Peckerman - Hypoperfusion in CFS/POTS leads to PENE

Resveratrol inhibits isoprostanes, and improve cerebral blood flow:

Resveratrol inhibits isoprostane production in young and aged rat brain.

Effects of resveratrol on cerebral blood flow variables and cognitive performance in humans: a double-blind, placebo-controlled, crossover investigation.

Dr Bell's views are not established and certainly not accepted by all researchers. Vanderbilt are currently reviewing whether abnormalities in kidney dopamine levels may effect postural salt handling and consequently overall blood volume.
Secondly many of the findings of abnormal autoregulation by Stewart and Medow point to impaired venous pressure and or changes in neuronal blood flow changes.
Finally the ventricular lactate studies are interesting given hits proximity to the hypothalamus.

Do you tolerate red wine? It also potently effects nitric oxide bioavailability - which may be adverse considering there is strong evidence of nitric oxide upregulation in many POTS patients.

And according to one of the researchers involved in a more recent research paper on ventricular lactate, the view that the etiological framework of primary cerebral antioxidant abnormalities is not uniformly accepted even in that group.

Impaired glucose metabolism alone can account for increased cerebral lactate. As can reduced blood flow from any of the pathological mechanisms in POTS and OI, many of which there is strong evidence for peripheral abnormalities rather than central.

Cerebral autoregulation in POTS with CFS was found to be poorly buffered, resulting in no buffering of BP variations in the cerebral vasculature. This again does not support this hypothesis.

Presuming peripheral vasoconstriction was a common finding in CFS with OI. WHich is isnt. Secondly how does this account for increases of norepinephrine and angiotensin II and potential baroreflex abnormalities?

Personally, I'm a big fan of Bell's hypovolemic vasoconstriction theory. I my case it explains a lot and it looks something like this:



It explains the hypovolemia and the secondary vasoconstriction response (SNS an RAAS). The same mechanism (high isoprostane/ET-1/ANP, hypovolemia, SNS and RAAS activation) are seen in diseases like obstructive jaundice/cholestase, pre-eclampsia and liver cirrhosis.

ANP = Atrial Natriuretic Peptide
ET-1 = Endotheline-1
SNS = sympathetic nervous system
RAAS = Renin–Angiotensin–Aldosterone System

Hi All,

I'm bumping this because I was telling someone here about this article by Peckerman. HTH ... X