBV virus: through vaccines and through antiviral medications. A vaccine is still in the early stages of development, and “There are…no regulatory agency-approved treatments for EBV-related diseases,” according to a study published in the Journal of Antimicrobial Chemotherapy. [2]
This means that currently there are no vaccines or drugs on the market to combat the active virus, let alone the latent virus.
However, the CBCD would like to point out a natural product designed to target the latent form of the virus. The name of that natural product is Gene-Eden-VIR. The CBCD encourages people infected with latent EBV to learn more about Gene-Eden-VIR.
For more information on the Center for the Biology of Chronic Disease, or to schedule an interview with one of our researchers, please visit http://www.cbcd.net or call 585-250-9999.
References:
[1] Goodrum F, Caviness K, Zagallo P. “Human Cytomegalovirus Persistence”, Cellular Microbiology, May 14, 2012
[2 Gershburg E., Pagano Joseph S., “Epstein Barr Virus Infections: Prospects for Treatment”, Journal of Antimicrobial Chemotherapy, 2005
http://jac.oxfordjournals.org/content/56/2/277.full
The Center for the Biology of Chronic Disease (CBCD, http://www.cbcd.net) is a research center recognized by the IRS as a 501(c)(3) non-for-profit organization. The mission of the CBCD is to advance the research on the biology of chronic diseases, and to accelerate the discovery of treatments for these diseases.
We invite biologists, virologists, scientists everywhere to download Dr. Polansky’s book, “Microcompetition with Foreign DNA and the Origin of Chronic Disease” here: http://cbcd.net/
The CBCD published the “Purple” book by Dr. Hanan Polansky.
The book presents Dr. Polansky’s highly acclaimed scientific theory on the relationship between the DNA of latent (chronic) viruses and the onset of chronic diseases. Dr. Polansky’s book is available as a free download from the CBCD website.

Chronic Chlamydia pneumonia is treatable

noreply@blogger.com (Unknown) — Sun, 11 Nov 2012 20:08:00 +0000

http://cid.oxfordjournals.org/content/29/2/452

Chronic Chlamydia pneumoniae Infection: A Treatable Cause of Chronic Fatigue Syndrome

Chronic fatigue syndrome (CFS), an elusive and controversial
illness, has been a difficult management problem for clinicians. A
number of infectious agents have been implicated as the cause of
CFS, although consistent and compelling evidence is still lacking
[1]. Few well-documented infections could cause persistent inflammatory
reaction leading to the symptomatology of CFS [2, 3].
Chlamydia pneumoniae is a common cause of respiratory infection
and has been demonstrated within plaques of the coronary arteries
years after initial infection [4]. Recently demonstrated replication
of C. pneumoniae within human macrophages and endothelial cells
[5] and a potent inducer of proinflammatory cytokines, such as
TNF-a and IL-1 [6], raised the possibility of chronic infection that
leads to persistent inflammatory response. A previous study failed
to demonstrate elevated titers of antibody to C. pneumoniae in 50
patients with CFS [7], although fatigue is a common symptom
reported by patients for whom sputum cultures are persistently
positive for C. pneumoniae [8].

