Latest Research Out Of Vandy

[juliegee]

Issie- I've been waiting for you to chime in on this one. I recently went back & re-read all of your salt postings as I realized they played into this. As you know, I was recently Dxed with diastolic dysfunction perhaps from too much salt loading. You predicted that that might be one outcome. I have voluntarily cut back on all added salt (not what naturally occurs in my food.) It's been tough on my autonomic symptoms, but I am hoping to reverse my heart damage... I'll know something on 2/24 when my echo is repeated.

Lenna- I am so excited about the Losartan!!! I have recently been studying Dr. Stewart's categories & am convinced that I am a "low-flow" too. What has jazzed me up is that losartan is also being used as a treatment for Reynauds. