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jangle

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Everything posted by jangle

  1. Exercise will improve you, but from my experience it doesn't necessarily last and I believe this is Rama's experience as well. At my best (mind you I was jogging 5-6 miles + weights + stairmaster + salt water fluids) I would have times when I felt near remission from POTS. Currently I'm starting to feel better again, but everything fluctuates for me. I had a pretty bad 2 month long relapse.
  2. I do think that the base abnormality of POTS is NET deficiency. The subsets are probably explained by additional confounding factors associated with NET deficiency. Some have MCAD, Mito, and/or EDS in addition to other yet to be determined that gives additional factors. Other autoimmune illnesses follow a similar pattern with different people under the same classification experiencing different symptoms yet having relatively the same underlying pathphysiology +/- some other unknown confounding factors. For instance some with lupus have anti phospholipid antibodies which explain the CNS symptoms, whereas others with Lupus have no CNS involvement, but both patients are still said to have Lupus from the underyling common autoantibodies and criteria they share. I guess it depends on your own individual threshold. For me, 1 in 4 is kinda rare. 1 in 10 virtually never happens, and 1 in 20 is basically like mini lottery odds, but when considering life or death I probably wouldn't do something willingly if I knew there was a 1 in 20 chance of me dying. 1 in 2000 though is two orders of magnitude more rare. That's not something I would even worry about.
  3. http://atvb.ahajourn...11.244343.short What this study found was that although people had normal NET genes, there's something going on acting on the normal gene that is repressing its transcription. In other words, there's something that's inhibiting your gene from producing enough NET proteins.
  4. Naomi are you talking about NET deficiency gene or the actual NET protein levels?
  5. Sounds like POTS research. There's articles saying our cerebral autoregulation is preserved, then there are articles that say it isn't. There are articles that say angiotensin ii is elevated, but only in a subset of patients. Then there are articles that say our autonomic nervous system is dysfunctional, and then there are articles that say it is normal and we only have low stroke volume. The only finding I'm willing to attach myself to anymore is the NET finding, because another study showed that POTS can be induced in normal volunteers by inhibiting their NET.
  6. Certainly I can imagine POTS being dramatic enough to induce PTSD. I don't think I have it as I don't have nightmares, flashbacks, or any of the other typical symptoms.
  7. Although there are different causes of POTS like there are for CFS, I don't think there are many different types of mechanisms. What I mean is, there's many different paths you can take to a building, but in the end there is one building. Now in the case of POTS, there very much likely are different mechanisms, so it's unlikely to be just one mechanism. But where I'm thinking is that the most prevalent mechanism is NET deficiency. I believe this afflicts most POTS patients as well as CFS patients. In addition to NET deficiency, there can be other things going on in addition to the NET deficiency which explains the additional symptoms people experience. Things like Mito, EDS, MCAD, etc. etc. It's sort of like Lupus, yes there is a diagnosis of Lupus, but some people with Lupus have CNS involvement. Yes there is a diagnosis of POTS, but some POTS patients have mitochondrial disorders or connective tissue disorders in addition to their baseline POTS. But I don't think there are many different causes of baseline POTS. If there were, then the NET deficiency study would have observed a large standard deviation in their NET study of POTS patients. The fact that it was small, pretty much says that the overwhelming majority of POTS patients have NET deficiency. Since people with CFS also have orthostatic tachycardia in large numbers, I'm assuming they too have NET deficiency.
  8. Nope, I will not take that. I did however do isolaz, which I recommend for acne. (But only if you can find someone who does it for max of $150/per)
  9. Oh sorry what I meant was I wish the researchers in that specific study tested their patients for POTS prior to giving them rituximab. This is because it has been shown that a lot of patients with CFS also have POTS, and if the responders (roughly 2/3 of their patient population) had their POTS reduced or taken away, then that would show efficacy for rituximab in POTS and implicate autoimmune etiology for POTS. It's almost as if one doesn't even need them to have done it. It's a pretty safe assumption a large portion of them did have POTS, in other studies it's well in excess that CFS patients have POTS and there's no way 30 randomly selected CFS patients, not one of them had POTS. But it needs to be "official" we need measurements and objective signs, not just speculation. Estimates are 25%+ of CFS patients have POTS, and lots more of them have exaggerated tachycardia upon standing suggestive of the same mechanism of POTS.
  10. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0026358 With 2/3 of their CFS patients responding to Rituximab, it seems highly likely that some of those responders had preexisting POTS. If they had POTS, it would have been interesting to see if the POTS also resolved with Rituximab. Interesting to note is that the study population had a very low frequency of detectable autoantibody, most were ANA negative even. I emailed the authors asking if they tested their patients for POTS, but I doubt they did. It just seems like they should have, they might have been able to help us POTSIES out.
  11. One thing I want to say is that, it is highly possible that these histone modifications are reversible. They have to be, because otherwise we wouldn't observe a significant percentage of people recovering. If the theory is correct, the remissions from POTS represents a reversion in the histone/epigenetic modification. Unless one argues these people who recover had something else other than NET, but that seems unlikely given the low standard deviation cited in the study of patients with low NET. (Meaning most of the POTS patients clustered around a lower than normal value for NET.) Which means that NET pretty much explains the majority of POTS patients' abnormalities. The most likely explanation for these reversals is a remission of the cytokine/autoimmune attack, but there could be something else to do with the transcription complex.
  12. Rama is correct, Issie. It is unlikely you will find any relevant findings from a serum IL-6 draw. For one thing, CNTF is just one of many IL-6 cytokines, you would need a test specifically for CNTF. However, even this would be flawed, as Rama correctly pointed out, cytokines involved in these types of inflammatory disorders tend to occur locally. For instance in Rheumatoid Arthritis, the increased IL-6 cytokines occur in the synovial fluid. However, there might be a way to test CNTF concentrations in the sympathetic neural cells, but I do not know of it. Yes Rama I also agree it is worth trying, and I will see if I can get a doctor on board.
  13. Makes me wonder if I have a cyst? I've had two brain MRIs, 5 years apart from each other. Multiple doctors reviewed it and told me it was normal, so I would think someone would have mentioned a cyst - but maybe not? I'm too afraid to look at the image myself.
  14. I imagine Mayo could get it approved through my insurance though.
  15. I've called neurologists in my area none have even heard of pots. One neurologist I went to told me to pretend the visit never happened - at least I got my money back. My rheumatologist only tested me for connective tissue disease which I do not have. I don't think I have achr autoantibodies but with the research on cytokines and NET I'd hope Dr. Goodman would be open to the idea.
  16. Ya Arizona girl I got your last PM. I would like to find an immunologist locally, I don't think I have an immunodeficiency, but I do believe POTS is autoimmune. My Rheumatologist is basically ignorning me and I can't seem to find an immunologist who does anything other than allergies. Even though I don't know the odds of getting Goodman on board some immunotherapy for POTS I figure my only chance is at Mayo, there's literally nothing doing here in Texas.
  17. Well I think I'm going to try Dr. Goodman. I'd like to get my NET gene sequenced to see if it's ok. If it is ok, I'd like to get my IL-6 levels measured and possibly other cytokine levels. Even if those come back normal, assuming my gene test comes back normal I'd like to go ahead and self experiment with a IL-6 blocker to try and increase NET expression. Hopefully Dr. Goodman is on board the new research.
  18. Yes, but with a drug that's already FDA approved for something else.
  19. Ok, well this doesn't really help me much, I'm 7 years into this. In fact this hurts me because it indirectly affects funding impressions for future research when an illness is thought to go away on its own.
  20. If you want to experiment on yourself and you have the money upfront to do so, will the Mayo Clinic allow you to try assuming of course you have a halfway good idea?
  21. NE reuptake inhibition would cause anxiety/effective NE surges. By losing the ability to remove NE from the synaptic cleft, your sympathetic nervous system stays activated. (It's activated by NE binding the synapse, gets "deactivated" when the NE leaves the synapse i.e. binding sites.) Really there are two options. 1.) Reduce NE concentration 2.) Increase NE reuptake. Option 2 would be most preferable as that's being implicated in causing POTS now.
  22. I'm thinking there has to be something in addition to NET deficiency. For instance, one would expect everyone who takes SNRI's to get POTS if NET alone was the causal mechanism. EDIT: Actually this may not be true, reboxetine used in the study is actually a very unique NET in that it binds only NET. The other SNRI's bind other parts of the ANS that might balance out NET inhibition and not cause POTS. Actually reboxetine is having difficulty getting approval in the USA because of its uncertain therapeutic benefit and potential side effects, (which probably includes drug induced POTS). I believe there is also autoantibodies involved. 15-20% of POTS patients have ACHR antibodies. There's probably other antibodies as well.
  23. It might be possible that even with A457P one could have normal NET expression. What I mean is, maybe the mutation only achieves 98% reduction in NET protein if an environmental cue also triggers it. Now if a person had that mutation and they measured their NET protein to be 98% reduced and they still did not have POTS then that would be confusing. But really the study where they blocked people's NET protein and it produced POTS pretty much sealed the deal for me already. There's no mistaking that.
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