Hi alex,
Could you elaborate more on your dosage and experience with resveratrol? i have bought the doctor's best bottle and have yet to start a trial. From what i have read, it is good for mitochondria. i would like to know your views and which biochemical process does resveratrol come into play.
Thanks.
I used to experiment with pycnogenol and grape seed extract. With the original pycnogenol (which was made from grape seed, not pine bark, pine bark was a later change to the formula) I got results at four capsules but not less, which made it very expensive. Resverotrol has a similar issue.
Lower dose resverotrol doesn't appear to do anything much. It must be making some small shift in antioxidant status and eicosanoid synthesis, but its not noticable up to about a month on 300mg or so. At 1.2mg I do notice a difference, even when only taken once.The particular resverotrol I am using also contains a small amount of grape seed, and the resverotrol is grape seed derived (not the other cheaper kind).
I am finding that resverotrol can counter-balance other antioxidants such as those that boost glutathione (and hence methylation protocols). This is, I theorize, because these protocols increase eicosanoid synthesis, whereas resverotrol decreases eicosanoid synthesis. There are issues here though. Reseverotrol shuts down PGD2 synthesis, do too much without a counter-balance and you could have major issues sleeping, as PGD2 is a critical sleep trigger. I am facing these symptoms at the moment - so in effect I am still experimenting to find a balance.
This of course presumes a balance can be reached. Many things have no static balance as they are too dynamic (read chaotic) to achieve a balance. This depends on the nature of the regulatory and non-regulatory feedback loops and is impossible to predict theoretically. It requires experimentation, which I am doing.It may also vary highly from individual to individual, a problem with many therapies in ME.
I find that there are two general symptom states in ME, after the work by Martinovic in the 90s. This is not quite true, its about as relevant as talkign of Th1/Th2 which is oversimplified. However its simpler to discuss it this way in a "brief" (but getting longer
) comment.
The two states could be summarized as excess eicosanoids and deficient eicosanoids, more or less (there are confounding factors). Excess gives muscle pain, headaches, fatigue, increased sleep, more brain fog etc. Its generally driven by omega-6 fats and antioxidants. Deficiency leads to less sleep, more neurological symptoms including pain and weakness. Its possible to have both states at the same time however due to these states being a composite of many types of eicosanoid effects. Generally speaking they tend to be separate however. The deficiency state is usually driven by glutathione depletion, a point I have been making since 1998.
Inflammation drives both states. First, it blocks synthesis by promoting oxidative stress. Second it promotes overutilization by driving the cyclooxygenase enzyme activity.
Resverotrol is anti-inflammatory, anti-oxidative and anti-eicosanoid synthesis. So in theory the issues raised by methylation and antioxidant therapies can be controlled by reseverotrol even though its an antioxidant. That makes it very interesting to me.
My suggestions for anyone trying resverotrol is either to balance it with other antioxidants or methylation aimed at boosting glutathione, or alternatively titrate the dosage to a low tolerated level.
Bye, Alex
PS Something I should have mentioned, eicosanoids are profoundly related to vasoregulation, I need to research this more.
