A week ago I took VIP for the first time. I took a "normal dose" (50 mg four times a day) but only for 1.25 days before stopping it on suspicion that my TGF-beta was increasing, which according to Shoemaker is a sign that I either have current mold exposure, have Lymes Disease, or have a TH-17 / Treg imbalance (I think it's current mold exposure).
Side Effects and Benefits
These days my brain functions decently for about 1.5 hours a day. About one day after I started taking VIP I noticed my ability to concentrate improving. This lasted for three days before dissipating. For each of those three days I was able to concentrate for 3-4 hours. I also went out to dinner with old friends one night. Usually I would be hard-pressed to engage in any kind of extended conversation, but that night I found myself telling jokes and laughing in a way I do not often do.
One of the things that tipped me off to potentially higher TGF-beta was bloody stool and a particular kind of poor sleep/insomnia. This started maybe a day after taking VIP and also continued for about three days. In this time I didn't change any other part of my treatment regimen, and I think having two changes appear and disappear concurrently suggests they might have the same cause.
The insomnia I experienced was a particular kind that I get when I don't eat raw beef or get enough zinc. As far as I can tell it's actually a problem with getting taurine to say inside of cells, and zinc helps with this.
Bloody stool tends to happen to me after repeated diarrhea, but in this case that didn't happen. It comes from bleeding, usually internal hemorrhoids.
TGF-beta
I think TGF-beta may be to blame for both of these effects, although I can only explain it halfway--TGF-beta blocks the vitamin-d receptor. Vitamin D increases metallothionein, which is necessary both as an antioxidant in the gut and for the absorption and use of zinc and copper. In the past I have used vitamin D to eliminate IBS-type symptoms, and I have thought it was due to an increase in metallothionein. In any case, decreased metallothionein would reduce the availability of zinc, and it seems to me that this is how TGF-beta would have caused that particular brand of insomnia.
A third thing that suggested high TGF-beta was that I had a spell of being "extra" tired each of the three days, although less so on the last one. The first day I know that it occurred after perhaps as much as an hour of sun exposure. The second time occurred following the use of boron. The first event may have occurred after boron as well, but I can't remember for sure. Boron increases the amount of active vitamin D in our blood. I've written elsewhere why I think that the marked fatigue some of us experience when we take vitamin D pills or even just expose ourselves to the sun is probably a result of high TGF-beta. This supports that theory. Here is what I wrote about it elsewhere:
Many of us with ME/CFS get quite exhausted from oral vitamin D (see
this thread). Personally, I suspect this is from an interaction between vitamin D and TGF-Beta, which "potently induce 5-lipoxygenase," at least in myeloid cells [1]. Many people with CFS have high TGF-Beta [2]. I tested this theory on myself by taking the 5-LO inhibitor acetyl-11-keto-beta-boswellic acid (AKBA), which proved successful in eliminating the vitamin d-induced fatigue--although over time it failed to prevent other side effects and I had to abandon oral vitamin D3 [3].
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Sources:
- Sorg BL, Klan N, Seuter S, Dishart D, Rådmark O, et al.Analysis of the 5-lipoxygenase promoter and characterization of a vitamin D receptor binding site.Biochim Biophys Acta2006;1761: 686–697.[PubMed]
- Bennett AL, Chao CC, Hu S, Buchwald D, Fagioli LR, Schur PH. Elevation of bioactive transforming growth factor-beta in serum from patients with chronic fatigue syndrome.J Clin Immunol.1997;17:160–166. doi: 10.1023/A:1027330616073.[PubMed][Cross Ref]
- Sailer ER, Subramanian LR, Rall B, Hoernlein RF, Ammon HP, Safayhi H. Acetyl 11-keto-b-boswellic acid (AKBA): Structure requirements for binding and 5-lipoxygenase inhibitory activity. Br J Pharmacol. 1996;117(4):615–618. doi: 10.1111/j.1476-5381.1996.tb15235.x. [PMC free article] [PubMed] [Cross Ref]