Lijdt uw kind aan ME, fibromyalgie, autisme of ADHD?

Er is een nieuwe Nederlandse ME website voor (ME) ouders met kinderen

www.everyoneweb.com/KinderenmetME/


De oprichter van de website nodigt u uit voor het besloten ouder FORUM: http://gratisforums.com/ouderskinderenmetme/

Problemen in verband met jeugdzorg kunnen hier besproken worden.



Jongeren van 15-25 jaar kunnen zich aanmelden op het besloten Jongeren FORUM : http://gratisforums.com/mejongerenforum/

Er zal tzt een FORUM worden opgestart voor 10-15 jarige die onder begeleiding daar kunnen praten.

Hoe gebruik je de ontstekingsremmer en pijnstiller Normast?

Normast oftewel palmitoylethanolamide is een natuurlijke ontstekingsremmer die in elke cel van ons lichaam aanwezig is.

Palmitoylethanolamide (PEA) wordt in ons lichaam zelf aangemaakt als antwoord op virale infecties, ontstekingen en pijnen. Door het aan te vullen help je dus de natuurlijke afweer van het lichaam te versterken.

Normast wordt in pijnklinieken gebruikt om chronische pijn te behandelen zonder veel neveneffecten. Honderden studies hebben de efficiëntie inmiddels bewezen. Bovendien is er geen interactie met andere medicatie zoals cortisone, de spierverslapper Baclofen, ...
MS, diabetes, hernia, neuropathie, fibromyalgie, ruggemergtrauma, endometriosis, het syndroom van Costen of het temperomandibulair syndroom (TMD) enz. zijn maar enkele aandoeningen die gebaat blijken te zijn met de stof PEA.


PEA vermindert:


1.de ontstekingsreacties in het ruggenmerg,
2.de neutrofiele celinfiltratie,
3.de productie van nitrotyrosine,
4.de expressie van proinflammatoire cytokines,
5.de kappa-B activiteit,
6.de expressie van stikstofmonoxide synthase, en
7.de apoptosis.


Vroeger werd het verhandeld onder de naam Impulsin. Nu kan je het vrij verkrijgen als supplement.
Best is je huisarts te betrekken bij je beslissing om deze stof te 'consumeren'.

Protocol:


Voor nieuwe gebruikers van Normast is het wenselijk om te beginnen met een starterprotocol van 50 dagen.


Het starterprotocol bestaat uit;

- één verpakking Normast 600 mg, 20 sachets

- vier verpakkingen Normast 600 mg, 20 tabletten

De eerste 10 dagen dient er, vanwege de snelle orale opname in het mondslijmvlies, tweemaal per dag een sachet met poeder te worden genomen.

De poeder langzaam laten smelten onder de tong, en zo min mogelijk doorslikken.

Na tien dagen wordt er overgegaan naar tweemaal daags één tablet. Neem de sachets en tabletten een uur voor of na een maaltijd in met ongeveer 12 uur verschil tussen de tijdstippen van inname.

Pas na vijftig dagen kan de werking van Normast goed beoordeeld worden en wordt het duidelijk of langer gebruik zinvol is.

Indien de pijn duidelijk is verminderd in deze eerste periode kan worden overgegaan op een lagere vervolg- of onderhoudsdosering van twee tabletten 300 mg Normast per dag.

Deze tabletten ook weer een uur voor of na een maaltijd innemen met ongeveer 12 uur verschil tussen de tijdstippen van inname.

Het vervolgprotocol bestaat uit vijf verpakkingen met 30 tabletten Normast 300 mg, voldoende voor 75 dagen.

Mochten gedurende het vervolggebruik de pijn en eventuele andere ongemakken toch weer toenemen, bestel dan nog een doos met Normast sachets en neem weer tien dagen de poeder onder de tong. Meestal neemt de pijn dan weer af.

Iedere patient moet in overleg met de behandelend arts individueel vaststellen of twee 300 mg tabletten voldoende is als onderhoud of dat toch meer nodig is. Ervaring leert, dat de werking van Normast bij iedere patiënt verschillend is.

Sommige patiënten hebben al baat bij de inname van tweemaal een tablet van 300 mg Normast per dag.

Andere patiënten hebben een hogere dosering nodig, bijvoorbeeld tweemaal daags tabletten van zowel 600 mg als 300 mg tegelijk, dus 900 mg per dag.

Het resultaat van het gebruik van Normast is bij elke patiënt dan ook verschillend.

De ene patiënt heeft al reductie van de pijn binnen één week nadat is begonnen met de inname van Normast, terwijl de andere patiënt deze reductie van de pijn pas na ruim een maand ervaart.

Raadpleeg altijd de huisarts bij de beslissing ten aanzien van het gebruik van Normast en ten aanzien van een van de bovenstaande adviezen voor de dosering van Normast.

Informeer uw huisarts eveneens over het resultaat van het gebruik van Normast, zodat met het doorgeven van deze kennis ook lotgenoten geholpen kunnen worden.


Prof. dr. Jan M. Keppel Hesselink, behandelend arts, januari 2011

Wat kost het? Voor een doosje van 20 sachets van 600 mg betaal je gemiddeld 30 euro + 4 euro verzendkosten.

Waar te bestellen? http://www.ergomax.nl/Normast_600mg_Microgranules_Ergomax.html

Hoe smaakt het? Het is een héél fijn poeder dat onder de tong vrij snel smelt. Het smaakt een beetje zoetig.

In de pijnkliniek te Soest, Nederland hebben ze de analyse, die Numbers Needed to Treat heet, ook op Normast losgelaten, en voor de 600 mg dosis twee maal daags is dat getal 2. Dat wil zeggen 50% van de mensen met veel pijn baat zullen hebben van Normast, maar de andere helft dus niet.

Eén kans op twee dus, de moeite waard. Vooral als je in gedachten houdt dat er vrijwel geen bijwerkingen optreden. Gewoon proberen dus. Als je na 50-60 dagen niets merkt, stop er dan mee of vraag aan je arts een voorschrift Algonerv crème. Daar zit ook PEA in maar oppassen, het bevat tevens capsaicine. Multiple Chemicle Sensitivity (MCS) patienten kunnen daar duidelijk niet tegen.
De crème kan een warmtegevoel geven de eerste dagen van gebruik.




Bronnen:

http://www.iocob.nl/multiple-sclerose/pijn-en-spasmen-bij-ms-behandeld-met-de-lichaamseigen-stof-palmitoylethanol.html

http://www.neuropathie.nu/ciap-chronische-neuropathie/50-jaar-getrouwd-ciap-en-revitalisatie-2.html

http://www.iocob.nl/ziekten/natuurlijk-middel-palmitoylethanolamide-werkzaam-bij-griep-proph-4.html

http://www.prohealth.com/library/showarticle.cfm?libid=15942


“Ik kan door ME zelf niet altijd meer zo vrolijk zijn, niet na wat ME ziekte ME heeft aangedaan.” door Catryn V

Statins kill your immunity

De uitslag van het labo liegt er niet om. Uw cholesterol is veel te hoog. U behoort misschien tot de categorie patienten die wegens een genetische afwijking in de familie teveel cholesterol produceert.

Men spreekt van familiale hypercholesterolemie als:

Onder de 16 jaar
- je totale cholesterolwaarden hoger zijn dan 6,7 mmol/l
- je LDL waarden hoger zijn dan 4,0 mmol/l
Volwassenen
- je totale cholesterolwaarden hoger zijn dan 7,5 mmol/l
- je LDL waarden hoger zijn dan 4,9 mmol/l

EN

- er in de tweede graad een geval van hartinfarct heeft voorgedaan voor de leeftijd van 50 jaar of
- er in de eerste graad een geval van hartinfarct heeft voorgedaan na de leeftijd van 60 jaar

OF

- een totale cholesterol hoger dan 7,5 mmol/l in de eerste of tweede graad
- een totale cholesterol hoger dan 6,7 mmol/l bij een kind < 16 jaar

The Dutch Lipid Clinic Network neemt ook het criterium tendinous xanthomata in overweging. Dat zijn kleine vetafzettingen op de pezen ter hoogte van de achillespees, knokkels op de handen en ellebogen.
Mensen die statines nemen, zien deze vetafzettingen na verloop van tijd weer verdwijnen. Kinderen zijn te jong om ze te hebben.

Als er meerdere mensen in je familie systematisch een te hoge cholesterol hebben en je leefwijze is gezond, dan is de kans groot dat je te maken hebt met een genetische afwijking.
Tot hiertoe heeft men drie dna-afwijkingen in kaart gebracht; de ldl receptor mutatie, de familiale defectieve apo B-100, en de PCSK9 mutatie.

In Engeland registreren ze deze patienten bij “The Simon Broome Familial Hyperlipidaemia Register”.
Eén op 500 mensen zou een defect gen van één van zijn ouders hebben meegekregen. De overlevingskansen van deze mensen liggen statistisch gezien wat lager. Mannen maken 50% meer kans op een hartaanval als ze 50 jaar oud zijn. Vrouwen hebben meer geluk, slechts 30% meer kans als ze 60 jaar oud zijn. Ik heb dus nog een paar jaar te gaan. Niet te verwonderen dat de verzekeringen je niet meer willen verzekeren of tegen een fikse surpremie.

Wetenschappers en dokters spreken graag van goede (HDL) en slechte (LDL) cholesterol. Eigenlijk zijn ze beide goed want als we geen slechte cholesterol hadden, bloedden we dood. De taak van LDL is gaatjes dichten in de bloedvaten.
Cholesterol hebben we nodig voor:

• de aanmaak van hormonen zoals testosteron, oestrogeen, progesteron en het groeihormoon DHEA;
• de aanmaak van cortisol, dat houdt de immuunbalans in evenwicht. Langdurig zieken hebben te weinig cortisol;
• de aanmaak van vitamine D, dat gaat ontstekingen te lijf. Je verbruikt het extra als je ziek bent;
• als anti-oxidant, en dat zorgt ervoor dat het immuunsysteem zijn defensie niet moet opstellen bij het ontmoeten van een indringer;
• om de celmembranen te stabiliseren. Als die in onevenwicht zijn, gaat de cel teveel vocht opnemen en stort het lichaam na verloop van tijd in;
• de omzetting van Q10. Dat is benzine voor de motor (mitochondria) van je cellen. Ze zetten voedsel om in energie. De mitochondria werken niet goed bij ME.

Maar met de cijfers hierboven, kunnen ze die boodschap niet meegeven. Bovendien zijn de officiële waarden waarbinnen uw cholesterol moet vallen, de laatste jaren stelselmatig naar beneden gehaald. Uw cholesterol zal en moet naar beneden gaan.

Het team gerespecteerde specialisten dat wereldwijd de normen herdefinieerde, bleek nauwe banden te hebben met de statines-producerende industrie. Acht van de negen leden hadden directe financiële belangen. Ze bezaten aandelen, gingen voor de respectievelijke bedrijven werken, zaten in de directie. Men kan zich afvragen in hoeverre deze adviseurs nog onafhankelijk waren. Het leven van miljoenen mensen wordt rechtstreeks beïnvloed door hun beslissing. Wetenschappelijk onderzoek in het algemeen is verre van onafhankelijk. Het merendeel van de experimenten aan de universiteiten wordt nu reeds gesponsord door de privé-fondsen.
Bron: http://www.usatoday.com/news/health/2004-10-16-panel-conflict-of-interest_x.htm

Uw specialist bekijkt uw blad met piekende cholesteroluitslagen dus meewarig en zegt voor de zoveelste keer dat het tijd wordt om medicatie te gaan nemen. Statines. De NICE guidelines heeft er haast 250 pagina's aan besteed, een ware lofzang. Geen scheef woord over die mirakelpillen staat erin beschreven. Alleen zwangere vrouwen mogen het niet nemen omdat het afwijkingen geeft aan de foetus. Heb ik even geluk gehad 18 jaar geleden tijdens mijn eerste zwangerschap. Mijn oudste heeft het heelhuids overleefd en blijkt bovendien hoogbegaafd en atletisch te zijn. Maar het was wel schrikken want die zwangerschap was niet echt duidelijk de eerste maanden.

De huisarts schreef anno 1990 statines voor en een dieet met weinig vlees en vet. Angstvallig wordt elke lepel mayonaise en teveel aan broodbeleg vermeden. Klanten kijken in mijn bord en vragen of ik vegetariër ben. Een bord rijkelijk gevuld met groenten. Zo ploeteren we voort, jarenlang. Zonder het te beseffen, ontzeg ik mezelf een belangrijke bron van vitamine B12. De cholesterol daalt wel maar niet drastisch. Op een dag besluit ik de statines te laten vallen. Het dieet met een minimum aan vetten zette ik voort, dat was inmiddels een levenswijze geworden.

Mijn gezondheidstoestand is inmiddels zo verergerd dat ik na het werk total loss op de zetel lig en de eerste uren niet meer bij bewustzijn ben of in staat om te reageren op mijn omgeving. Elke zaterdagochtend draait dezelfde film. Mama gaat naar de winkel, komt thuis, zet de boodschappentas voor de koelkast en tegen de avond ligt ze nog steeds in bed om bij te komen van deze inspanning. Op mijn opnameformulieren van het ziekenhuis staat genoteerd dat ik de schuld geef aan de statines. Telkens ik die pillen erbij slik, wordt het erger. Ik kan niet eens meer blokje rond rijden met de fiets. Mijn beenspieren lijken wel van lood.

De bijsluiter in het doosje van uw medicijn zal het u vertellen. Alle mogelijke neveneffecten dat een mens kan krijgen, staan netjes gerangschikt in minuscule lettertjes. Hoofdpijn, vermoeidheid, spierpijnen, leververgiftiging, bedenk het maar. Het zal vermeld staan. Zwangere vrouwen en kinderen worden gewaarschuwd. Uw dokter heeft een bijbel met duizenden namen van medicijnen om zich te informeren. Medisch afgevaardigden komen met de regelmaat van de klok langs om hen op de hoogte te brengen van de laatste ontwikkelingen in het landschap van de farma-industrie. Congressen worden gesponsord als ware het trouwfeesten met gratis eten en drank. Het geld vloeit rijkelijk. Er wordt niet gekeken op een servetje.

Maar wat deze medicatie echt met een mens doet, dat staat niet in de NICE-guidelines. Dat lees je niet in de bijsluiter. Dat zal de vertegenwoordiger niet komen vertellen. Je moet het zelf gaan zoeken. 

Statines maken je immuniteit kapot en het bewijs zal ik u geven in een volgend artikel. Het zou me verbazen dat de heren onderzoekers en ontdekkers van de statines dit niet wisten.

Hoog tijd dat statines een belangrijke waarschuwing krijgen in de bijsluiter.

Dag 449 Planten

De energie blijft pieken. Ik laat me verleiden tot een dans met een natte zwabber en de stofzuiger helpt een handje mee. De wasmachine draait een toer extra. De was wappert vrolijk aan de wasdraad. Tegen de middag heb ik meer werk verzet dan de afgelopen week tezamen.

De vermoeidheid trekt tegen dan als een magneet mijn gewicht naar de aarde. Mijn matras is een welgekome rustplek. Het waait te hard voor de hangmat vandaag.

In de late namiddag staat een vriendin aan de deur om samen planten te gaan kiezen. Vlakbij is het uitverkoop van plantjes en ik heb mijn oog laten vallen op een perzikenboompje, een hazelnotenstruik, een paar vlinderstruiken en meer van dat moois.

Samen smeden we plannen om die woestenij in de tuin om te toveren. Ze heeft heel leuke en haalbare ideeën. Alles lijkt zo vanzelfsprekend en soms vergeet men zelfs zijn ziekte. Totdat je de plantjes in de grond mag steken. Delegeren gaat me gelukkig goed af. Jammer dat het plezier van zelf iets te kunnen verwezenlijken er zo bij inschiet.

Dag 448 Spieren

Nieuwe reeks powerbaxters in het dagziekenhuis. De eerste verpleegster prikt verkeerd. Mijn aders lopen nochtans als blauwe rivieren rijkelijk onder mijn huid. De tweede verpleegster blijkt een botte naald te hebben. Dit heb ik nog niet eerder meegemaakt, de naald prikt niet eens door mijn vel.
Een martelpoging komt in de buurt van deze prikoperatie en ik vraag met aandrang de procedure stop te zetten en de zetel plat te leggen. Mijn huidskleur zou de gelijkenissen met een melkfles doorstaan hebben. De bloeddruk wordt voor de zekerheid gemeten en bevestigt de kleur, 8 op 5.

Ik blijf ondanks de pogingen gemotiveerd vanwege de vorige baxtersessies. Ze gaven me 24 uur extra energie en minder ziektegevoel. De internist opperde dat in een ideale wereld ik twee weken continue aan een infuus zou moeten hangen om beter te kunnen worden. Waarom niet 's nachts een baxter en dan overdag kunnen leven ...

Volgens zijn laatste testen mis ik 5,5 kilo spiermassa om aan mijn minimumgewicht te komen. Qua vet- en vochtgehalte was het in orde.

Dag 447 Geheugen

Honderden keren heb ik mijn telefoon mislegd, afspraken met vriendinnen vergeten, ontelbare rekeningen verkeerd en/of te laat betaald, de namen van mijn eigen kinderen en ex-collega's door elkaar gehaald, me afgevraagd in welk jaar en welke maand we nu toch alweer waren, wie dat vertrouwde gezicht toch zou kunnen zijn, dagelijks google gebruikt om te weten hoe je een woord weer moest schrijven, cognitieve testen afgelegd die bevestigden dat mijn geheugen een slag van de molen had gekregen, telkens opnieuw moeten vragen wat men nu eigenlijk bedoelde, geen 7 + 17 kunnen optellen uit mijn hoofd, ...


En toch maakte het me niet bang, ik werd er alleen maar boos om. Vandaag is dat gevoel veranderd. Hubby zei me doodleuk dat hij vanaf morgen drie dagen weg zou zijn vanwege een cursus. Hij zou me dit verteld hebben. Ik val uit de lucht. Geen boze gevoelens als herinnering. Mijn fysiek en emotioneel geheugen laat me volledig in de steek. Wat overblijft is een zwart gapend gat.

