I wonder whether any of Dr Ritchie Shoemaker's idea might help throw light on the nature of ME/CFS. Even though he focuses on mold-induced illness, the fact that Dr Joseph Brewer found that prior mold exposure is common in ME/CFS patients suggests there may be some common areas between mold-induced illness and ME/CFS.
If you look at Shoemaker's
11 step treatment plan for mold-induced illness, which I have been scrutinizing in recent days, there are some interesting interventions there — interventions which might both throw light on the nature of ME/CFS, as well as serve as possible treatments for ME/CFS.
One of those 11 steps that stood out for me was step 10: the lowering of elevated TGF beta-1 in mold patients, which Shoemaker achieves using the drug
losartan at a low dose of 25 mg twice daily. Ref:
1
And there are
several supplements that reduce TGF beta-1 as well, including: curcumin, vitamin D, Rhodiola rosea, ginkgo biloba, taurine, EGCG, genistein, licorice, N-acetyl-cysteine and resveratrol.
TGF beta-1 is elevated in both mold illness and in ME/CFS, and Shoemaker explains
here the possible autoimmune consequences for having high TGF beta-1:
Underlying these new insights into abnormalities in T-reg cells is the role of Th17 immunity, in which plasma TGF beta-1 is a major marker.
When we have the combo of high TGF beta-1 and low T-regs what is happening is that the helpful, good guy T-regs are being directed into tissue by TGF beta-1 where the wonderfully helpful T-regs are converted (plasticized) into pathogenic T-cells that make more TGF beta-1 (OH NO!) which sends more T-regs to their death in tissue.
Get used to hearing Th17/T-reg imbalance: it is the new jargon word in modern immunology. We are now seeing countless references to Th17/T-reg imbalance in assessment of inflammatory illness from acute coronary syndrome to cirrhosis. No where can we show such abnormalities better than in mold illness.
So Shoemaker is basically saying that high TGF beta-1 kills T-regs.
The Th17/T-reg ratio is much higher than normal in several autoimmune diseases, and it is thought this ratio may play a causal role in such diseases. The high TGF beta-1 found in mold illness and ME/CFS likely contributes to this elevated Th17/T-reg ratio, because high TGF beta-1 kills T-regs, thereby increasing the ratio.
If we wanted to bring the Th17/T-reg ratio down, then inhibiting TGF beta-1 using losartan might be the first step; there are also a number of supplements and drugs (see
here) that desirably inhibit Th17, and other which desirably boost T-regs, which will both serve to reduce a high Th17/T-reg ratio, and thereby possibly ameliorate autoimmunity.
Supplements and drugs that increase T-regs include: IGF-1, andrographolide (from Andrographis paniculata), selenium, vitamin D and rituximab.
Caveat:
this study on the CVB4 triggering of type 1 diabetes in mice found that
increasing TGF beta helped prevent diabetes from arises after CVB4 infection.