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Posted

"

As perhaps you might know we published on increased ANF-II well before Satish and also established the role of ACE2 in certain forms of POTS.

Florinef is more or less artificial aldactone which had been shown to be decreased in Satish’s patients while ANG-II is increased.

Spironolactone is a diuretic and might have an adverse effect in patients, but it is a thought.

Recent work in animal; models of CHF and hypertension show that ACE2 is abnormal and

exercise makes it normal."

Exercise makes it normal. :)

Posted

I also take a diuretic, small dose, Hydrochlorothiazide 12.5 with the Losartan 100mg, because I was retaining fluid in my ankles. I actually have to watch my salt intake, and can only take so much fluid, too, so it's like a double edged sword! "But I am fearfully and wonderfully made." :)

Posted

Yeah, and if you need to increase your potassium that drug would do it.

But, if there are auto antibodies to ace 2 and you have low renin and aldosterone - this would probably be bad for you. With the kidney dysfunction - the thought is these people have too much potassium. The usual treatment is diuretics - but that won't work for us potsies. The other possibility is instead of having vasodilitation issues we may have vasoconstriction issues. The possibility of auto antibodies to ace is increased if there are connective tissue disorders and autoimmune problems. I think allot has to be discovered before the true picture will come to light. The studies I read on this said that some women have pre-eclampsia and this can be the issue with this. That would explain why some have developed POTS issues with pregnancy.

I think there are different subsets of us and we don't all fit into the same little box. We need to figure out all the components of each individual person and then catagorize us and then the solutions for each group - will be totally different. I don't believe that has been done yet - and I think it's a major flaw in the treatments being done today. (For what my opinion is worth. LOL)

Posted

Yeah, and if you need to increase your potassium that drug would do it.

But, if there are auto antibodies to ace 2 and you have low renin and aldosterone - this would probably be bad for you. With the kidney dysfunction - the thought is these people have too much potassium. The usual treatment is diuretics - but that won't work for us potsies. The other possibility is instead of having vasodilitation issues we may have vasoconstriction issues. The possibility of auto antibodies to ace is increased if there are connective tissue disorders and autoimmune problems. I think allot has to be discovered before the true picture will come to light. The studies I read on this said that some women have pre-eclampsia and this can be the issue with this. That would explain why some have developed POTS issues with pregnancy.

I think there are different subsets of us and we don't all fit into the same little box. We need to figure out all the components of each individual person and then catagorize us and then the solutions for each group - will be totally different. I don't believe that has been done yet - and I think it's a major flaw in the treatments being done today. (For what my opinion is worth. LOL)

Hi issie, you mention pre-eclampsia. I actually developed pre-eclampsia about two weeks after I developed pots at the end of my pregnancy. Do you think they are related?

Posted

I'm thinking!!! I'm really excited about what I'm uncovering in regard to the autoantibodies to ace. It could be the answer for us ODDITIES - that don't fit into the picture. It just might be the reason for our high bp's, and lack of response to typical POTS solutions. It's way out there - but, very possible - this could be an answer for us. Maybe not an answer - but, a reason.

Posted

I like Dr Stewart. Top guy. And he must get some far out emails... You guys should consider donating to his research. And now everyone knows that he occasionally replies he might get a few more...

there are alterative reasons for why ang II might be high in some POTS.

Posted

I'm thinking!!! I'm really excited about what I'm uncovering in regard to the autoantibodies to ace. It could be the answer for us ODDITIES - that don't fit into the picture. It just might be the reason for our high bp's, and lack of response to typical POTS solutions. It's way out there - but, very possible - this could be an answer for us. Maybe not an answer - but, a reason.

Issie, do you ever talk to dr goodman about your theories? I know he is of the mind set that pots is autoimmune endocrine. It sounds like you have a lot of knowledge and he does do research.... Just a thought!

Posted

yes, I run it past him. He's the quiet type and I never know what he's thinking I hope one day - we'll hit on answers. At least, he - so far, has let me try out what I want to try. So, we'll see if he'll go for this one. He will read studies. I've had to eat crow on some of the things I thought would work - FOR ME. But, at least he let me try it. I talk to the docs on behalf of all us POTSIES. Even when it doesn't apply to me.

Issie

Posted

Hate to be the bringer of negative scientific debate - but ACE 2 would only have any relevance if you had actually evidence - that is plasma assay - demonstrating you have elevated angiotensin II. If you dont - and I am yet to talk to any patient on these forums that has either had the test or tested positive to it - then ace 2 probably has no relevance at all.

Posted

Ya I just want to say that I'm not sure about spironolactone and I wouldn't want anyone getting hurt trying that medicine from my suggestion. But hopefully we can get something going here.

EDIT: Do you think we can get our angiotensin ii levels checked? I'll ask my doctor when I see him.

Double EDIT: Also Rama, the study I linked from Raj did show that POTS patients tended to have higher angiotensin ii levels. Also Stewart's research established this as well. It might not be universal in POTS patients, but for some it could be their major issue.

Posted

Oh my yes, the poor guy has pages and pages of stuff from me. I run it all past him. He's the quiet type and I never know what he's thinking - but, I do believe he is aware of what I'M thinking. LOL :) I hope one day - we'll hit on answers. At least, he - so far, has let me try out what I want to try. So, we'll see if he'll go for this one. Have to get all my thoughts together and get all the studies printed and deliver them to him. (Nice that I live here.) He will read studies - but, not our conversations. But, I make sure there is a really nice cover letter - explaining the whys. I've had to eat crow on some of the things I thought would work - FOR ME. But, at least he let me try it. I talk to bunch of the docs on behalf of all us POTSIES. Even when it doesn't apply to me.

