Re: striking new CFS findings by M Maes

[Guest guest]

This is very good news. So how many different ways do you think people looking at these results might interpret them? penny <usenethod@...> wrote: These are very welcome studies, but probably won't take the world bystorm unless/until others replicate them. I sure hope someone willtry. Maes states an impressive p of 0.0002 for the amount of NFkB p50in "peripheral blood lymphocytes of 18 unmedicated patients with CFS"vs

"18 age-sex matched controls." That's a hell of a p for a study this small. He may have foundsomething very robust here.2: Maes M, Mihaylova I, Bosmans E. Not in the mind of neurasthenic lazybones but in the cell nucleus:patients with chronic fatigue syndrome have increased production ofnuclear factor kappa beta.Neuro Endocrinol Lett. 2007 Jul 11;28(4) [Epub ahead of print]PMID: 17693979 [PubMed - as supplied by publisher]3: Maes M, Mihaylova I, Kubera M, Bosmans E. Not in the mind but in the cell: increased production ofcyclo-oxygenase-2 and inducible NO synthase in chronic fatigue syndrome.Neuro Endocrinol Lett. 2007 Jul 11;28(4) [Epub ahead of print]PMID: 17693978 [PubMed - as supplied by publisher]4: Mihaylova I, Deruyter M, Rummens JL, Bosmans E, Maes M. Decreasedexpression of CD69 in chronic fatigue syndrome in relation toinflammatory markers: evidence for a severe disorder in the

earlyactivation of T lymphocytes and natural killer cells.Neuro Endocrinol Lett. 2007 Jul 11;28(4) [Epub ahead of print]PMID: 17693977 [PubMed - as supplied by publisher]

[Guest guest]

> This is very good news.

>

> So how many different ways do you think people looking at these

results might interpret them?

Pretty much just one way - inflammation. At least, that's my guess.

Haven't got the full text so far. NFkB is the master molecule of

inflammation. I just have to make sure this particular *subunit* (p50

was it?) is involved in NFkB's function in the straightforward way I

assume it probably is.

The inflammation could cause the disease - or instead, as Rich

proposes, a metabolic/physiologic dysfunction that is the real

fundamental cause, could impair control of normal bacteria and

viruses, causing inflammation and perhaps some of the symptoms.

As you know I personally am strongly in favor an inflammatory root

cause for many reasons.

[Guest guest]

> Pretty much just one way - inflammation.

A main reason CFS has not necessarily been considered an immune

disease is the nonresponse to immunosuppressants. Long ago, P Behan, a

sympathetic UK neurologist, reported a formal open trial of

azathioprine. Actually he didn't even report it, just mentioned it and

said the patients got worse if anything. As far as steroids go, there

have been randomized trials over the years; some are cited in this

insurance co coverage position paper:

http://www.cigna.com/customer_care/healthcare_professional/coverage_positions/me\

dical/mm_0102_coveragepositioncriteria_chronic_fatigue_syndrome_treatment.pdf

I haven't yet nailed down whether cyclophosphamide has been tried,

though this paper claims it has been citing McBride 1991 British Med

Bulletin, which I don't have access to right now.

Since corticosteroids are supposed to suppress NFkB signaling, I'm not

sure the experience with them in CFS jives too fantastically with

Maes' new finding. Steroids also are supposed to not work well in

scleroderma, but I'm not sure how well the pathogenesis of scleroderma

is understood, though it does have some immune hallmarks.

[Guest guest]

I meant to add that the same analysis might apply to depression. The

immune hypothesis of depression has existed for quite some time, and

some strong results exist. I've never heard of immunosuppressant

treatment for depression, though I haven't looked.