Remy
Administrator
I recently did the CellTrend testing for CFS/POTS...came up with two positive results, so I'm trying to figure out what my next steps might be.
I don't think I understand exactly how these antibodies work...or what treatments might be most effective. Does anyone have any good sources of information on this?
Here is the full list of the antibodies tested with my positive results in bold:
but then this:
Midodrine is an alpha 1 agonist...so does that mean that the antibody is actually blocking the receptor site, keeping it from functioning properly? Or is it activating it, in which case an alpha 1 blocker might seem to make more sense? It seems like the two quotes are actually contradictory.
So wouldn't it be likely that blocking the exaggerated catecholamine response would improve symptoms? Is there a good way to do this?
Does this also go along with the lowered levels of neuropeptide Y that have been reported in cases of lowered resilience to stress and PTSD? https://www.ncbi.nlm.nih.gov/pubmed/8752116
I don't think I understand exactly how these antibodies work...or what treatments might be most effective. Does anyone have any good sources of information on this?
Here is the full list of the antibodies tested with my positive results in bold:
- Beta-1 adrenergic receptor auto-antibodies
- Beta-2 adrenergic receptor auto-antibodies
- Muscarinic cholinergic (M1) receptor auto-antibodies
- Muscarinic cholinergic (M2) receptor auto-antibodies
- Muscarinic cholinergic (M3) receptor auto-antibodies
- Muscarinic cholinergic (M4) receptor auto-antibodies
- Muscarinic cholinergic (M5) receptor auto-antibodies
- Alpha-1 adrenergic receptor auto-antibodies
- Alpha-2 adrenergic receptor auto-antibodies
- The autoantibodies may also exert an allosterically mediated positive modulatory effect upon b1AR and a negative modulatory effect on a1AR activity.
but then this:
These autoantibodies appear to function as partial agonists and the absence of measurable direct activation of the transfected receptors in vitro in the absence of their normal ligand does not exclude their presence. It is possible this allosteric impact on the activity of the a1AR ligand norepinephrine represents the distinct pathophysiological feature characteristic of POTS.
Midodrine is an alpha 1 agonist...so does that mean that the antibody is actually blocking the receptor site, keeping it from functioning properly? Or is it activating it, in which case an alpha 1 blocker might seem to make more sense? It seems like the two quotes are actually contradictory.
We have recently demonstrated an exaggerated catecholamine response in postural tachycardia among patients with syncope and dysautonomic cardiovascular response to orthostasis.19 The catecholamine surge may be seen as a compensatory mechanism to override the a1AR malfunction associated with the proposed autoimmune blockade as present in POTS patients but this explanation is unlikely in those with recurrent VVS.
So wouldn't it be likely that blocking the exaggerated catecholamine response would improve symptoms? Is there a good way to do this?
Does this also go along with the lowered levels of neuropeptide Y that have been reported in cases of lowered resilience to stress and PTSD? https://www.ncbi.nlm.nih.gov/pubmed/8752116