Over the past 3 years, we encountered 10 of 171 patients with
symptoms of chronic fatigue who had elevated titers of antibody to
C. pneumoniae long after initial respiratory infection. Most patients
had favorable clinical and serological responses to a 1- to
2-months course of azithromycin therapy, although relapse was
common. The clinical symptoms of and titers of antibody to
C. pneumoniae for our 10 patients over the course of treatment are
summarized in table 1.
A 32-year-old female developed pharyngitis, cough, cervical
lymphadenopathy, low-grade fevers, severe fatigue, and myalgia
in January 1993 (patient 1). A medical evaluation showed a normal
complete blood cell count and normal results of thyroid function
test and serum chemistry analysis. IgG antibody to Epstein-Barr
virus was positive. During the following 3 years, the patient had
frequent relapses of severe fatigue, diffuse myalgia, night sweats,
pharyngitis, headaches, insomnia, and painful, swollen cervical
lymph nodes (especially following exertion) that resulted in total
disability.
Repeated evaluation in August 1996 revealed small nontender
anterior cervical lymph nodes. Results of routine laboratory studies
and serologies for several viruses were unremarkable. The titer of
IgG antibody to C. pneumoniae was 1:256. Magnesium sulfate
injections and salt loading failed to alleviate symptoms. One
month later, when the patient was having increasing fatigue, the
titer of antibody to C. pneumoniae rose to 1:1,024. Azithromycin
(500 mg) was administered by mouth the first day, followed by
250-mg doses for the subsequent 4 days. The patient’s condition
improved by day 3 of therapy, although her symptoms relapsed 12
days later.
Similar improvement and relapse followed a second 5-day
course of azithromycin treatment. Thereafter, 250 mg of azithromycin
was given daily for a total of 30 days; this therapeutic
course resulted in a marked decrease in her symptoms. She returned
to full-time work as a manager at her company and maintained
an energy level of 8–9 of 10 for the next 2 years. Follow-up
antibody titers are shown in table 1.
Most of our patients had symptoms referable to the upper or
lower respiratory tracts, but radiographic studies of the sinuses
and chest were unremarkable. Seven of the 10 patients had high
levels of total antibody to C. pneumoniae 0.5 to 3 years following
an episode of symptomatic respiratory infection. Three
patients had low antibody titers of 1:128 and 1:256, but their
symptoms did decrease with antibiotic therapy. Low or absent
antibody response to C. pneumoniae was documented for patients
with persistently positive respiratory cultures [8]. Comparatively,
the mean titers 6 SD for 90 controls were 32 6 36
(range, ,8 or 4 to 256). Only two of 19 fatigued patients with
reciprocal titers between 32 to 64 responded to 1 month of
azithromycin treatment (data not shown).
The spontaneous rise of titers for several patients correlated with
an increased severity of fatigue and a concomitant increase in
respiratory symptoms. This observation suggests that relapses of
symptoms could be due to persistent infection with periodic reactivation
rather than reinfection. All of the patients with relapses
responded to additional azithromycin treatment.
C. pneumoniae is a common copathogen in patients with respiratory
infection [9]. Symptoms of acute purulent sinusitis and mastoiditis
in patients 7 and 8, respectively, did decrease after 2–3 weeks of
ceftriaxone treatment, but severe fatigue persisted for the next 2 years;
fatigue resolved only after 2 months of azithromycin treatment.
Recently, Falck et al. [10] found C. pneumoniae DNA in throat
secretions from 10 of 11 patients with chronic rhinorrhea, fatigue,
and throat biopsies positive for C. pneumoniae. Seventy percent of
the patients had elevated titers of IgG (1:512) or IgA (1:128)
antibody. All of their patients responded to prolonged courses of
macrolide therapy, but symptoms frequently recurred.
Collectively, these results suggest that C. pneumoniae is an
uncommon yet treatable cause of chronic fatigue. The sensitivity,
specificity, and interlaboratory variability of the DNA test will
need to be better defined. Although seemingly less sensitive and
prone to interlaboratory variation, the widely available microimmunofluorescence
test may be a practical screening test for this
entity before throat biopsy is performed.

John K. S. Chia and Laura Y. Chia
Torrance Memorial Medical Center, Torrance, California

Source: http://cid.oxfordjournals.org/content/29/2/452

More options about treatments can also be found at www.cpnhelp.org

Videotalks by Rich von Konynenburg

noreply@blogger.com (Unknown) — Fri, 02 Nov 2012 21:31:00 +0000

http://iaomt.media.fnf.nu/2/skovde_2011_me_kroniskt_trotthetssyndrom/$%7Bweburl%7D

If you like to learn more about methylation (vit B12, folate, sulphur, gluthation and detox), go to minute 35 in the first film right away!

9 bartonella species known to infect humans

noreply@blogger.com (Unknown) — Thu, 01 Nov 2012 10:32:00 +0000

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2100128/

Do Bartonella Infections Cause Agitation, Panic Disorder, and Treatment-Resistant Depression?

In the last 15 years, 9 Bartonella bacteria have been identified that are known to infect humans: B henselae, B elizabethae, B grahamii, B vinsonii subsp. arupensis, B vinsonii subsp. berkhoffii, B grahamii, B washoensis, and, more recently, B koehlerae and B rochalimae.[16–20] Currently, the largest national laboratories offer tests for only 2 species[21–23] (B quintana and B henselae).

Some Bartonella cases have “atypical” presentations with signs or symptoms lasting more than weeks, causing diverse medical problems. For example, Bartonella can cause vision abnormalities, prolonged fever, joint pain, lung inflammation, respiratory disease, and granulomas throughout the body. It can occasionally cause abdominal pain, liver and spleen tissue abnormalities, thrombocytopenic purpura, bone infection, papules or pustules, maculopapular rashes, arthritis, abscesses,, – heart tissue and heart valve problems,– and neurologic illnesses.–

Traditionally, cognitive neurology has been related to some psychiatric illnesses. A search of PubMed with “Bartonella” and the search words “depression,” “mania,” “bipolar,” “major depression,” “depression,” “anxiety,” “panic,” “panic attack,” “psychosis,” and “schizophrenia” yielded the limited journal results below:

Depression
Dementia
Encephalopathy
Violent behavior
Confusion
Combative behavior
Substance abuse disorders[43–48]

Conclusion

We note that the number of Bartonella species that infect humans currently outpaces the number of Bartonella species that can be tested by top national labs. Some antibiotics seem to have an effect, but dosing and duration are not clearly established or indicated by a broad literature review. Further, clinical improvement and the cessation of symptoms do not always signify complete eradication. That is, it may be possible for a patient to relapse due to a significant medical stress to the body or a decrease in immune system capacity. Of greatest importance, we believe that Bartonella can enter the brain and cause not only well-documented neurologic disorders, but also some psychiatric disorders as well.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2100128/

How and why herpes virus reactivate

noreply@blogger.com (Unknown) — Thu, 01 Nov 2012 10:20:00 +0000

How and why herpes virus reactivate

http://www.sciencedaily.com/releases/2012/10/121031125516.htm

ScienceDaily (Oct. 31, 2012) — The mere mention of the word "herpes" usually conjures negative images and stereotypes, but most people have been infected with some form of the virus. For most, a sore appears, heals and is forgotten, although the virus remains latent just waiting for the right circumstances to come back. Now, the mystery behind what triggers the virus to become active again is closer to being solved thanks to new research published in the Journal of Leukocyte Biology's November 2012 issue.

