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Pupil disfunction in POTS and OI

Discussion in 'Problems Standing: Orthostatic Intolerance; POTS' started by ramakentesh, Mar 7, 2012.

  1. ramakentesh

    ramakentesh Senior Member

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    Something to look out for as it usually suggests an autoimmune basis (Autoimmune autonomic gangliopathy with autoantibodies against nicotinic a3 autonomic acetylcholine receptors.)
     
  2. merylg

    merylg Senior Member

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    I get enlarged pupils if I take Tramadol (look like a druggy!) :rolleyes:
     
  3. Hip

    Hip Senior Member

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    I am trying to figure out why there are so often autoantibodies against various receptors. Any ideas on this, ramakentesh?

    Some autoantibodies seem to activate a receptor when they attach to it (agonize the receptor); other autoantibodies block the normal functioning of the receptor (antagonize the receptor). In either case, these autoantibodies that target receptors obviously may significantly hinder normal communications in the body (communications mediated by receptors and their ligands), and this communications dysfunction likely underlies many of the pathophysiologies of a disease.

    But why, out of all the different molecular targets in the human body, do autoantibodies so often target receptors?

    For example, ME/CFS has autoantibodies that target the M1 subtype of muscarinic receptor, in 50% of patients. Orthostatic hypotension has autoantibodies that target both the M2 and M3 subtypes of muscarinic receptor (and in this case, the autoantibodies activate these two muscarinic receptors), as well as autoantibodies to ?1 and ?2 adrenergic receptors. Sjgren's syndrome has autoantibodies that target the M3 subtype of muscarinic receptor (and in this case, the autoantibodies block this M3 muscarinic receptor).

    And you say above that POTS has autoantibodies to the A3 subtype nicotinic receptors.


    I'd like to know what (pathological) processes in the body, or during an infection, set the molecular targets of autoantibodies? Knowing this may provide a way to stop the production of autoantibodies, and this could dramatically improve if not cure these autoantibody-associated diseases.
     
  4. fla

    fla Senior Member

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    What sort of pupil dysfunction? I've always been especially prone to red eyes on photographs but I assumed my retina was just more reflective than everyone else's?
     
  5. ramakentesh

    ramakentesh Senior Member

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    In this case we are probably looking for abnormal responses to light - particular in one pupil. In my case the pupils were different sizes for about two weeks unless I was in a dark room.

    Are you referring to the work of David Kem et al on Orthostatic hypotension? Previously all of the work I was aware of was looking at autoantibodies that bind to or block a3 acetylcholine receptors in POTS, OH and in Sjorgens Syndrome. Can you refer me to the research that talks about muscarinic receptors? Other than perhaps mediating vasodilation I am confused about how muscaranic receptors would effect autonomic control as they are generally not ganglionic. i guess vasodilation?

    Doc have also looked into autoantibodies against Norepinephrine transporter, beta 2 activating or binding, and perhaps ang II receptor binding but apparently finding autoantibodies does not automatically prove a conclusion that they have a pathological role in a disease state even when it involves those receptors.

    As for why - gees if they knew that you'd be seeing some pretty impressive treatments for all autoimmune disease right across the board. Its alwasy the same situation - loss of self tolerance and then different arms of the immune system perpetually attacking specific targets - the targets being the main delineator of the disease.

    Molecular mimicry is a popular possibility on patient discussion and some research theory - at least for Ankylosing Spondylitis. A bacteria enters the body that has the ability to trick a suspectible host into attacking antigens in the body that are similar to those attached to the bacteria. Much of the newer reseatch also points to a poor immune system going crazy because it cannot competantly rid the body of certain pathogens that contain proteins similar to the patient's histocompatibility.
     
  6. ramakentesh

    ramakentesh Senior Member

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  7. Hip

    Hip Senior Member

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    Yes. I put these references in an earlier thread on acetylcholine and the parasympathetic nervous system.



    I find the idea that microbes trick the host into attacking antigens in the body quite interesting; there are a lot of tricks that microbes employ for immune evasion purposes (immune evasion = thwarting the action of the immune system, to ensure the survival of the microbe), and autoimmune attacks might just be one of their more clever immune evasion tricks.


    I am particularly interested in enteroviruses in ME/CFS (and its co-morbid diseases like POTS). Autoimmunity can appear within hours of the initial enterovirus infection, and its appearance seems to be driven by certain key cytokines, such as IL-1? and TNF-?. Ref: here.

    Perhaps inhibiting IL-1? and TNF-?, even after autoimmunity has begun, may help reverse it?
     
  8. ramakentesh

    ramakentesh Senior Member

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    yeah that is what I am looking at also because i have Ank Spond.
     
  9. Hip

    Hip Senior Member

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    In which case, you might be interested in the list of TNF-alpha inhibiting supplements I compiled. I did some experiments a while back taking lots of these TNF-alpha inhibiting supplements simultaneously.

    Supplements that inhibit TNF-alpha:


    Cat's claw - a remarkably potent inhibitor of TNF-alpha production

    5-Loxin extract from Indian Frankincense (Boswellia Serrata) is a very potent inhibitor of TNF-?

    Acetylcholine significantly inhibits the release of TNF (so acetylcholine boosters like choline bitartrate, alpha GPC, carnitine may well reduce TNF. However, "piracetam alone markedly increased choline content in hippocampus (88%) and tended to decrease acetylcholine")

    Astragalus
    Burdock (Arctium lappa)
    Ginger
    N-acetyl-l-cysteine
    Chondroitin sulfate
    Devil's Claw
    Curcumin
    Milk thistle
    Alpha lipoic acid
    Allicin (from Garlic)
    Stinging nettle leaf
    Magnesium
    Vitamin C
    ECGC Green Tea
    Vitamin E
    Tea tree
    Ashwagandha
    Rehmannia root
    Coptis root
    Anethole (in fennel)
    Frankincense
    Xylitol
    Fish Oil (Omega-3)
    Oxymatrine
    Artesunate
    Dietary fiber
    Colostrum: Soluble TNF-? receptors in human colostrum neutralize TNF-? bioactivity
    Niacinamide
    Benicar
    Quinine
    Naltrexone
    Deprenyl
    Azithromycin - selectively reduces TNF-alpha levels in cystic fibrosis airway epithelial cells
    Royal Jelly
    Oregano
    Gingko
    Licorice
    Clove
    Q10 - a moderate anti-inflammatory effect
    Evening primrose oil (gamma-linolenic-acid) - converts to Prostaglandin E1, which suppresses TNF-alpha


    The Following Supplements INCREASE production of TNF-alpha:

    Reishi mushroom
    Rhodiola rosea
    Elderberry juice (Sambucol)
    Chlorella
    Spirulina
    Ginseng
    Dandelion root
    Honey
    Chocolate
    Echinacea
    Silica
    Lactoferrin
    Biotin deficiency - up-regulates TNF- production in murine macrophages
     
  10. fla

    fla Senior Member

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    Montreal, Canada
  11. ramakentesh

    ramakentesh Senior Member

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    I am very interested so thank you very much Hip! And I have some experiences with many of those:

    Licorice improves both my POTS and my AS
    Rehmannia improves my POTS
    Rhodiola rosea improves my POTS for about two days before ALWAYS bringing on a massive relapse of AS - which may tie in with your observations.
    Astralagus helps both POTS and AS for me.
    Stinging nettle tea works wonders for AS but seems to bring on POTS for me although this could be random
    Similarly, ginger lowers my BP and Curcumin makes POTS much worse for me.

    I guess ill find the balance one day!
     
    ahimsa likes this.

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