Het gevaar van vitamine D

Mijn aandacht werd vandaag getrokken door een artikel over de gevaren van vitamine D suppletie.
Het werd geschreven door Stephanie Seneff, a Senior Research Scientist in the Computer Science and Artficial Intelligence Laboratory bij MIT die zich de laatste jaren terug heeft geconcentreerd op biologie en het verband tussen voeding en gezondheid.

Hieronder zal ik pogen een stuk van haar artikel omtrent de gevaren van vitamine D suppletie te vertalen. Vroeger was ik een heel andere mening toegedaan over vit D gebruik maar na het lezen van haar tekst, ben ik aan het denken gezet. Misschien jullie ook.

Deel 1

Stel dat je vitamine D gehalte te laag is, dan hebben we heden de neiging om dat aan te vullen met een supplement. Echter, biologie zit gecompliceerder in elkaar.
Orale vitamine D en deze geproduceerd door de zon zijn totaal verschillend van elkaar. Degene die je van de zon binnenkrijgt, wordt onmiddellijk in de huid omgezet om je te beschermen tegen o.a. huidkanker. Door je systematisch in te smeren zoals ons wordt aangeleerd door de media en artsen, schakelen we de reactie van cholesterol die vitamine D moet omzetten, simpelweg uit.

Tweede probleem, door het uitschakelen van ons eigen systeem en het vervangen van dit mechanisme door supplementen, is als diabetes creëren. We vernietigen als het ware de alvleesklier en dienen vervolgens insulineshots toe. Daarmee kan je het vergelijken.

Teveel zonlicht? Stel dat je teveel vitamine D hebt door zonlicht, dan vernietigt het lichaam dit tot een reeks inactieve metabolieten. Ten tweede het bruine kleurtje in de huid zorgt ervoor dat we niet teveel vitamine D opnemen eenmaal we aan onze limieten zijn gekomen.

Deel 2

De argumenten die heden worden aangehaald om vitamine D te suppleren, zijn te eenvoudig en bedriegelijk. Vit D is noodzakelijk tegen infectie en kanker, daarover is geen twijfel. Het is essentieel in botontwikkeling en calciumhuishouding. Echter in plaats van iedereen aan te raden vaker in de zon te zitten, moet men zonnecrème smeren en supplementen nemen.

Dat is niet zonder gevaar.

Vit D is immuunmodulerend en het chronisch gebruik ervan in geconcentreerde dosissen, moet men vergelijken met antibioticakuren. Het doodt goede bacterieën en is misschien mede de oorzaak van obesitas net zoals chronisch gebruik van corticoiden.

Nog alarmerender is dat de darmbacterieën zich aanpassen aan deze chronische vitamine D dosissen. Omdat de bacterieën willen overleven, gaan ze dus muteren en ervoor zorgen dat de vit D niet meer omgezet kan worden in een actieve vorm (van 25-D naar 1,25-D). De analogie met bacterieën die resistent worden aan antibiotica is niet ver weg! Hier hebben we te maken met darmbacterieën die ervoor zullen zorgen dat de omzetting van een immuunmodulerende vitamine niet meer kan uitgevoerd worden.

Men riskeert zo verhoogde kans op auto-immuunziekten, kanker en infecties om maar een voorbeeld te geven.

Bron: http://people.csail.mit.edu/seneff/statins_pregnancy_sepsis_cancer_heart_failure.html

Punt 10

WHO Petition for Tick Born Diseases

http://www.change.org/petitions/world-health-organization-who-take-action-on-tick-borne-diseases?

It takes less than a minute to sign and send it to your friends!

Adrenal insuffiency in critical illness

Hypothamic-pituitary adrenal insufficiency in critical illness   7/20/2001

(Critical care clinics volume17 number1 January 2001)

INTRODUCTION

ü          Cortisol is the major glucocorticoid produced by the adrenal cortex and is required for normal function of all cell in the body. Deficiency of cortisol is associated with increased morbidity and mortality during critical illness.

ü          Cortisol is required for carbohydrate, protein, and lipid metabolism; immune function, synthesis and action of catecholamines and adrenergic receptors; cardiac contractility; wound healing; vascular tone, endothelial integrity, normal vascular permeability; and numerous other functions.

ü          Hemodynamic benefits of glucocorticoids also related to the action beta-adrenergic receptor desensitization/uncoupling, and inhibition of nitric oxide sythase. Mineralocorticoids are important in the maitenance of fluid and electrolyte balance.

Regulation

ü          Cortisol circulates in the blood in bound and unbound forms. The bound form is primarily carried on cortisol binding globulin(90%). It is unbound or free cortisol that is physiologically active and hemeostatically regulated.

ü          Although levels of free cortisol have not been well studied in critically ill patients, studies in critically ill patients suggest that there is a decreased in cortisol binding rather than an increased. The cause for this decrease in binding is not unknown, but it may increased cortisol availability to the cell during stress.

ü          The bioavailabilty of cortisol to its sites of action (i.e., nucleus) has not been well studied during critical illnesss. There are no clinically useful tests for assess cellular actions of cortisol (end-organ affects) during illness.

CAUSES OF ADRENAL INSUFFICIENCY

ü          Systemic inflammatory states such as sepsis are associated with primary and secondary adrenal insufficiency that is reversible with treatment of the inflammation.

