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Hunting down the cause of ME/CFS & other challenging disorders - Lipkin in London
In a talk to patients in London on 3rd September, Dr. W. Ian Lipkin described the extraordinary lengths he and his team are prepared to go to in order to track down the source of an illness, with examples ranging from autism to the strange case of Kawasaki disease.
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Peckerman - Hypoperfusion in CFS/POTS leads to PENE

Discussion in 'Problems Standing: Orthostatic Intolerance; POTS' started by xchocoholic, Sep 18, 2011.

  1. adreno

    adreno 3% neanderthal

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    Tundras of Europa
  2. ramakentesh

    ramakentesh Senior Member

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    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.
     
  3. ramakentesh

    ramakentesh Senior Member

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    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.
     
  4. ramakentesh

    ramakentesh Senior Member

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    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.
     
  5. ramakentesh

    ramakentesh Senior Member

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    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?
     
  6. Emootje

    Emootje Senior Member

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    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
     
  7. xchocoholic

    xchocoholic Senior Member

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    Florida
    Hi All,

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

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