Issie

Thanks for advocating on behalf of all of us issie, I try to do the same :)

Posted

No doubt. But Stewarts work demonstrated a subset of patients only with elevated angiotensin II levels and these were nearly exclusively females. The Vandy work suggests that they included 15 female patients who just happened to also have elevatede angiotensin II levels. They believe a larger portion do, but again you will notice that all the patients in that research were also female.

Email Dr stewart again - i think you'll find he thinks its about 20-25% ish.

This isnt criticising you, the idea or anything like that. Just applying some observations to the idea. I have often thought about whether inflammation could effect angiotensin II catabolism and I know that some studies suggest that C-reactive protein does as an example.

As for advocacy and sending stuff to doctors - the dangers of emailing and sending doctors volumes of research is that unless its relevant, demonstrates a basic understanding of physiology and is supported by actual peer-reviewed science relevant to POTS patients it probably just reinforces the belief that we are all obsessed with our symptoms and are crazy. The likelihood that a bunch of patients are going to solve the etiology of POTS based on random internet searches is probably pretty low simply because we cant test any of our hypothesis on patients and because we cant actually test any favourable results. But more often, it is because the theories are based on incomplete understanding of what has already been established about POTS or the physiology of the vascular / autonomic system.

Posted

No doubt. But Stewarts work demonstrated a subset of patients only with elevated angiotensin II levels and these were nearly exclusively females. The Vandy work suggests that they included 15 female patients who just happened to also have elevatede angiotensin II levels. They believe a larger portion do, but again you will notice that all the patients in that research were also female.

Email Dr stewart again - i think you'll find he thinks its about 20-25% ish.

This isnt criticising you, the idea or anything like that. Just applying some observations to the idea. I have often thought about whether inflammation could effect angiotensin II catabolism and I know that some studies suggest that C-reactive protein does as an example.

As for advocacy and sending stuff to doctors - the dangers of emailing and sending doctors volumes of research is that unless its relevant, demonstrates a basic understanding of physiology and is supported by actual peer-reviewed science relevant to POTS patients it probably just reinforces the belief that we are all obsessed with our symptoms and are crazy. The likelihood that a bunch of patients are going to solve the etiology of POTS based on random internet searches is probably pretty low simply because we cant test any of our hypothesis on patients and because we cant actually test any favourable results. But more often, it is because the theories are based on incomplete understanding of what has already been established about POTS or the physiology of the vascular / autonomic system.

It is a complex problem not just for us but for the researchers as well. But we shouldn't let that deter us from trying to see if we can find something that might be of use. Even if it isn't everything, making any little bit of progress down the right direction can shave years off of our suffering as well as future POTS sufferers.

The way to move forward from here is to see if we can get those ACE2 autoantibody/ACE2 tests. Without objective evidence as to the pathology we have nothing.

Posted

I think the way forward would be to get the angiotensin assay. Quest do it.

I didnt mean to sound mean or personal with the comment above. it wasnt directed at anyone specifically. But I know for a fact that many POTS docs get volumes of information and research from various patients all the time. Some of it might open up whole new avenues but Im sure many dont even look at any of it and they probably just cringe. Science is about testing hypothesis - about being the worst enemy of your own hypothesis - instead of trying to find all the things that support it its also important to have a look and be open to the things that dont.

I like your idea and it may prove valid. Anyone here at any time may stumble upon something fantastic. Tumeric was an example that helped many people. But angiotensin II is not elevated in all POTS patients. It may be in many or it may only be in a small portion depending on which research group your following. that doesnt mean I think you should stop thinking about POTS - on the contrary.

POTS is somewhat complex but the difference between us and doctors is that they communicate with one another, share ideas and unpublished data and I can tell you that they know more about POTS than many here give them credit for. We as patients, are out in the cold - we can only read what gets published after peer review and we rarely get to hear about any of the unpublished findings that often shape the direction of research. We dont get to hear about the results of medical trials of an array of new medications for POTS. We dont get to see hypothesis tested or get to see patients all day every day. I know that there is a lot more established about POTS than has been published. Often we dont get to see the full context and sometimes we even apply those findings incorrectly because we dont have all the data.

So we are probably as likely to stumble upon something by luck as by reasoning. :) I always keep a good tab on the self-prescribers on CFS forums who take all manner of drugs to see if they help. I figure that someone will be chance stumble on something one day! :)

The moment I have certainty about the etiology of my POTS is the moment I spend a month on the net. Until then I just read the POTS research only.

Posted

This is definitely Dr. Stewart's and Raj's idea. I'm just trying to take their idea and form a treatment on it.

Right now it seems like Vitamin D would be the best option, namely because it is safe. But obviously that hasn't helped many people on this forum.

Also exercise, which has shown to help some people.

There is a lot of guess work, I'm honestly at a point where I wouldn't mind trying things that haven't been proven yet.

Posted

ive been there myself. TCM was one of those.

Stewarts idea is that angiotensin II is elevated because of genetic faults within ace 2 not an autoimmune mediated change in ace 2 gene expression.

Raj and Roberston's idea is that ang ii is elevated. No explanation of why.

Autoimmunity is pretty much something that most patients would agree plays a role in POTS in their opinion so this could indeed by the 'bridging theory' at least for some. And I hope it is. But not all docs accept that POTS has a definate autoimmune basis.

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