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Peckerman - Hypoperfusion in CFS/POTS leads to PENE

ramakentesh

Senior Member
Messages
534
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.
 

ramakentesh

Senior Member
Messages
534

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.
 

ramakentesh

Senior Member
Messages
534
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.
 

ramakentesh

Senior Member
Messages
534
with a potent vasoconstrictor
effect on peripheral vasculature lead to decreased regional

cerebral blood flow, with consequent increases in anaerobic
glycolysis and brain lactate, the end product of glycolysis

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?
 

Emootje

Senior Member
Messages
356
Location
The Netherlands
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:

isoprostane F2.jpg

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
 

xrayspex

Senior Member
Messages
1,111
Location
u.s.a.
Hi All,

I'm bumping this because I was telling someone here about this article by Peckerman. HTH ... X
hey xchocoholic I was researching and came upon this thread again and wanted to follow up---you had mentioned that you were able to deal with a lot of your symptoms through diet etc Would you mind saying how that is going for you now and what you have found to be the most useful in dealing with these issues? what drinking, eating, supplementing, resting etc habits? (I was going to PM you but looks like you aren't open for that option?)