ü          The adrenal insufficiency is believed to result from hypothalamic-pituitary-adrenal suppression by cytokines and other inflammatory mediators.<=The immune and endocrine systems share common mediators that are capable of regulating each other..

INCIDENCE

ü          The incidence of adrenal insufficiency in critically ill patients is variable and depends on the underlying disease and severity of the illness.

ü          The authors define adrenal insufficiency as an inappropriately low cortisol response to stress (i.e.,<25 a="a" acth="acth" cortisol="cortisol" dl="dl" endogenous="endogenous" exogenous="exogenous" for="for" is="is" mcq="mcq" of="of" p="p" secretion="secretion" stimulation="stimulation" stimulus="stimulus" stress="stress" superior="superior" tests.="tests." than="than" use="use">

ü          The incidence increased with severity of illness (critical illness and sepsis>elective surgery >ward admits) with most studies in critically ill patients reporting incidences of 25% to 40%

CLINICAL MANIFESTATIONS

ü          Adrenal insufficiency should be suspected in patients with clinical features or disease processes associated with adrenal dysfunction. These include sepsis, HIV infection, head trauma, bilateral flank pain, and DIC.

ü          Hypotension that is refractory to fluid and requires vasopressors is a common presentation. One should always suspect adrenal insufficiency in patients with unexplained hyponatremia, hypokalemia, hypoglycemia, or eosinophilia.

EVALUATION OF ADRENAL FUNCTION

ü          The best stimuli for testing adrenal function are endogenous stresses such as hypotension, hypoglycemia, and hypoxemia. The tests evaluate the integrity of the entire brain (the sensor), hypothalamus-pituitary-adrenal axis.Endogenous stresses such as hypotension, hypoxemia, and hypoglycemia are superior stimuli for cortisol secretion compared with ACTH testing.

ü          When the level of stress is low or uncertain, cortisol production can assessed by induction of hypoglycemia (i.e., insulin tolerance test) and injection of exogenous ACTH (i.e., corticotropin) . It is important to realize that administration of exogenous ACTH bypasses the brain-hypothalamic-pituitary axis and tests the integrity of the adrenal gland directly. Failure of the adrenal gland to secrete adequate cortisol in response to ACTH is diagnostic of primary or secondary adrenal insufficiency (high positive predictive power); however, a normal response to ACTH dose not rule out adrenal insufficiency (low negative predictive power).

ü          The traditional approach to the short Corticotropin stimulation test (also known as the cosyntropin stimulation test) is to administer 250 mcg of synthetic corticotropin intravenously. Serum is obtained for cortisol analysis before and 30 and 60 minutes after corticotropin. A subnormal response (indicative of adrenal insufficiency) is a cortisol level less than 25 to 30 mcg/dL

ü          Importantly, a normal response to 250 mcg corticotropin(high dose) does not ru1e out adrenal insufficiency. This is amount of corticotropin is supraphysiologic (over one hundredfold greater than normal stress-induced ACTH levels). The very high levels of Corticotropin obtained with 25O mcg can override adrenal resistance to ACTH and result in a normal cortisol response (similar to the effect of insulin in patients with type 2 diabetes mellitus).These levels also can result in normal responses in patients with acute secondary adrenal insufficiency.

ü          Many patients with normal responses to high-dose(25O mcg) corticotropin fail to respond normally to stress or CRH.

ü          Patients with partial adrenal insufficiency and acute adrenal insufficiency can have normal responses to exogenous ACTH. It can take 10 to 14 days for the adrenal gland to atrophy enough so that responses are subnormal to ACTH after the acute onset of secondary adrenal insufficiency (as may be seen in patients with sepsis)．

ü          It is interesting that very high cortisol levels (markers of severe stress) and blunted increases in cortisol (lack of adrenal reserve) are associated with high mortality. Of course low cortisol response to stress also is associated with high mortality.

ü          The traditional high-dose (25O mcg) Corticotropin stimulation test administers supraphysiologic doses of Corticotropin, so many clinicians use the more physiologic low-dose (1 to 2mcg) Corticotropin stimulation test, which better approximates ACTH levels found in severe stress.

ü          Blood samples for cortisol analysis are obtained before and 30 and 60minutes after administration of 1to 2mcg of Corticotropin. An appropriate response is a circulating cortisol level greater than 25 to 30mcg/dL Using the low-dose Corticotropin stimulation test, the authors and other investigators have found that in most critical1y ill patients with stress-related cortisol levels 15mcg/dL cortisol levels do not increase higher than 20 mcg/dl following certicotropin. The authors believe that patients in whom Cortisol levels do not rise have adrenal insufficiency. Many affected patients wi1l have a normal cortisol response(25mcg/L) Using the high-dose Corticotropin stimulation test. Thus,it appears that the low-dose Corticotropin stimulation test is more sensitive than the high-dose test for detecting adrenal insufficiency

ü          In the authors’ experience, most patients with adrenal insufficiency diagnosed by the low dose corticotropin test improve clinically(i.e., improved blood pressure)with hydrocortisone treatment. In a recent study,³³ the authors reported that 40% of patients with hypotension and sepsis who require vasopressors and 30 of patients with HIV admitted to the ICU have adrenal insufficiency diagnosed with the low-dose corticotropin stimulation test.

ü          Endogenous ACTH levels range from 100 to300 pg/mL during severe stress. These levels produce maximal secretion of the adrenal gland. Postoperative ACTH levels average 100 to 125pg/mL. Critically ill patients typically have ACTH levels of 80 to 150 pg/mL. Normal ACTH levels in nonstressed individuals range from 9 to 50 pg/mL. Corticotropin levels (ACTH) can aid in the diagnosis of adrenal insufficiency. Low plasma cortisol levels in the face of high Corticotropin levels (i.e. 100 pg/mL or 22 pmol/L) suggest primary adrenal insufficiency. Normal or low Corticotropin levels m the presence of low cortisol levels suggest secondary adrenal insufficiency

ü          The adrenal axis can be evaluated using Corticotropin releasing hormone (CRH). After administration of CRH, corticotropin(ACTH) peaks at 15to 30minutes and cortisol peaks at 30to 60minutes.This test can distinguish between corticotropin deficiency and deac1ency of CRH. The authors have noted an occasional patient in the ICU who fails to respond normally to CRH but does respond normally to high-dose (250 mcg) corticotropin. These patients have secondary adrenal insufficiency.．

ü          There is much controversy regarding levels of cortisol that are considered an adequate stress response. Many textbooks and published manuscripts state that the normal cortisol response to stress is a level＞18to 2O mcg/dL. .The choice of 18to 20 mcg／dL is based primarily on the response to exogenous ACTH（25O mcg）in patients who are not stressed or critically ill. When the physician examines the cortisol  response to severe stress （i.e., critical illness，hypotension，hypoxemia）, the majority of patients are found to achieve levels in excess of 25to 30mcg/dL* An uncomplicated cholecystectomy in a normal person increases cortisol concentrations to 27 to 34mcg/dL at 30minutes after the start of surgery and to 46 to 49mcg/dL at 5 hours after surgery. Melby and colleagues ³⁷ reported a mean cortisol level of 63mcg/dL in 2O patients with hypotension and sepsis (range 30 to 160 mcg/dL). Thus, many critical care metabolism experts believe that the cortisol response to critical illness should exceed these levels. The authors use 25mcg/dL as the lower normal response to stress. It is not necessary to obtain cortisol levels at a specific time of the day because most critically ill patients lose the diurnal variation in their cortisol levels. The level should be obtained during the stress(i.e., hypotension，hypoglycemia， hypoxemia).

ü          The acute and chronic responses to ACTH differ. The acute response may not always predict the chronic response. Thus, patients with chronic critical illnesses or stresses should be re-evaluated at intervals to determine if their adrenal function is adequate (even if initial adrenal function was adequate for the level of stress)．The authors call the failure to maintain cortisol secretion in the face of chronic stress the adrenal exhaustion syndrome. Chronically elevated cytokine levels or persistent or recurrent infections may contribute to adrenal exhaustion．

ü          The initial step is to determine whether the patient has primary or secondary adrenal insufficiency. This determination can be accomplished using ACTH levels or prolonged ACTH infusion. The next step is to image the brain (secondary adrenal insufficiency)or adrenals (primary adrenal insufficiency). Magnetic resonance(MR) imaging is the most sensitive test for detecting abnormalities m the hypothalamic-pituitary-adrenal axis. Disease in the adrenal glands is best imaged with computed tomography(CT) scanning. Enlarged adrenal glands suggest tuberculosis (unless long standing), fungal disease, cancer, hemorrhage, and AIDS. Small adrenal glands suggest autoimmune adrenal atrophy or long-standing infectious or vascular disease. A biopsy specimen from the involved area may be required for definitive tissue diagnosis. Patients with secondary adrenal insufficiency should be evaluated for loss of other hormones such as thyroid hormone.

TREATM ENT

1.          Supportive care and treatment underlying disease: It includes administration of fluids, electrolytes, nutrition, needed medications such as antibiotics and organ support (i.e., respiratory  cardiovascular support). It is important to maintain body temperature and glucose levels(With dextrose and normal saline solutions).

2.          Hydrocortisone replacement

ü          Adrenalectomy in animals increases mortality after septic and hypovolemic shock. Glucocorticoid replacement improves survival in these models. Thus it is believed that hydrocortisone treatment is lifesaving in patients with adrenal insufficiency ; however, most of this belief is based on pathophysiologic reasoning and case studies.For example, Soni and colleagues identified and treated thee patients with septic shock and adrenal insufficiency with glucocorticoids. All thee were weaned off pressor support within several hours of receiving steroid.

ü          Survival was not improved Mckee and colleagues reported that the mortality from critical illness increased from 27 in patients with stress cortisol levels 125mcg/dL  and 97 to 100m patients with stress cortisol level 125rncg/dL n 36.

ü          Beishuizen and colleagues diagnosed adrenal insufficiency in 10 of 40 medical-surgery ICU patients. Treatment with hydrocortisone improved hemodynamics in seven of eight patients.

ü          Mark and colleagues diagnosed adrenal insufficiency in seven patients. In all of them blood pressure improved with hydrocortisone treatment

=>There are a few studies in the literature that have compared treatment of patients with adrenal insufficiency with glucocorticoids versus placebo.

ü          Mckee and colleagues randomized18 critically ill patients with adrenal insufficiency (stress cortisol 125mcg/dL and no response to corticotropin) to glucocorticoid treatment or placebo. One of eight(13) steroid-treated patients died compared with nine of ten (9) of patients given placebo.

ü          Evidence for high mortality from untreated adrenal insufficiency in critically ill patients also comes from the report of Ledingham andWatt , who reported increased mortality from use of etomidate(a sedative agent that causes adrenal insufficiency) in multiple trauma patients (44 etomidate versus 27 other sedatives).

ü          Bollaert and colleagues randomized 41 critically ill patients with septic shock to hydrocortisone (100 mg every 8hours)or placebo. The glucocorticoid-treated patients had a greater reversal of shock at 7and 28days and reduced 28-day mortality compared with the placebo group.

ü          In a recent study Bnegel and colleagues randomized 40 critically ill patients with sepsis and hypotension who required vasopressor support to hydrocortisone or placebo. Hydrocortisone treatment was associated with improved shock reversal and decreased days of vasopressor support. There also was earlier resolution of organ dysfunction, shorter ventilator time and shorter ICU stay. Mortality was 4of 20 of the steroid-treated patients versus 6 of 20 of the placebo group. The authors of this study did not evaluate the patients for the presence of adrenal insufficiency; however, this group reports an incidence of adrenal insufficiency of 40 to 50. These studies used stress doses of glucocorticoids (300 mg hydrocortsone per day) in contrast, a number of large multicenter studies that used massive doses of glucocorticoids (30 mg/kg methylprednisolone) failed to and benefit in patients with sepsis.

ü          Annane and colleagues evaluated adrenal function in 189 patients with septic shock. Interestingly, compared with survivors/nonsurvivors had significantly higher basal plasma cortisol levels and lower cortisol response to high-dose (0.25mg) Corticotropin(decreased adrenal reserve) The increased basal cortisol levels and lower response to corticotropin may reflect a higher degree of illness in the nonsurvivors. The relative lack of a serum Cortisol response to Corticotropin insome critically ill patients may be related to the fact that the hypothalamic-pituitary-adrenal axis is already maximally stimulated. Similar observations have been noted by other investigators, Thus, patients with low stress cortisol values(adrenal insufficiency)and those with high values (severe stress or illness) have increased morta1ity.

THERAPEUTIC APPROACH TO ADRENAL INSUFFICIENCY

ü          Patients with diseases known to cause adrenal insufficiency and clinical features of adrenal insufficiency should be evaluated for adrenal dysfunction . Patients with hypotension refractory to fluids and who require vasopressors are at very high risk. Hyponatremia, hyperkalemia, hypoglycermia, and eosinophilia also suggest the diagnosis of adrenal insufficiency.

ü          A stress serum cortisol sample should be obtained for analysis. The patient should be started on hydrocortisone (100 mg every 8hours) empirically pending results of testing. If the serum cortisol level is found to be less than 25mcg/dL the hydrocortisone should be continued. In addition, if the patient has improved clinically with hydrocortisone, the author favor continuing the hydrocortisone for a few days (unless there is a specific contraindication). The authors and other believe that some patients may have cellular resistance or deficiency of glucocorticoids despite high serum levels. Until there is an adequate end-organ assay for glucocorticoid actions,they recommend continuing glucocorticoid treatment in patients who improve on thesteroid, despite adequate circulating levels. The does of hydrocortisone should be tapered down toward maintenance doses as the patient’s clinica1status improves.

ü          If the level of stress is uncertain and adrenal insufficiency is suspected, the authors favor adrenal testing with the low-dose (1 to 2mcg) corticotropin stimulation test. The authors usually treat the patient with hydrocortisone empirically pending results. If the corticotropin stimulation test can not be performed immediately, dexamethasone (2mg) should be administered, and the test should be performed within the next 12 hours. Dexamethasone does not significantly cross-react with cortisol in the assay for cortisol l and can be given to patients spending the results of adrenal testing.

ü          There is debate regarding whether asymptomatic patients with borderline adrenal insufficiency should be treated with hydrocortisone. The authors believe that all critically ill patients are symptomatic and warrant treatment because many of the clinical features of adrenal insufficiency are nonspecific and easily masked by critical illness.

ü          Once their conditions are stable, patients should be tapered to maintenance does of hydrocortisone appropriate to their levels of stress. In nonstressed patients 15mg hydrocortisone in the morning and 10mg in the afternoon are usually adequate for replacement. Definitive adrenal testing should wait until the patient is well. Most critically ill patients with acquired adrenal insufficiency recover adrenal function after recovery from illness and will not require life-long replacement of adrenal hormones.

ü          Patients with primary adrenal insufficiency develop both glucocorticoid and mineralocorticoid hormones. Mineralocorticoids can be replaced with fludrocortisone(50 to 200 mcg/d)

SUMMARY

ü          Adrenal insufficiency is a common and underdiagnosed disorder that develops in critically ill patients. Most forms are acquired and will resolve with treatment of the underlying disease. Hypotension that is refractory to fluids and requires vasopressors is the most common presentation of adrenal insufficiency in the ICU. It is important to make the diagnosis of adrenal insufficiency, because current data suggest that treatment with glucocorticoids improves outcome.

ü          Diagnosis usuallv can be made on the basis of a stress cortisol level. Occasionally, when the level of stress is uncertain,the low-dose corticotropin stimulation test will be required for definitive diagnosis. A therapeutic trial with hydrocortisone should be started in patients with suspected adrenal insufficiency pending results of diagnostic testing．

Lesson 1: Inflammation causes adrenal insufficiency
Lesson 2: This is mediated by cytokines
Lesson 3: Endocrine health is intimately linked with immune health. You can't have one without the other.




PS: If you are the author of this article, please contact me and I will add your name/references.

Prozac works antiviral

Onderzoek naar het postpoliosyndroom en chronische vermoeidheid heeft voor een verbazingwekkende ontdekking gezorgd. Het virus dat de belangrijkste trigger is voor ME/cvs is nauw verwant aan het virus dat polio veroorzaakt.

Bron: http://www.me-cvsvereniging.nl/sites/default/files/120929%20ME%20CVS%20Artikel%20ME%20of%20Polio.pdf

Een beetje geschiedenis: 

Dr Ramsay stelde samen met collega’s vast dat sinds 1916 een reeks epidemies van de soort encephalitis lethargica (EL) plaatsvonden. Deze gebeurden rond dezelfde periode als de beruchte griepepidemie van 1918. De symptomen evolueerden door de tijd heen maar ook van plek tot plek en hij en collega’s hadden een sterk vermoeden dat een nieuwe ziekte zich had gevormd. Rosemary Lindan bevestigde dit hetzelfde jaar en schreef “there can be no doubt a new disease entity had appeared”.

Tegen het einde van de tweede wereldoorlog verschoof de aandacht naar poliomyelitis en verschillende bronnen vestigden er de aandacht op dat de onbekende ziekte evolueerde in aard. Uitbraken van poliomyelitis in de zomer en herfst gingen steeds vooraf aan deze nieuwe ziekte. Deze laatste bleek ook veel besmettelijker te zijn en veel meer slachtoffers te vellen.  

Coxsackie, het virus dat het vaakst voorkomt bij ME, is een virus dat deel uitmaakt van de poliofamilie samen met andere enterovirussen.  
http://virology-online.com/viruses/Enteroviruses.htm

Fluoxetine (Prozac) is a Potent Inhibitor of Coxsackievirus Replication

1. Jun Zuo1,
2. Kevin K. Quinn1,
3. Steve Kye1,
4. Paige Cooper1,
5. Robert Damoiseaux2 and
6. Paul Krogstad1,3,*

+ Author Affiliations

1. ¹Departments of Pediatrics
2. ²California Nanosystems Institute
3. ³Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, University of California, Los Angeles CA 90095

ABSTRACT

No antiviral drugs currently exist for the treatment of enterovirus infections, which are often severe and potentially life-threatening. Molecular screening of small molecule libraries identified fluoxetine, a selective serotonin reuptake inhibitor, as a potent inhibitor of coxsackievirus replication. Fluoxetine did not interfere with either viral entry or translation of the viral genome. Instead, fluoxetine and its metabolite norfluoxetine markedly reduced the synthesis of viral RNA and protein. In view of its favorable pharmacokinetics and safety profile, fluoxetine warrants additional study as a potential antiviral agent for enterovirus infections.

FOOTNOTES

• ↵*Correspondent Information: Paul Krogstad, Dept of Pediatrics, David Geffen School of Medicine at UCLA, 615 Charles, E. Young Drive South, BSRB 173, Telephone 310 825 5235, Fax: 310 206 4764, Email: pkrogstad@mednet.ucla.edu

• Copyright © 2012, American Society for Microbiology. All Rights Reserved.

ME is no more 'in the mind' than Multiple Sclerosis.

http://poultonblog.dailymail.co.uk/2012/09/me-no-more-in-the-mind-than-multiple-sclerosis.html

thank you sooooo much Sonia Poulton

19 September 2012 9:03 PM

ME is no more 'in the mind' than Multiple Sclerosis. When is the world going to get that?

Ever since I first wrote on the subject of Myalgic Encephalomyelitis - or to afford it a more user-friendly title, ME - earlier this year for MailOnline, http://www.dailymail.co.uk/debate/article-2141230/All-mind-Why-critics-wrong-deny-existence-chronic-fatigue.html  I have been overwhelmed by the response from patients and their loved ones.

The over-riding message I have received has been one of gratitude. I can tell you that this is something of an unusual experience for a journalist writing for national newspapers.

These people have Facebook-ed and Tweeted me. I have received calls and e-mails. There have been forums addressing the article and pictures and cards received which outlined a sense of relief for millions of people.

Many of these voices – including some of the greatest scientific, legal and academic minds in the ME world – have echoed a collective sigh to see their illness validated in the media.

The very notion that the media, and the press in particular, can actually serve a positive purpose in society may come as a surprise. But sometimes it does. And my piece, according to the phenomenal response that greeted it, was just one of those times.

Here's why. For decades, people who have suffered the debilitating – and sometimes fatal – condition of ME have been forced into a type of denial.

They have been told that their illness doesn't really exist on the scale that they claim to experience it (due, in part, to it being labelled a 'chronic fatigue syndrome'. A highly controversial description because it creates an image of something substantially less than what ME actually is).

They have been told, repeatedly, to 'pull themselves together' and to 'G.E.T. A G.R.I.P.' (a vile acronym actually used to describe the graded exercise prescribed, wrongly, to ME patients).

In short, it is not enough for people to have to endure serious multi-system issues that can leave them bed-bound for months at a time, but they are also made to feel bad for, well, feeling bad.

What an injustice. 

...


For full article and comments see the website
http://poultonblog.dailymail.co.uk/2012/09/me-no-more-in-the-mind-than-multiple-sclerosis.html

Sinusitis

Er is misschien hoop voor de vele mensen met een chronische snotneus (sinusitis voor de geleerden onder ons). Uit recent onderzoek blijkt dat er een huidbacterie woekert in de neusholtes. Deze zou men niet hoeven te doden met antibiotica of ander zwaar geschut, nee nee een spray met probiotica (meer bepaald Lactobacillus sakei) zou volstaan om de bacterie de kop in te drukken.

Och was alles maar zo eenvoudig op te lossen ...

http://www.standaard.be/artikel/detail.aspx?artikelid=DMF20120918_00300735
http://stm.sciencemag.org/content/4/151/151ra124

The fall of the biopsychosocial model

While both CBT and GET are not often discussed directly in biopsychosocial terms, its alluded to frequently.
GET is of course the bio- part;
CBT (under a presumption of a psychosomatic illness) is the -psycho- part,
and denying patients support and benefits that will enable their illness is the -social part.

Source: http://forums.phoenixrising.me/entry.php?1347-The-Rise-and-Fall-of-the-Biopsychosocial-Model

One Link Established- Chronic Fatigue Syndrome (CFS), Lupus, Fibromyalgia, Autoimmune disease and Chronic Lyme Disease

http://www.envita.com/lyme-disease/finally-one-link-established-chronic-fatigue-syndrome-cfs-lupus-fibromyalgia-autoimmune-disease-chronic-lyme-disease

An Easy Explanation to Idiopathic (unknown Cause of Disease) – But is it the Right One? 

Idiopathic disease is defined as one that develops without any apparent or known causes.  That is the term used for fibromyalgia, autoimmune diseases, including Lupus and Chronic Fatigue Syndrome. While many of these diseases have recognizable signs and symptoms, the lack of causality haunts medical schools, doctors, practices, and hospitals. The only one benefitting from the lifelong symptom treating associated with Chronic Fatigue Syndrome, Lupus, Autoimmune disease, or Fibromyalgia are the pharmaceutical companies who sell billions in medication to treat them. A long list of pain medications, sleep-aids, anti-depressants and anti-inflammatories is not sufficient because the diagnosis is incorrect. So let’s look at what the possible causes are to these diseases.

Here is the conventional Scientific Overview of What Causes (Chronic Fatigue Syndrome) CFS and Fibromyalgia

Below, is a quick list of causes and we will give a clinical review and explanation as to what takes place.

• Brain abnormalities
• Genetic factors (HPA) axis
• A hyper-reactive immune system
• Viral or other infectious agents like (Chronic Lyme disease Complex)
• Psychiatric or emotional conditions

Are Genetics to Blame? Fibromyalgia and Chronic Fatigue Syndrome

Chronic Fatigue Syndrome and Fibromyalgia have been linked with genes involved in the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. These genes regulate response to trauma, injury, and other stressful events. 10 years of Envita’s clinical experience shows that while such traumas could play a role in the etiology (the trigger to exhibiting symptoms) of the disease, they are not likely the causes of these conditions.

What is the HPA (Hypothalamic-pituitary- adrenal axis)?  Does Lyme Disease Play a Role?

HPA makes up a multi-set of direct influences and feedback interactions among the hypothalamus, the pituitary gland (a pea-shaped structure located below the hypothalamus), and the adrenal, also called “suprarenal,” glands which are small, conical organs on top of the kidneys.
The interactions among these organs constitute the HPA axis, a major part of the neuroendocrine system that controls reactions to stress and regulates many body processes including digestion, the immune system, mood, emotions, sexuality, as well as energy storage and expenditure. Infectious disease, such as chronic Lyme Disease Complex, impacts the HPA-axis via neurotoxins that compete for the same receptor sites used by the HPA-axis. In fact, such infections can bring about identical symptoms of some idiopathic diseases listed above and many of the symptoms associated therewith. This should bring our attention to the Lyme Disease Complex, which is composed of a number of infections and neurotoxins that bring about even more symptoms than those listed earlier in this article.

Does HPA Affect Fibromyalgia and Chronic Fatigue Syndrome?

Abnormal levels of certain chemicals regulated in the HPA axis area of the brain system, have been proposed as a cause of Chronic Fatigue Syndrome and also have some influence in Fibromyalgia. This system controls important functions, including sleep, stress response, and depression. Of particular interest to researchers, are the chemicals and other factors listed below that are controlled by the HPA axis.
The HPA axis is involved in the neurobiology of mood disorders and functional illnesses, including anxiety disorder, bipolar disorder, insomnia, post-traumatic stress disorder, borderline personality disorder, ADHD, major depressive disorder, burnout, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome, and alcoholism. Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA axis function. All of these conditions and their symptoms are commonly seen in Chronic Lyme disease patients that contain a host of infections and neurotoxins that block serotonin receptors in the brain.

