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I would give my entire net worth up to this point to just be able to spend a week with the POTS researchers and present all the research we've accumulated and ideas for treating angiotensin ii. If we can work together we can find a cure for POTS.

There is always hope. We're going to figure this thing out!

Julie I absolutely love you! That study explains the anomaly that was confusing me so much with POTS. Why would saline work but not drinking + salt intake? At this point we have a working model. Now we need to figure out how to treat it. And that goes back to what caused the high angiotensin ii like you mentioned. Could it be a compensatory mechanism to low aldosterone, is it an autoimmune attack to ACE2 enzymes, is it a genetic deficiency, is it a receptor abnormality? Any other theories as to what can cause high angiotensin ii in us? For me I think it was a genetic deficiency of ACE2 enzymes, because I distinctively remember having symptoms (though much milder) since I was a child. It could be that any of these causes can eventually lead to POTS in patients and that might explain the heterogeneity of presentations. However, the specific cause is most definitely going to have a dramatic impact on the type of treatment to lower angiotensin ii. For instance, one wouldn't want to give spironolactone to someone whose high angiotensin ii is caused by low aldosterone, that would be very dangerous and make it much worse.

There is still a possibility that aldosterone isn't the primary cause. Drugs like mestinon work well for pots patients despite not influencing the raas directly. Rather the primary defect is the vagus nerve. Perhaps aldosterone secretion is mediated by the parasympathetic nervous system. Therefore a faulty pns would create the environment of low aldosterone. I believe that indeed the faulty pns is due to high angiotensin ii levels and that correcting that should ne the focus of treatment. Maybe it isn't a compensatory mechanism to low aldosterone.

Lemons that is true, the parenteral delivery is definitely the difference but I think angiotensin ii is what males the difference occur. Issie, ya it would not be safe. But now im beginning to think neither would spironolactone. The thing is we have unbalanced steroids that is causing our problems but the body is very sensitive to shifts on steroids so that makes treatment so much more difficult.

Do you think we could get synthetic aldosterone? Im wondering if that might be a better way. Like florinef is still sufficiently different than aldesterone. Florine is more like spironolactone.

Oh gosh ill have to look them up. I know I've had a few.

Im thinking that would cause the racing heart as well as gastrointestinal and blood flow issues. Like this makes sense too because like why would spironolactone decrease angiotensin ii? Well spironolactone binds to the aldesterone receptor which would then shut off the angiotensin ii compensatory mechanism thus resulting in lower angiotensin ii.

Issie that's a good idea especially since aldesterone tends to be on the low end of the spectrum in pots. Maybe the high angiotensin ii is a failed compensatory mechanism. I mean failed in that once triggered it starts blocking the vague nerve

Lemons ace2 converts angiotensin ii to 1-7. So high ACE2 would mean low angiotensin ii. Conversely low ACE2 would mean high angiotensin ii. Lissy that is interesting I haven't thought about the potential of antibodies to interrupt in some way the function of ACE2. It might not be a binary thing (either you have normal ACE2 or you don't) but rather having abnormally functioning ones. That would make treatment much different.

Okay, that would make sense. I wonder if because my renin and aldosterone levels are nearly non-existent - if lowering the angiotension II levels (If they were high, in the first place - don't know) was the wrong thing to do - because maybe with those levels already being nearly non-existent - the angiotension may not need to be lowered - it could have been high (if it is) for a reason. Maybe something to do with the autoantibodies. Maybe it's keeping potassium levels in check. But, if the chain of breakdown in the kidneys (renin, angiotension 1, angiotension 2, aldosterone) is how it goes - than it's not likely that an elevated angiotension level would be coming from the kidney chain of events because that would be low too. (low renin on one end and low aldosterone on the other - makes the inbetween low too) So, if that's the case - then where would the high angiotension levels be coming from? They can be produced in the heart and liver. So, maybe if angiotension is high and someone's renin and aldosterone levels are low - the dysfuction of the paradox of high angiotension could be from somewhere else in the body. But, WHERE? (I hope people are able to follow my rambling line of thought.) Just trying to make this make sense. I was so sure that the Lorsartan would work for me and when it didn't - I really couldn't figure that one out. There seems to be a connection with the autoantibodies to ACE2 and connective tissue disorders (possibly EDS) which I have also. Not sure how to tweek this. THAT! is a very interesting question. One I hope we do not have to answer, sort of like solving an equation like (x^3+SQRT(EXP(x^2+SQRT(x))) * Log(x) * 0 = 0 If that 0 wasn't there, that'd be really difficult to solve for x. But hopefully we won't have to answer that question, hopefully we can just find a medicine that ups ACE2 levels and gets us better without ever having to know the gory details. (In this example the medicine would have the effect of putting the 0 in the equation) Otherwise we're in for some rough science.

Figured I'd make a new thread on this topic. http://www.ncbi.nlm....pubmed/20228119 Angiotensin ii definitely has some type of mitigatory effect on water consumption associated with some type of protein receptor downregulation. However this doesn't seem to affect saline administration. Now there might be more studies that elucidate more on this topic, I haven't thoroughly searched for them yet, but I believe this explains why saline helps POTS patients and not water + salt (as much) and provides very strong evidence for angiotensin ii.

http://www.ncbi.nlm....pubmed/20228119 Could this explain why saline helps POTS patients but not water + salt intake? (not as much anyway) It seems angiotensin ii affects something about water intake, but not saline intake.

honestly the best way to go would be just to get some synthetic ace2 enzymes and throw em in. Don't know if that's possible. If we can get a researcher interested, they might have some ideas.

Ya Rama, I'm beginning to think that the therapeutic value of Florinef isn't just an enhancement of blood volume, but rather I think it is doing an activity similar to spironolactone. Dr. Stewart did mention that Florinef is essentially artifical spironolactone, and if spironolactone drastically raises ACE2 levels and lowers angiotensin ii, then maybe Florinef is having some type of attenuated ACE2 enhancement as well. Still, I think spironolactone would have a much more drastic ACE2 elevation effect. Either way, there might be an even better therapeutic option for raising ACE2 levels/lowering angiotensin ii. Exercise might work for some, but I got to believe there's some type of hormonal medication that would also work well. I've been searching but thusfar I haven't found anything outside of the herbs and spironolactone already posted.

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http://www.heartrhyt...1204-X/abstract Julie, also I found in this article that despite POTS patients having higher angiotensin ii levels, they had similar to slightly lower aldesterone numbers. (p = .111) only p < 0.05 is considered statistically significant. So in other words there was not a statistically significant difference in aldesterone levels between POTS and controls. Now why that is? I have no idea. EDIT: Lemons I would love for Rama to help me mow my lawn. Did that sound as wrong as it did to me?

Julie that is true. A higher angiotensin ii level shouldered make a high aldesterone level. There has to be something going on one abstraction level above what we are looking at. I don't think it is a dysfunction of the receptors because that would cause chronic symptoms i.e. structurally abnormal nerve receptors would have produced POTS all of one's life, but because POTS is something that one develops it suggests an alteration in chemical environment rather than structural genetic change. However I do think it is possible to have elevated angiotensin ii in localized regions I.e. the heart perhaps has a local deficiency of ace ii enzymes while maintaining overall serum levels constant.

Julie I've heard the method of testing angiotensin ii is quite involved so hopefully they did it right. There could be a connection between nitric oxide and angiotensin ii.

http://www.ncbi.nlm....v/pubmed/512963 I found this study that showed that angiotensin ii concentration effectively blocks nerve signals from the vagus nerve. Essentially what I think is happening is that systemically (kidneys, brain, heart) there is an elevated level of angiotensin ii (Might show up in serum samples, might not - for those that it doesn't, the angiotensin ii might only be localized to certain regions - perhaps due to localized ACE2 autoantibodies.) I don't think it is the nerve that is damaged but rather the method for the nerve to communicate its signals to the various organs. Interestingly enough I think this might also have a role in anxiety disorders. People with mitral valve prolapse often have anxiety/dysautonomia and sure enough this study showed they have a faulty angiotensin ii system: http://www.ahjonline...0015-9/abstract Now that's more of a speculation. Anyways, I recently got referred to Doctor Levine and I sent him my idea about angiotensin ii/vagus nerve. He said he was very impressed and that he will have a lot to talk about with me. I know of all the POTS researchers he's the most steadfast against there being a problem with the autonomic nervous system. But I have found that life is full of ironies. EDIT: Also, I think the reason Astronauts develop POTS is because their angiotensin ii levels go up during spaceflight. http://www.ncbi.nlm.nih.gov/pubmed/2147850

These seem much safer than experimenting with unknown medications!

Is subway gluten free? They have like 5 dollar subs I've been living off those for lunch and dinner XD

Ill try going glutton free but it seems impossible as every food seems to have a million ingredients in it.

No, I've never worn aftershave, but I could always try it out and see what happens.

So it's possible to be Pretty much every breakfast item contains starch. You'd almost have to just skip breakfast. kayjay your igG test was negative? I think I read somewhere that that detects celiac disease for up to 85% of celiac patients.