Dag 446 Wegenwerken

Zolang ik tussen de lijntjes kleur, functioneer ik vandaag. Liggen, braaf zijn en een paar uren bewegen. Een vriendin wil de jongste wel opvangen tijdens de middag, dat bespaart me een uur minder in de file staan met de wegenwerken voor de deur. She saves my day. De gemeente mag een helikopter inlassen wat mij betreft om de 2 km te overbruggen de komende maanden.

The PACE Trial “did not study CFS/ME patients dixit prof Peter White

18th May 2011

On 17th May 2011 Zoe Mullan, Senior Editor at The Lancet, sent an email to Professor Hooper in response to the complaint he submitted about the PACE Trial article published online by The Lancet on 18th February 2011 and subsequently in the journal on 5th March 2011. In her email, Zoe Mullan wrote: “We asked the authors of the PACE trial to respond to your concerns, which they have duly done. Your complaint and their response were discussed at the highest management level and this group of executive editors was fully satisfied that there were no grounds whatsoever on which to take further action. We attach the response provided to us here. From an editorial perspective, the case is now closed”.

The undated response to Professor Hooper’s complaint by Professors White, Sharpe and Chalder that was sent to Dr Richard Horton (Editor-in-Chief of The Lancet) on behalf of all the co-authors will, in the interests of openness and transparency, be placed in the public domain and will be fully addressed in due course, as will Professor Hooper’s concerns over what he believes is the failure of The Lancet’s editorial process in this instance, but there is one point in Professor White’s letter that is of particular importance, so it is addressed in this initial response.

In their letter, Peter White et al state: “The PACE trial paper refers to chronic fatigue syndrome (CFS) which is operationally defined; it does not purport to be studying CFS/ME”.

The sentence continues by stating that the PACE Trial studied: “CFS defined simply as a principal complaint of fatigue that is disabling, having lasted six months, with no alternative medical explanation (Oxford criteria)”.

This is exactly what the ME/CFS community has been saying from the outset, namely that the PACE Trial was not studying those with ME.

Soon after the Oxford criteria were published in 1991, one of the co-authors, psychiatrist Anthony David, wrote in the British Medical Bulletin: ““British investigators have put forward an alternative, less strict, operational definition which is essentially chronic…fatigue in the absence of neurological signs, (with) psychiatric symptoms…as common associated features” (AS David; BMB 1991:47:4:966-988).

Given that ME is a classified neurological disorder (ICD-10 G93.3), there thus ought to have been no dispute that the PACE Trial Investigators were not studying those with ME, but the Investigators have persistently confirmed that they were studying those with ME, for example:

1. The PACE Trial Identifier is clear: “Myalgic encephalomyelitis is thought by most to be synonymous with CFS” (PACE Trial Identifier; 2.1). The cited references for this statement are given as (i) Fukuda K et al. The chronic fatigue syndrome: a comprehensive approach to its definition and study. Ann Intern Med 1994; 121: 953-959; (ii) Sharpe MC et al. A report – chronic fatigue syndrome. JR Soc Med 1991; 84: 118-121; (iii) Wessely SC et al. Chronic fatigue and its syndromes. Oxford, Oxford University Press, 1998; (iv) Working group report to the Chief Medical Officer, www.doh.gov.uk/cmo/cfsmereport 2002 and (v) NHS Centre for Reviews and Dissemination. Interventions for the management of CFS/ME. Effective Health Care 2002; 7(4): 1-12.

2. The two versions of the PACE Trial Protocol (both the Full Protocol and short version that was published in BMC Neurology 2007:7:6) are equally clear; the PACE Trial was: “A randomised controlled trial of adaptive pacing, cognitive behaviour therapy, and graded exercise as supplements to standardised specialist medical care versus standardised specialist medical care alone for patients with the chronic fatigue syndrome/myalgic encephalomyelitis or encephalopathy”.

3. In the Glossary to the Full Protocol, Professor White et al specifically state that CFS/ME is the official term for the illness described in the “Working Group Report to the Chief Medical Officer (2002) and the MRC RAG Report (2003)”.

4. In the PACE Trial Patient Clinic Leaflet, Professor White et al state: “This illness is also known as post-viral fatigue syndrome, myalgic encephalomyelitis (ME) and myalgic encephalopathy (ME). Medical authorities are not certain that CFS is exactly the same illness as ME…but we will be calling this illness CFS/ME”.

In The Lancet article itself, Peter White et al use the term myalgic encephalomyelitis throughout the text and actually state: “Myalgic encephalomyelitis is thought by some researchers to be the same disorder….Several diagnostic criteria exist for chronic fatigue syndrome and myalgic encephalomyelitis”, thus implying that they had indeed studied those with ME.

Moreover, in the authors’ reply published in the Lancet on 17th May 2011 (The PACE trial in chronic fatigue syndrome – Authors’ reply), Peter White is unambiguous: “…however we defined CFS and myalgic encephalomyelitis, we found that cognitive behaviour therapy and graded exercise therapy provided a significant and clinically useful advantage….”.

Here, though, Professors White, Sharpe and Chalder have categorically stated that the PACE Trial “does not purport to be studying CFS/ME”.

This may explain why so many recruits were not accepted into the PACE Trial on the stated grounds they did not fulfil the Oxford criteria for “CFS” (which according to the Principal Investigators themselves, is not the same as “CFS/ME”).

If the PACE Trial was not studying CFS/ME (as now asserted by Professor White et al), then the results cannot be used by NICE to support its Clinical Guideline 53 for CFS/ME.

NICE, however, announced on 14th March 2011 that there will be no review of CG53 until 2013: “…interventions recommended in the original guideline, such as CBT and GET, were described as the interventions for which there is the clearest evidence-base of benefit. This is supported by the recently published PACE trial….The results of the study are in line with current NICE guideline recommendations on the management of CFS/ME….There are no factors…which would invalidate or change the direction of the current guideline recommendations. The CFS/ME guideline should not be updated at this time”.

Most certainly, this statement by the Principal Investigators that the PACE Trial did not purport to be studying those with CFS/ME raises important issues about the alleged generalisability of the PACE Trial results, given that The Lancet article unambiguously states: “The PACE findings can be generalised to patients who also meet alternative diagnostic criteria for chronic fatigue syndrome and myalgic encephalomyelitis but only if fatigue is their main symptom”.

That The Lancet supports the Principal Investigators’ inconsistent and indefensible position and refuses to engage with clearly articulated complaints must be of concern to anyone interested in the integrity of the scientific process.

Glyphosate found to infect plants with AIDS-like disease, animals and people victim too

Remember my blog on glyphosate a few days ago?

Monsanto pesticide found to infect plants with AIDS-like disease


Wednesday, May 18, 2011 by: Ethan A. Huff, staff writer

When Dr. Don Huber, professor emeritus at Purdue University and internationally-recognized plant pathologist, wrote a letter back in January to US Department of Agriculture (USDA) Secretary Tom Vilsack, warning him about a new mystery disease showing up primarily in genetically-modified (GM) crops, the notice fell on deaf ears.

Research conducted by a team of senior plant and animal scientists found that Monsanto's glyphosate chemical, which is the primary ingredient in its popular RoundUp herbicide formula, appears responsible for infecting plants with an AIDS-like syndrome that destroys their immunity, blocks their absorption of certain vitamins and minerals, and eventually kills them.

Dr. Huber explains in his letter that the destruction caused by glyphosate does not appear limited to plants, either -- animals and humans alike that consume foods tainted with the chemical, or that are exposed in some other way to it, are potentially susceptible to developing the same autoimmune disorder. For this reason, Dr. Huber urged the USDA to further investigate RoundUp, as well as to deny the deregulation of GM alfalfa.

You can read a copy of Dr. Huber's letter for yourself here:

http://es-la.facebook.com/notes/wood-prairie-farm/the-complete-text-of-dr-don-m-hubers-letter-to-usda-secretary-vilsak/197340006962367

The key factor of Dr. Huber's discovery was a microscopic pathogen specifically prevalent in GM crops. The pathogen, he explained in an interview with Food Democracy Now! (FDN) as well as in his letter, is common. But an apparent weakening of plant immunity by glyphosate makes plants treated with the chemical more susceptible to contracting the harmful pathogen. And as a result of exposure, large swaths of GM farmland have died, and many animals that feed on GM-tainted meal have become infertile or have had abortions.

But instead of listening to the scientifically sound advice of Dr. Huber and withholding deregulation of GM alfalfa until more intense safety studies could be conducted, the USDA decided to ignore it all and approve the "Frankencrop" anyway.

To watch the full video interview between FDN and Dr. Huber, visit:
http://vimeo.com/22997532

Sources for this story include:
http://www.bnet.com/blog/food-indus...


Bron: www.naturalnews.com/032441_pesticide_AIDS.html#ixzz1NTZhwhhs

The Prevalence and the Effect of Anti-TNF-α Treatment

Everyday Cognitive Failure in Sarcoidosis: The Prevalence and the Effect of Anti-TNF-α Treatment


Marjon D. Elffericha–c, Patty J. Nelemansa, f, Rudolf W. Pondsa, d, Jolanda De Vriesa, g, Petal A. Wijnena, e, Marjolein Drenta, caild care center and Departments of Physical Therapy, Respiratory Medicine, Psychiatry and Psychology, and Clinical Chemistry, Maastricht University Medical Center, and Department of Epidemiology, University of Maastricht, Maastricht, and Departments of Medical Psychology, CoRPS, Tilburg University, and St. Elisabeth Hospital, Tilburg, The Netherlands

Address of Corresponding Author

Respiration 2010;80:212-219 (DOI: 10.1159/000314225)

--------------------------------------------------------------------------------
Abstract


Background: Cognitive symptoms, such as concentration problems, are frequently recorded by sarcoidosis patients.

Objectives: The aim of this study was to assess the prevalence of perceived everyday cognitive failure in sarcoidosis patients and healthy controls. Furthermore, the effect of treatment on cognitive functioning was examined.

Methods: The study included 343 sarcoidosis patients (44.6% females; age 49.3 ± 11.0 years). They completed the Cognitive Failure Questionnaire (CFQ) and Fatigue Assessment Scale (FAS) at baseline and the 6-month follow-up to evaluate the effect of treatment on cognitive functioning. The control group consisted of 343 age- and sex-matched healthy controls.

Results: The mean CFQ score was significantly higher in sarcoidosis patients (37.3 ± 16.1) compared with the controls (31.3 ± 10.1; p < 0.0001).A high CFQ sore (≧43) was found in 35.0% of the patients and only 14.3% of the controls. No relation with disease severity and duration, or disease location was found. The proportion of patients receiving treatment did not differ among the groups with high and normal CFQ score. At the 6-month follow-up, only patients recently treated with anti-TNF-α therapy (n = 42) demonstrated a significant improvement in the CFQ score (Δ –7.07 ± 7.23) compared with the untreated patients (Δ –0.08 ± 9.35) and patients treated with prednisone with or without methotrexate (Δ 1.67 ± 9.22; p < 0.0001). After adjustment for the concomitant decrease in fatigue, the effect of anti-TNF-α therapy remained high and significant. Conclusions: Subjective cognitive failure is a substantial problem in sarcoidosis patients regardless of disease severity. Anti-TNF-α therapy had a positive effect on cognition, fatigue and other symptoms of sarcoidosis.

Copyright © 2010 S. Karger AG, Basel
--------------------------------------------------------------------------------
Introduction

Cognitive impairment, characterized by memory loss and concentration problems, has been observed in several chronic disorders in previous studies. Severe chronic obstructive pulmonary disease was associated with lower cognitive performance over time [1]. Patients suffering from sarcoidosis often report cognitive complaints, such as memory loss, concentration problems and other mental problems. However, up to now no studies have been performed to assess this problem extensively in sarcoidosis.

Sarcoidosis is an inflammatory disease with a high incidence among young adults. The clinical course of sarcoidosis is highly variable [2,3,4,5]. A spontaneous remission may occur or it may become chronic. Patients often present with symptoms that do not correspond with objective physical evidence. Patients with pulmonary sarcoidosis may present with symptoms related directly to the chest, such as cough, dyspnea on exertion, retrosternal chest pain, chest discomfort and wheezing. Fever, anorexia, weight loss, general weakness, fatigue, pain, mental problems and reduced quality of life are also associated with sarcoidosis [6,7,8]. These symptoms are disabling, particularly when they become chronic. Previously, we found that sarcoidosis patients with current symptoms displayed more depressive symptoms and health status scores were lower compared with patients without current symptoms [7]. In line with this finding, Cox et al. [9] found that higher scores on depressive symptoms and perceived stress were related to lower health status scores in sarcoidosis. Furthermore, Chang et al. [10] found a prevalence of depression of 60% in their sarcoidosis population.

Broadbent et al. [11] described ‘cognitive failure’ as a cognitive error that occurs during the performance of a task that a person normally would execute successfully. They developed the Cognitive Failure Questionnaire (CFQ, see Appendix), a self-report questionnaire assessing failures in everyday errors of attention, perception, memory and motor function [11]. In general, the CFQ appears to be a reliable and brief measure useful in clinical practice.

The aim of this study was to assess the prevalence of perceived cognitive problems using the CFQ in patients with sarcoidosis compared with healthy controls. Moreover, within a subpopulation of these patients, perceived cognitive functioning levels evaluated at baseline and after 6 months of treatment were compared. The effect of different types of treatment initiated for sarcoidosis-related problems, but not cognitive failure, were also assessed using the CFQ.

Patients and Methods

Sarcoidosis patients (n = 441) attending the outpatient clinic of the Department of Respiratory Medicine of the Maastricht University Medical Center were sent a set of questionnaires in November 2007. Exclusion criteria were poor knowledge of the Dutch language (n = 4) and co-morbidity, such as a malignancy (n = 24). The diagnosis was based on clinical features consistent with sarcoidosis, according to the guidelines of the World Association of Sarcoidosis and Other Granulomatous Diseases [12]. Biopsies were available in 80% of cases; no biopsy was obtained in patients with Löfgren’s syndrome.

Of the 441 patients, 343 (77.8%) returned the questionnaires and were included in the study. To assess the effect of treatment on cognition, the questionnaires were completed for the second time 6 months after baseline (324/343 = 94.5% of cases). Demographic and medical data of all participants were obtained. Healthy volunteers (n = 1,357), who participated in the Maastricht Aging Study, served as a sex- and age-matched control group (n = 343) for comparison of the CFQ scores [13].

This study was performed in accordance with the Declaration of Helsinki and its amendments. The protocol was approved by the local medical ethics board of the Maastricht University Medical Center. Written informed consent for participation in this study was obtained from all subjects.

Clinical Data

Relevant clinical data including treatment, lung function measurements and chest radiographs were obtained. With respect to the use of medication during follow-up, patients with sarcoidosis were categorized into three treatment groups: (1) no immunomodulating drugs; (2) prednisone with or without methotrexate (MTX), and (3) anti-TNF-α drugs. Furthermore, it was recorded whether patients received medication at baseline. Forced expiratory volume in 1 s and forced vital capacity were measured with a pneumotachograph (Masterlab, Jaeger, Würzburg, Germany). Diffusing capacity for carbon monoxide was measured by the single-breath method on the Masterlab (Jaeger). Values are expressed as a percentage of predicted values.

Chest radiographs were graded according to the radiographic staging of DeRemee (0–III), adding stage IV: with signs of pulmonary fibrosis, loss of volume, hilar retraction and bullae. Two groups were distinguished: the first group included stages 0 and I, and the second stages II–IV.

Questionnaires

The sarcoidosis patients completed the CFQ developed by Broadbent et al. [11] and the Fatigue Assessment Scale (FAS) [14,15] (http://www.ildcare.eu/index.php?id=100), the Center for Epidemiological Studies-Depression Scale (CES-D) [16], and the Small Fiber Neuropathy Screening List (SFNSL) [17] (http://www.ildcare.eu/index.php?id=100).

The CFQ is a self-report questionnaire consisting of 25 items assessing impairment in attention, perception, memory and motor functioning in everyday life [11]. In addition to these 25 items, all participants indicated on a 5-point Likert scale if they had experienced an increase in cognitive failures in the past 5 years (termed ‘increase’, ranging from ‘no increase’ score 1, to ‘very strong increase’ score 5), and to what extent these cognitive impairments affected their daily life, ranging from ‘no hindrance at all’ (score 1) to ‘very much hindrance’ (score 5), how worried they were about these cognitive failures, ranging from ‘not worried at all’ (score 1) to ‘very much worried’ (score 5) and finally how annoying they found these cognitive failures, ranging from ‘not annoying at all’ (score 1) to ‘very much annoying’ (score 5). The total CFQ score was calculated by summing up all items, with the total score ranging from 0–100. A high CFQ score was defined as a score ≧43 (mean of the controls plus one standard deviation).

Statistical Analysis

Differences in mean scores between two groups were compared using Student’s t test for independent samples and differences in mean scores between more than two groups were compared using analysis of variance. The proportions of patients with a high CFQ score within the sarcoidosis and control group were compared using the χ2 test.

Within the group of patients with sarcoidosis, the difference between the baseline score and the score at the end of the 6-month follow-up was calculated for both questionnaires (CFQ and FAS). The baseline score was subtracted from the follow-up score. Decreases in CFQ and FAS scores indicate decreased cognitive failure and fatigue and thus improvement. For the total group of patients with sarcoidosis, the one-sample t test was used to test whether there was a significant change in scores during follow-up.In order to evaluate the effect of different types of medication on the CFQ score, mean changes between baseline and follow-up scores in the two treatment groups treated with immunomodulating drugs during the follow-up were compared with a reference group of patients without immunomodulating drug treatment using Student’s t test for independent samples.

In order to evaluate whether treatment affected the change in the CFQ score that is independent of changes in self-reported fatigue, a multivariate linear regression model was used with change in CFQ score as dependent variable. In this model, treatment group was coded by two dummy variables, using the group who received no immunomodulating drugs as reference group. Change in FAS score was coded as a continuous variable. Statistical analyses were performed using SPSS (version 15.0) for Windows. A two-sided p ≤ 0.05 indicated statistical significance.

Results

The CFQ data of the sarcoidosis population and the matched control group are summarized in table 1. The mean CFQ total score was significantly higher in sarcoidosis patients (37.3 ± 16.1) than in the controls (31.3 ± 10.1; p < 0.0001). More than one third of the patients had a high CFQ score (54.0 ± 8.8) versus 14.3% of the matched controls. Moreover, patients experienced significantly higher increases in cognitive failures in the past 5 years and were more hindered, annoyed and worried about these cognitive failures.

Table 1. Characteristics of sarcoidosis patients (cases, n = 343) and matched controls (n = 343) at baseline





The demographic characteristics of the sarcoidosis population are summarized in table 2. Patients were not suffering from anemia. No relation was found with serum calcium levels, electrolytes or inflammatory parameters: C-reactive protein, angiotensin-converting enzyme or soluble interleukin 2 receptor. Moreover, lung function test results, arterial oxygen levels (at rest) and dyspnea did not correlate with the CFQ scores (data not shown) and no differences were found in lung function test results between patients with a high CFQ compared to those with a normal CFQ score (table 2) at baseline. Of the studied patients, 70.6% had involvement of the lungs, 67.1% of lymph nodes; 34.5% of the eyes; 32.2% of the joints; 9.2% had cardiac involvement; 5.9% had signs of neurosarcoidosis and 11.4% had other manifestations of sarcoidosis; 16% of the patients had only extrathoracic signs of sarcoidosis. No differences regarding these mentioned clinical data were found between those patients with a high or normal CFQ score.




Table 2. Characteristics of the total sarcoidosis population subdivided by normal and high CFQ scores at baseline

In the group with high CFQ scores, the number of women was significantly higher than in the group with normal CFQ scores, and this difference was also found in the healthy control group. No substantial differences were found in clinical data, including disease presentation, severity and duration, and lung function test results, between patients with a normal or a high CFQ score (table 2). At baseline, 42.3% (n = 145) of the patients with sarcoidosis used no immunomodulating drugs (no treatment), 37.3% used prednisone (daily dose 9.1 ± 7.5 mg; range: 1–60), and 20.4% used prednisone and MTX (10.4 ± 5.5 mg once a week; range: 5–20). Thus, 57.7% (n = 198) of the patients were treated. Moreover, 35% of the cases received pain killers (non-steroidal anti-inflammatory drugs but none of the patients used opiates); 6.3% antidepressant drugs, and 8.2% sleep medication. None of the patients received treatment for cognitive problems. At baseline, the percentages of patients receiving treatment were similar for the group with high and normal CFQ scores (table 2).

After 6 months of follow-up, the effect of treatment was evaluated. The reason for initiating treatment hereafter was never cognitive failure. Only the effect of the various treatments on cognitive functioning was evaluated. At baseline and after 6 months, 324 cases completed the questionnaires: 189 of them were not treated with either prednisone and/or MTX during this 6-month follow-up period (group 1). Group 2 consisted of 93 patients, of which 48 used corticosteroids only and 45 used low-dose corticosteroids together with MTX and folic acid. Group 3 comprised 42 of the 324 patients who were treated with anti-TNF-α drugs during these 6 months [infliximab 5 mg/kg every 4 weeks (n = 31) or adalimumab 40 mg s.c. once a week (n = 11)]. At baseline, this latter group, suffering from refractory sarcoidosis, used prednisone with MTX but did not demonstrate clinical improvement after the initially started therapy. After starting anti-TNF-α treatment this co-medication was reduced to, either to 7.5 mg MTX once a week or to 5 mg prednisone once a day (in case they developed side effects during MTX treatment), to avoid antibody formation.



Table 3 shows that for the total group of patients with sarcoidosis, the mean change in CFQ and FAS scores during follow-up was very small and not significant. However, when patients were categorized according to treatment (groups 1–3), the group of patients who received anti-TNF-α therapy during the follow-up period (group 3), showed substantial improvement in both CFQ and FAS scores. This change in scores is significantly higher than in the reference group of untreated patients (group 1) and the patients who were treated with prednisone with or without MTX (group 2) during the 6-month follow-up (p < 0.0001; table 3). After restriction to only those patients with a high CFQ score at baseline (n = 121), the results remained similar and significant (p < 0.0001). Improvement was still much higher in the group treated with anti-TNF-α drugs [group 1 (n = 67; ΔCFQ: –1.75; ΔFAS: 0.59); group 2 (n = 29; ΔCFQ: –0.86; ΔFAS: 0.86), and group 3 (n = 25; ΔCFQ: 8.48; ΔFAS: –5.36)]. After adjustment for change in FAS score using a multivariate linear regression model, the change in the CFQ score in the group of patients treated with anti-TNF-α drugs remained significant and higher than in the other groups. The change from baseline to 6 months was –4.94 (95% confidence interval: –8.10 to –1.79) compared with non-significant changes of –0.25 (95% confidence interval: –1.53 to 1.02) and 1.46 (95% confidence interval: –0.76 to 3.69) in the reference group without any treatment and the group treated with prednisone with or without MTX, respectively.


Table 3. Results (means ± SD) with respect to CFQ and FAS scores according to treatment categories











Discussion



This study is the first to demonstrate that everyday cognitive failure is a substantial problem in sarcoidosis patients. This is remarkable, because sarcoidosis predominantly affects young adults. A high CFQ sore (≧43) occurred in more than one third of the sarcoidosis patients compared with 14.3% in matched healthy controls. Patients experienced more failures in the past 5 years compared to controls. Moreover, these failures had more (emotional) effects on the patients; patients were significantly more hindered, annoyed and worried about their cognitive failures. No substantial relationship was found with disease presentation, severity or duration. Although the primary reason for initiating treatment was not cognitive failure but other sarcoidosis-related symptoms, only treatment with anti-TNF-α drugs resulted in an improvement in cognitive functioning, whereas untreated patients and patients treated with corticosteroids with or without MTX did not show progress in cognitive functioning. Moreover, the results indicate that a low cognitive performance (high CFQ score) is associated with more fatigue, depressive symptoms and symptoms related to small fiber neuropathy.



The findings in the present study raise the question of whether the higher frequency of cognitive impairment in patients with sarcoidosis can be explained by the higher frequency of fatigue, depression and symptoms related to small fiber neuropathy or whether the strong concordance between all these symptoms and cognitive impairment can be explained by a common underlying mechanism. Strong support for the latter explanation is given by the finding that treatment with anti-TNF-α drugs resulted in an improvement in the CFQ and FAS scores and that this treatment effect on the CFQ score was independent of the improvement in the FAS score. After adjustment for change in FAS score using a multivariate linear regression model, the change in the CFQ score in the group of patients treated with anti-TNF-α drugs remained high and significant. Therefore, it is hypothesized that the common underlying mechanism is associated with an increase in TNF-α levels. The most widely held view is that chronic disorders including sarcoidosis cause changes in the central nervous system (CNS) through possible processes such as vascular disease due to inflammation, including an increase in TNF-α, oxidative stress and inflammation-induced changes in neurotransmitter metabolism [18,19]. Such CNS changes then lead to a lower cognitive function. Autonomic dysfunction and fatigue are both a dominant symptom of and risk factor for depression, and the conditions may share several neurobiological abnormalities, for example an increase in TNF-α.



There is evidence that TNF-α regulates synaptic transmission in the brain and that this cytokine is involved in the spatial memory impairment in mice [20]. It is also assumed that neuroinflammation with overexpression of cytokines is a standard characteristic of the brain pathology present in Alzheimer’s disease. Tobinick and Gross [21] reported rapid cognitive improvement in Alzheimer’s disease following treatment with etanercept, which binds TNF-α and blocks its interaction with cell surface TNF-α receptors.



Recent evidence also suggests that TNF-α may induce the expression of inducible nitric oxide synthase (iNOS). Overexpression of iNOS was found in the brains of Alzheimer’s disease patients. As a strategy to prevent the cognitive decline in Alzheimer’s disease, anti-oxidants are well recommended based on the association of oxidative damage with the progress of the disease [18,22]. More recently, the TNF-α inhibitor thalidomide was found to be effective in reducing the iNOS/peroxynitrite-related pathology via restraining the increase in TNF-α without eventually harming the physiological function of iNOS [22]. Involvement of excess TNF-α in the pathogenesis of cognitive impairment and fatigue in patients with sarcoidosis would explain the favorable effect of anti-TNF-α drugs in this study.




The present study also draws attention to the high prevalence of everyday cognitive failure in patients with sarcoidosis. The results stress that sarcoidosis patients are at a higher risk for developing cognitive problems compared to healthy controls. In many chronic disorders it is well known that the decline in cognitive performance is likely to have important clinical consequences [1]. In sarcoidosis patients, this is even more important as this disorder affects mainly young adults. In this part of their lives, cognitive abilities are necessary for personal health, their social lives and maintenance of their abilities to function appropriately at work and to finish their studies successfully, for example. Providing effective medication for the treatment of cognitive deficits in general can have a dramatic effect on the quality of life of a patient dealing with this problem.



In sarcoidosis, inflammation results in an increase in TNF-α [23]. In the present study, anti-TNF-α treatment appeared beneficial in reducing cognitive failure, as well as disease activity and fatigue. Two randomized, double-blind, placebo-controlled trials have been performed in pulmonary sarcoidosis. Baughman et al. [24] found a significant improvement in the forced vital capacity of patients receiving infliximab compared to placebo, in agreement with Rossman et al. [25]. More recently, Moravan and Segal [26] demonstrated that combination treatment with mycophenolate mofetil and infliximab is a promising therapeutic approach for refractory neurosarcoidosis. Case reports suggest that this agent can be beneficial in patients with neurosarcoidosis and small-fiber neuropathy [27]. Also, thalidomide treatment was effective in sarcoidosis [28]. However, cognition was beyond the scope of these studies and not evaluated.



One of the limitations of this observational study was that the neuropsychological assessment for cognitive dysfunctions was restricted to a rather global and subjective screening instrument. Labeling oneself as absent-minded or forgetful depends upon the perceived discrepancy between the subject’s everyday memory functioning and her/his everyday memory demands. Self- reported cognitive changes or decline do not necessarily reflect actual cognitive decline. Beliefs about cognitive changes are strongly influenced by self-efficacy beliefs, personality, vitality and coping styles [29]. This influence might explain the higher proportion of women with high CFQ scores in both the sarcoidosis group and the matched control group. Future studies using objective measures of cognitive performance to estimate the prevalence of everyday cognitive impairment in patients with sarcoidosis are recommended. Nevertheless, it seems unlikely that the favorable effect on cognitive function reported by patients who were treated with anti-TNF-α drugs is attributable to the use of a subjective screening instrument.

Another limitation of the study was that it was not feasible to evaluate whether or not the improvement in CFQ after anti-TNF-α treatment was direct or mediated through decreases in depressive symptoms. Patients completed the CES-D questionnaire at baseline, but results on CES-D scores at 6 months were not available. Both depression and fatigue are very important issues regarding cognition. Moreover, we found that autonomic dysfunction is also involved. However, in our population fatigue appeared the most prominent of these three factors. Therefore, we decided to evaluate fatigue, next to cognition, after the 6-month follow-up (table 3). One of the main reasons for this was to prevent patients refusing to participate in the second round because they got the impression that they needed to complete too many questionnaires. Our experience is that patients are willing to participate, if this is not too time consuming. The relationship between depression and cognition should be addressed in further studies. Furthermore, there might be a concern that improvement in cognition could be associated with improvement in lung function test results. However, at baseline, no association was found between lung function and cognitive failure. Patients with cognitive failure had either normal lung function or moderately decreased values. These lung function test results were comparable with those of patients without signs of cognitive failure.

Conclusions

In conclusion, everyday cognitive failure is a substantial problem in patients with sarcoidosis. More than one third of the sarcoidosis patients exhibited cognitive deficits compared to 14.3% of healthy volunteers. Our study should raise awareness that sarcoidosis patients, similar to patients with other chronic disorders, are at higher risk for developing cognitive impairment. This will likely further worsen their general health. Anti-TNF-α treatment was found to be successful in the treatment of refractory sarcoidosis. It not only reduced fatigue but, interestingly, also had a positive effect on the cognitive functioning of sarcoidosis patients. These results emphasize the need for further research to integrate knowledge about neuropsychological deficits, coping, cognitive failure and cognitive performance, fatigue, depressive symptoms and treatment strategies in sarcoidosis into clinical management. These findings render managing sarcoidosis patients even more challenging.