How Can Chronic Lyme Disease Complex or Infectious Disease Affect HPA?

Patients may have contracted an infection at any point in their life-time; however, the symptoms of Chronic Lyme disease Complex or its co-infections may remain unseen or dormant until the individual is weakened by a trauma or trigger. This could be anything from child birth or a car accident to the death of a loved one, a divorce, or even a vaccine as seen among children with weakened immune systems.
In the etiology of chronic infectious disease, the traumatic event is a trigger but not the cause of autoimmune disease, Chronic Fatigue Syndrome, or Fibromyalgia. Nevertheless, treating these triggers is critically important to the new patient’s care. What we find is that infection and not genetic defects are at the root of HPA axis disruption in the brain itself.

The Major Impact of Epigenetic Changes

A number of studies have found that alterations in genes are caused by infections involving immune function, intercellular communication and energy transfer.
Researchers have identified many different genes in patients with Chronic Fatigue Syndrome that relate to blood disease, immune system function, and infection. However, despite these identifications, there is no clear pattern to them and it is quite possible that it is the infections alone that are altering these genes and are responsible for impacting mental and emotional health as well. It is very possible that the infections can alter these genes that impact mental and emotional health as well.

Important Neurotransmitters Changed by Neurotoxins Competing for Receptor Sites

Some patients with Chronic Fatigue Syndrome have abnormally high levels of serotonin – a neurotransmitter (chemical messenger in the brain), and also show deficiencies in dopamine – an important neurotransmitter associated with feelings of reward. In some cases there is also a demonstrable imbalance between norepinephrine and dopamine.
A number of studies on Chronic Fatigue Syndrome have shown patients with lower cortisol levels, a stress hormone produced by the adrenal glands. It has been suggested that such cortisol deficiencies are responsible for Chronic Fatigue Syndrome patients having impaired or weakened responses to psychological or physical stresses like worry, infection, or exercise. However, administering replacement cortisol improves symptoms only in some patients. Why? Infection and their toxins (neurotoxins) must be cleared before hormone replacement can begin to be effective in these patients. It is also common for these patients to have thyroid, testosterone and cortisol issues.

Idiopathic Diseases are at the Root of Many Psychological Disorders: Sleep disorders Explained

Evidence suggests that certain CFS, Fibromyalgia, and Autoimmune patients have disturbed circadian rhythms (disorder of the sleep-wake cycle), which is regulated by the so-called circadian clock, a nerve cluster in the HPA axis. These are commonly seen in Lyme Disease Complex along with a number of other neurological symptoms.
A mentally or physically stressful event, such as a viral infection, may disrupt natural circadian rhythms. An inability to reset these rhythms results in a perpetual cycle of sleep disturbances. Medications that improve sleep can be very helpful for certain patients with Chronic Fatigue Syndrome, Fibromyalgia, and Autoimmune diseases. But, until the infections are cleared and hormones are rebalanced, long-term improvement is unlikely.
Psychological, personality, and social factors are strongly associated with Chronic Fatigue Syndrome, Fibromyalgia, and Autoimmune disease like Lupus. There is a distinct complex relationship between physical and emotional factors.

What Specific Infections are Responsible

Because most of the features of Chronic Fatigue Syndrome resemble those of a lingering viral illness, many researchers have focused on the possibility that a virus or some other infectious agent, in some cases, causes the syndrome.
At Envita, we have clinically determined that these patients usually have a group of viral, bacterial, parasitic, and fungal infections that make up what we call Lyme Disease Complex. Some patients may or may not have actual Lyme disease but may have another type of tick-borne illness along with a host of co-infections that have brought about immunological, hormonal, and neuroendocrine changes.
Still, not all Chronic Fatigue Syndrome patients show signs of infection. And although experts have long been divided on whether infections play any role in this disorder at all, it does seem clear that subtypes of both viral and non-viral Chronic Fatigue Syndrome exist. That being said, researchers have seemingly overlooked the complexity of mute-infections, multi-toxins, and heavy metal components that complicate these conditions making them extremely difficult to diagnose on a case to case basis. When a complex of infections exists, they can affect the activation and replication of each other via biofilm communities. To be certain, most patients are never tested thoroughly and correctly for all the infections that make up, chronic Lyme Disease Complex.

Infections, Looking More Like the Cause

The theory for Chronic Fatigue Syndrome having a viral cause is not based on hard evidence, rather, on an ever-growing series of observations that suggest this association:
Chronic Fatigue Syndrome as well as Fibromyalgia and Autoimmune disease patients are often found with elevated levels of antibodies to many organisms that cause fatigue and other Chronic Fatigue Syndrome symptoms. Such organisms include those that cause Lyme disease, Candida (“yeast infection”), herpes virus type 6 (HHV-6), human T cell lymph tropic virus (HTLV), Epstein-Barr, measles, coxsackie B, cytomegalovirus, or parvovirus.
Many of these infectious agents are very common; however, none have emerged as a definitive cause of CFS. Well-designed studies of patients who met strict criteria for CFS without any known cause have not found an increased incidence of any specific infection(s).
In up to 80% of cases, CFS starts suddenly with a flu-like condition. In the U.S., there have been reports of cluster outbreaks of CFS occurring within the same household, workplace, and community (but most have not been confirmed by the Centers for Disease Control and Prevention). However, most cases of CFS occur sporadically in individuals, and do not appear to be contagious. These all have the pattern of infections and more importantly, complexes of infections taking over the patient’s immune system, which is clearly seen in the depressed CD57 markers found in almost all of this population.