In the report, scientists show how the immune system may lose its control over the virus when facing new microbial threats, such as when it must fend off other viral invaders or bacteria.
"Because almost all people are infected by one or more herpes family viruses during their lifetime, the potential impact of these findings are significant," said Charles H. Cook, M.D., FACS, FCCM, director of surgical critical care at The Ohio State University College of Medicine in Columbus, Ohio, and a researcher involved in the work. "We hope that by understanding how these latent viral infections are controlled that we can prevent reactivation events and improve people's lives."
To make this discovery, researchers studied mice with latent herpes family cytomegalovirus (CMV) during severe bacterial infections. They found that T-cells responsible for CMV control were reduced significantly during a new infection with bacteria. This, in effect, reduced the "brakes" which kept the virus under control, allowing the virus to reactivate and cause disease. When the immune system eventually sensed the reactivation, the memory T-cell levels returned to normal, effectively restoring the body's control over the virus.
"Finding ways to control herpes flare ups is important, not only for the health of the person with the virus, but also for preventing its transmission," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "This report highlights the important interplay when we are 'co-infected' with more than one microbe and provides important insights into why the immune system sometimes fails as well as how it can regain control of latent herpes virus infections."

http://www.sciencedaily.com/releases/2012/10/121031125516.htm

High CD8+ and low CD57+, what does it mean?

noreply@blogger.com (Unknown) — Wed, 24 Oct 2012 19:09:00 +0000

Scand J Infect Dis Suppl. 1995;99:69-77.

The role of CD8+, CD57+ cells in human cytomegalovirus and other viral infections.

Wang EC, Borysiewicz LK.

Source

Department of Medicine, University of Wales College of Medicine, Heath Park, Cardiff, UK.

Abstract

Peripheral blood lymphocytes expressing CD8 and CD57 determinants are a small (1-15%) subset in healthy humans. CD8+, CD57+ peripheral blood lymphocytes may be divided by the level of CD8 expression, into CD8+high (CD57+) T-cells and CD8+low (CD57+) natural killer (NK) cells. CD8+high (CD57+) T-cell numbers are increased in human cytomegalovirus (HCMV)-seropositive subjects, and there is substantial evidence that HCMV is integral in the development of this subset in health and disease. Furthermore, the CD8+high (CD57+) subset is clonally derived, expressing a limited range of T-cell receptors, and are therefore likely to have restricted antigen specificity. Functionally, CD8+low(CD57+) cells exhibit NK activity, while CD8+high(CD57+) T-cells from healthy subjects mediate contact-dependent suppression in several in vitro systems including: (i) pokeweed mitogen-induced proliferation and immunoglobulin synthesis, and (ii) generation of antiviral MHC-restricted cytotoxic T-lymphocytes. This is distinct from the nonspecific, soluble factor-mediated suppression exhibited from a phenotypically similar subset in human immunodeficiency virus (HIV) and bone marrow transplant recipients. This suggests an important immunoregulatory, suppressive role for CD8+high(CD57+) T-cells that may be potentiated by HCMV and altered in diseases associated with higher numbers of this subset including HIV, allograft recipients and rheumatoid arthritis.

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Signs and Symptoms of Autonomic Dysfunction

Some of the listed symptoms are always present while others occur when a person with Autonomic Dysfunction has been standing or sitting too long:

Why do you need trace elements?

Chronic immune activation

Crossreaction between bartonella and chlamydia

Serological cross-reactions between Bartonella and Chlamydia species: implications for diagnosis.

Source

Abstract

Severe lactic acidosis reversed by thiamine within 24 hours

Severe lactic acidosis reversed by thiamine within 24 hours

Letter

Competing interests

Acknowledgements

References

Chronic latent (!) viruses cause disease

Latent Viruses Cause Disease; CBCD Explains

Many scientists believe that latent viruses can only cause disease if reactivated. This is simply untrue.

Chronic Chlamydia pneumonia is treatable

Chronic Chlamydia pneumoniae Infection: A Treatable Cause of Chronic Fatigue Syndrome

Videotalks by Rich von Konynenburg

9 bartonella species known to infect humans

Do Bartonella Infections Cause Agitation, Panic Disorder, and Treatment-Resistant Depression?

Conclusion

How and why herpes virus reactivate

How and why herpes virus reactivate

High CD8+ and low CD57+, what does it mean?

The role of CD8+, CD57+ cells in human cytomegalovirus and other viral infections.

Source

Abstract

Cite this article as: BJMP 2010;3(1):301
Download PDF

Some of the listed symptoms are always present while others occur
when a person with Autonomic Dysfunction has been standing or sitting too long: