Dr Stoff

Dr. Stoff  was a compassionate man who really seemed to understand what a CFS sufferer was going through. Here is a passage from his book that I thought was beautiful and still makes me cry. The journey inward is like a quest to the top of the mountain that rises above the chaos in your life and body. The trek is not by way of an escalator. It is a long, hard climb. The only way out of this mess is through it. Together we will walk the path, guided by signposts. The climb to the top, beyond illness, is worth the effort. When we have reached the summit you will have learned more about yourself and grown more than you ever dreamed was possible. There will be many hills and valleys along the way, and there may be times when you wonder, "Why bother?" Just remember this: when you are ascending the mountain you can look back down and know what was. But when you're deep in the valley you can't look up through the fog to see what will be. Trust.
When you cross a small valley along your trek, the memory of what you have already seen and learned will sustain you. If you stop along the way to really take in the signposts, then you are a special person indeed, for you are ready to put aside the fear of the unkown, of yourself, and really examine who and what you are. You are ready to love, accept, and appreciate yourself for who and what you are. You will learn to listen to yourself and to your body to fulfill its needs. When you reach the summit, you can pause and reflect on what you have learned and re-create yourself. the power to do so is yours. And with your new strength you can now bring greater love to your family and friends.
You will have gained a sense of maturity and perspective with which you can offer them a hand. THIS IS WHAT I WILL SEE WHEN I LOOK AT YOU ON THE MOUNTAINTOP: A PERSON WHO CAN LOVE, A PERSON WHO CAN LISTEN. AN AUTHENTIC HUMAN BEING. When you look back, there will be no regret and remorse over lost time and opportunities. Instead, you will see that the greatest opportunity of your life is the illness now before you. Give me your hand and let us begin our journey.

Dr. Stoff quit his practice and went into research only.

Gras maaien

Vandaag voor het eerst in twee maanden weer een goede dag gehad. Van de gelegenheid gebruik gemaakt om de moestuin onder handen te nemen. Dit jaar groeit er niets behalve metershoog onkruid. Om 12 uur nog even een paar uurtjes in bed gekropen maar tegen 15 uur zijn we erin gevlogen. Voor de gelegenheid mijn strakste sportoutfit van enkele jaren geleden aangetrokken. Felt great!

De grasmaaier kreeg ik niet aan de praat. Een paar keer aan de draad trekken met een stel pijnlijke armen is voldoende om de motor te doen verzuipen. De puberzoon wilde wel even helpen en vond het geronk van de nieuwe machine blijkbaar leuk genoeg om de grasmachine te bedienen. Onderweg hebben we nog een jonge pad van een bloederige dood gered. Met de hark in de hand heb ik wat instructies gegeven en de rest zo goed mogelijk bijeen geveegd. Cardio!

De moestuin is weer een lapje grond geworden. De wildernis is tegen de vlakte gegaan. De vlinders kunnen nog naar hartelust op het veld er vlak achter rondfladderen.

De jongste heeft nog wat zwarte bessen geplukt die als bij wonder tussen het onkruid groeiden. Vanavond lekker smullen!

Lyme tijdens zwangerschap

Deze avond bijna van mijn stoel gevallen van het verschieten bij het zien van onderstaande foto.
Dit zou een reactie op antibiotica na een tekenbeet bij een zwangere vrouw in haar zesde maand.
Toeval wil dat ik een gelijkaardige uitslag heb gehad in augustus 1995 en zeven maanden zwanger was.
De arts van dienst weet het aan oververhitting en warmte-uitslag wat me toen wel mogelijk leek omdat we pas naar de tropen waren verhuisd.

Mijn zoon is kort na de geboorte op intensive care beland met een macrocytose en sepsis door bacteriële besmetting. Ikzelf heb kort daarna drie maanden mijn bed niet kunnen verlaten voor een tot nu toe onbekende reden.

De Nederlandse Vereniging voor Lymepatienten bevestigt dat een besmetting kan doorgegeven worden via zwangerschap en dat babies o.a. milde sepsis, systemische ziekten en andere vervelende kwalen kunnen krijgen. Mijn aandacht is alvast gewekt.

Bronnen
http://www.dr-hopf-seidel.de/mediapool/87/874128/data/Vortrag_fuer_Europaem_7-12.pdf
http://server1.lymevereniging.nl/LJNL/NVLP_LJNL%202007_3.PDF

Nog andere interessante documenten ivm Lyme (en zwangerschap):
http://www.neurologie.nl/uploads/131/144/richtlijnen_-_niet-NVN_protocollen_CBO_lyme.pdf

Dit document vermeldt dat pas bevallen vrouwen lange tijd uitgeput zijn in de maanden na de bevalling als ze Lyme besmetting oplopen tijdens de zwangerschap.
http://www.ilads.org/lyme_disease/B_guidelines_12_17_08.pdf

Autoimmunity in CFS

Interesting article to read!

http://bb-cfs.blogspot.be/2012/07/autoimmunity-in-cfs.html?utm_source=BP_recent

Whilst autoimmunity in CFS may be considered a peripheral phenomenon, it’s potential importance is highlighted by the recent Rituximab study (B-lymphocyte depletion) which demonstrated significant therapeutic benefit ⁸. Putative factors underpinning autoimmunity in CFS include oxidative stress, altered gut permeability, chronic inflammation and chronic immune activation ^3,9.

Anti-neural antibodies in lupus and Lyme

http://www.ncbi.nlm.nih.gov/pubmed/20227484

 

Brain Behav Immun. 2010 Aug;24(6):1018-24. Epub 2010 Mar 18.

Anti-neural antibody reactivity in patients with a history of Lyme borreliosis and persistent symptoms.

Chandra A, Wormser GP, Klempner MS, Trevino RP, Crow MK, Latov N, Alaedini A.

Source

Department of Neurology and Neuroscience, Cornell University, New York, NY 10065, USA.

Abstract

Some Lyme disease patients report debilitating chronic symptoms of pain, fatigue, and cognitive deficits despite recommended courses of antibiotic treatment. The mechanisms responsible for these symptoms, collectively referred to as post-Lyme disease syndrome (PLS) or chronic Lyme disease, remain unclear.

We investigated the presence of immune system abnormalities in PLS by assessing the levels of antibodies to neural proteins in patients and controls. Serum samples from PLS patients, post-Lyme disease healthy individuals, patients with systemic lupus erythematosus, and normal healthy individuals were analyzed for anti-neural antibodies by immunoblotting and immunohistochemistry. Anti-neural antibody reactivity was found to be significantly higher in the PLS group than in the post-Lyme healthy (p<0.01) and normal healthy (p<0.01) groups.
The observed heightened antibody reactivity in PLS patients could not be attributed solely to the presence of cross-reactive anti-borrelia antibodies, as the borrelial seronegative patients also exhibited elevated anti-neural antibody levels. Immunohistochemical analysis of PLS serum antibody activity demonstrated binding to cells in the central and peripheral nervous systems. The results provide evidence for the existence of a differential immune system response in PLS, offering new clues about the etiopathogenesis of the disease that may prove useful in devising more effective treatment strategies.
Copyright 2010 Elsevier Inc. All rights reserved.

Source: http://www.ncbi.nlm.nih.gov/pubmed/20227484

Antiphospholipiden in Post Lyme Disease?

http://www.ncbi.nlm.nih.gov/pubmed/21729977

 

Lupus. 2011 Nov;20(13):1372-7. Epub 2011 Jul 5.

Antiphospholipid antibodies in patients with purported 'chronic Lyme disease'.

Greco TP Jr, Conti-Kelly AM, Greco TP.

Source

St Mary's Hospital, Department of Medicine, Waterbury, CT, USA. tgreco@stmh.org

Abstract

BACKGROUND:

Antiphospholipid antibody (aPL) positive patients and patients with purported chronic Lyme disease ('CLD') share many clinical features. After identifying significant aPL in sera of several index patients with 'CLD', we performed aPL tests on all patients referred in whom 'CLD' was suspected, diagnosed or treated.

METHODS:

All patients with suspected, diagnosed or treated 'CLD' and reportedly 'positive' Lyme assays were studied. aPL testing included anticardiolipin antibodies (aCL), anti-beta-2-glycoprotein-1 antibodies (anti-β2GP1) and lupus anticoagulant (LAC). Patients were classified into four newly described categories of CLD and data was analyzed.

RESULTS:

One hundred and six patients were evaluated, of whom 82% had neurologic symptoms and 51% rheumatologic symptoms. Eighty-eight of 106 (83%) patients had positive Lyme serologies (enzyme-linked immunosorbent assay [ELISA] 62/106, 58.4%; western blot [WB] 64/106, 60%), while 18/106 (16.9%) were negative or equivocal. aPL was found in all 'CLD' categories. aCL and/or anti-β2GP1 were positive in 85/106 (80%), with aCL present in 69/106 (65%) and anti-β2GP1 present in 69/106 (65%). For all assays, IgM isotypes predominated: WB 55/64 (85%), aCL 63/69 (91%), anti-β2GP1 52/69 (75%), aCL and/or anti-β2GP1 74/85 (87%). Anti-β2GP1 assays occurred in higher titer than aCL: 36/69 (52%) versus 63/69 (91%), p<0.001. Seventeen patients had aPL-related events. Only 12/106 (11.3%) had true post-Lyme syndromes (PLS), category IV, or late Lyme disease (LLD). Most patients had been treated for Lyme: 82/106 (79%).

CONCLUSION:

aPL occurs frequently in patients with 'CLD'. IgM anti-β2GP1, IgM aCL and IgM WB were frequently found. Documented PLS or LLD was uncommon. The role of aPL in patients with 'CLD' needs further investigation.

Source: http://www.ncbi.nlm.nih.gov/pubmed/21729977

Lupus of Lyme

Reumatologen en ik, het zal nooit wat worden.

Bah, heb er al zoveel spijt van. Echt met een sisser afgelopen.

Ik kreeg mijn klachten niet uitgelegd want het moest in chronologische volgorde en daar liep het al fout. En toen wilde die man weten wat mijn ergste klachten vandaag waren maar voor inspanninsgintolerantie en krachtverlies bleek ie oostindisch doof.

Wie had ooit de diagnose lupus en botschade vastgesteld? Die botscan, dat wilde niets zeggen.

En na wat fysiek onderzoek bleef ie maar doordrammen waarom ik niet kon sporten. Zwemmen, dat was toch iets voor mij? Te koud water? Kom kom, er bestaan zwembaden met warm water. Fietsen? Lopen? Nee, ook niet? Waarom niet? Oma probeerde nog eens als oud-gediende.

Hij wilde mijn onderzoeken van naderbij bekijken en binnen een maand mag ik terugkomen. Mijn dikke map dus achtergelaten. Duizenden euro's studiemateriaal gratis in zijn handen. Dat kan hij in zijn sofa in het gezelschap van een glas cognac eens gaan doorbladeren.

SPORT dat is Luxe. Als ik kon sporten, dan was ik al lang gaan werken!!! Maar daar ben ik natuurlijk niet opgekomen toen ik binnen zat. Wat een kl*thommel.

De enige troost die ik eruit haal, is dat als de botscan volgens hem niets zegt, dat het misschien nog Lyme-artritis of iets van die aard kan zijn. Dat liever dan een systeemziekte dat mijn botten opvreet.

Ongelovige reumatoloog

Morgen een afspraak bij een bekende reumatoloog. Oma is verpleegster en heeft zo haar connecties.

Zijn eerste reactie aan de telefoon was (zoals ik dat wel vaker hoor): "En wie heeft u die diagnose gegeven?"
Aargh, daar word ik nu eens nijdig van. Alsof mijn klachten ongeloofwaardig zijn en een diagnose van een collega minder waard zou zijn dan de hunne.

Dus zei ik: "De naam van de arts ontglipt me maar de botscan was wel redelijk overtuigend."
En toen mocht ik komen.

Supplementen nieuwe lading

ik heb een fortuin aan supplementen gekocht. En nu gaan we het uitproberen. Alles is onderweg via iHerb.

Jarrow Formulas 5mg Methyl B12
Enzymatic Therapy 1mg B12 infusion
Solgar Metafolin 800mcg
Country Life Dibencozide (adenosylb12)
Jarrow B-Right b-complex,
Potassium
Omega3 fishoils
Zinc - 50 mg
Calcium/magnesium
D3 - 3000-5000 IU total
Vitamin E, Gamma complex
Vitamin C – 4000+mg/day
L-carnitine fumarate
Alpha Lipoic Acid
D-Ribose
Selenium
Lecithin
Chromium GTF
Copper

Raw Thyroid
Biotin
Saw Palmetto
Q10 ubiquinol
Super Minerals
...

Toelichting bij methylation test

En dit is de toelichting die ik kreeg op mijn resultaten van Rich Van Konynenburg in person:

Hi, Marlene.

Here are some comments on your lab test results:

You have glutathione depletion (based on low Glutamic acid lactam (pyroglutamic acid)).
You have a B12 deficiency, probably a functional B12 deficiency (based on low glutathione and low methylcobalamin). Note that MMA is not elevated, probably because it is masked by deficiencies in vitamin B6 and biotin.

You have a partial block of methionine synthase, which links the methylation cycle with the folate metabolism (based on low-normal SAM, high SAH, low-normal 5-methyl THF and low THF).
You have loss of folates from the cells (based on low levels of most of the folates).

In view of the above, I would say that you have the vicious circle mechanism that characterizes ME/CFS, as described by the Glutathione Depletion--Methylation Cycle Block hypothesis, and that a methylation protocol would be likely to help you.

The low red blood cell folic acid level indicates that you have oxidative damage to your cell membranes, which is to be expected with low glutathione.

In addition, you have low vitamin B6 (based on low pyridoxic acid, and low or low-normal values for the first five amino acid metabolites).

Your glycolysis appears to be operating somewhat more slowly than normal (based on low-normal pyruvic acid).
Your body is not in ketosis, and fatty acids are not undergoing omega oxidation at an elevated rate. This is somewhat surprising, because the low citric acid level indicates that the Krebs cycle is being fed at a lower than normal rate, and in fact, your Krebs metabolites are low in general. This would likely produce fatigue. Perhaps the thyroid and adrenals are not stimulating the gene expression of enzymes in glycolysis and the Krebs cycle as much as normal. I understand that your thyroid hormones may be a little low.

I don't know whether Alkala N would cause this, but I suspect it wouldn't. Usually when a person's glycolysis is slow, I see the fatty acid markers go up, indicating that the cells are trying to burn fat in order to make up for the lack of carbohydrates, but your fatty acid markers are not raised, and your citric acid is low.

I forgot to mention that your vitamin B5 level is also low, and that could be contributing to the low citric acid, because B5 is needed to make coenzyme A, and Co A is part of acetyl CoA, which reacts with oxaloacetate to make citric acid.

Your B2 looks O.K. I don't have data for your B3. Both B2 and B3 are needed for burning fatty acids.

You might have low vitamin C or low copper (based on high-normal HVA with low-normal VMA). Low vitamin C would be expected with glutathione depletion, because glutathione normally recycles vitamin C.

I don't have a unique explanation for the abnormalities in your sulfur metabolites. You might have elevated production of hydrogen sulfide by bacteria in the gut or possibly due to the partial methylation cycle block combined with an upregulating polymorphism in the gene for cystathionine beta synthase (CBS).

Also, you might have a polymorphism in the gene for the sulfite oxidase enzyme, or you might have a molybdenum deficiency. Your high thiosulfate together with low thiocyanate, combined with your history of cyanide intolerance suggests that you might have a polymorphism in the gene for rhodanese, which is the enzyme that normally converts cyanide to thiocyanate by reacting it with thiosulfate. I'm not able to sort this out with the available data.

You could do the home test for hydrogen sulfide in the urine that is supplied by ProteaPharma there in Belgium. You could also run the stool test offered by RedLabs in Belgium to see what the bacterial populations are in your gut. If you do that, I suggest that you ask them to add the Desulfovibrio genus from their library when they run the analysis. Genomic testing would show whether you have the polymorphisms I suggested. You could run tests for the metals at the ELN lab in the Netherlands.

I hope this is helpful.

Best regards,

Rich