Infection Complexes Leading to Immune System Abnormalities and Immuno-Compromised States

CFS is sometimes referred to as “Chronic Fatigue Immune Dysfunction Syndrome.” In many cases, studies have detected many immune system irregularities. Some components appear to be over-reactive, while others appear to be under-reactive, but no consistent picture has emerged to explain CFS as a disease of the immune system in conventional medical practices. Chronic Lyme Disease patients almost always have depressed CD57 marker called the striker panel and this is almost never run on chronic fatigue patients when they go to their doctor. Almost 100% of the time we find decreased key immune function in all CFS patients because we are running the correct diagnostics.

Environmental Toxins Impact Chronic Fatigue Syndrome and Fibromyalgia

Some studies have reported that a majority of CFS patients have allergies to foods, pollen, metals (such as nickel or mercury), or other substances. One theory is that allergens, like viral infections, may trigger a cascade of immune abnormalities leading to CFS. However, most allergic people do not have CFS. In our clinical setting, patients often have pesticide, heavy metal and chemical toxicity along with chronic infections which explains the abnormal and inconstant responses to allergies. Environmental toxins complicate these conditions and require targeted treatments to overcome them.

Autoimmunity Overlaps with other Conditions

The risk profile for CFS is similar to the risk profiles for a number of autoimmune diseases. Studies are inconsistent with regards to the presence of auto-antibodies (antibodies that attack the body’s own tissues) in CFS, so the disease is unlikely to be due to auto-immunity – making it more likely connected to infectious disease. In Lyme disease patients, we typically see that the patient was diagnosed at one time or another with several autoimmune diseases but almost certainly the previous physicians were confused.

Where Can You Find Help?

Envita Medical Centers has been leading the way in comprehensive, personalized patient care.  Contact us for more information. We will answer any health questions you may have.

http://www.envita.com/lyme-disease/finally-one-link-established-chronic-fatigue-syndrome-cfs-lupus-fibromyalgia-autoimmune-disease-chronic-lyme-disease

The Invitation by Oriah

It doesn’t interest me
what you do for a living.
I want to know
what you ache for
and if you dare to dream
of meeting your heart’s longing.

It doesn’t interest me
how old you are.
I want to know
if you will risk
looking like a fool
for love
for your dream
for the adventure of being alive.


It doesn’t interest me
what planets are
squaring your moon...
I want to know
if you have touched
the centre of your own sorrow
if you have been opened
by life’s betrayals
or have become shrivelled and closed
from fear of further pain.


I want to know
if you can sit with pain
mine or your own
without moving to hide it
or fade it
or fix it.


I want to know
if you can be with joy
mine or your own
if you can dance with wildness
and let the ecstasy fill you
to the tips of your fingers and toes
without cautioning us
to be careful
to be realistic
to remember the limitations
of being human.


It doesn’t interest me
if the story you are telling me
is true.
I want to know if you can
disappoint another
to be true to yourself.

If you can bear
the accusation of betrayal
and not betray your own soul.
If you can be faithless
and therefore trustworthy.


I want to know if you can see Beauty
even when it is not pretty
every day.
And if you can source your own life
from its presence.


I want to know
if you can live with failure
yours and mine
and still stand at the edge of the lake
and shout to the silver of the full moon,
“Yes.”


It doesn’t interest me
to know where you live
or how much money you have.
I want to know if you can get up
after the night of grief and despair
weary and bruised to the bone
and do what needs to be done
to feed the children.


It doesn’t interest me
who you know
or how you came to be here.
I want to know if you will stand
in the centre of the fire
with me
and not shrink back.


It doesn’t interest me
where or what or with whom
you have studied.
I want to know
what sustains you
from the inside
when all else falls away.


I want to know
if you can be alone
with yourself
and if you truly like
the company you keep
in the empty moments.


By Oriah © Mountain Dreaming,
from the book The Invitation
published by HarperONE, San Francisco,
1999 All rights reserved

http://www.oriahmountaindreamer.com/

Chronic diseases can stem from infectious agents

Evidence now confirms that noncommunicable chronic diseases can stem from infectious agents. Furthermore, at least 13 of 39 recently described infectious agents induce chronic syndromes.

Identifying the relationships can affect health across populations, creating opportunities to reduce the impact of chronic disease by preventing or treating infection. As the concept is progressively accepted, advances in laboratory technology and epidemiology facilitate the detection of noncultivable, novel, and even recognized microbial origins. 

A spectrum of diverse pathogens and chronic syndromes emerges, with a range of pathways from exposure to chronic illness or disability. Complex systems of changing human behavioral traits superimposed on human, microbial, and environmental factors often determine risk for exposure and chronic outcome. Yet the strength of causal evidence varies widely, and detecting a microbe does not prove causality.

Nevertheless, infectious agents likely determine more cancers, immune-mediated syndromes, neurodevelopmental disorders, and other chronic conditions than currently appreciated.

full paper
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291059/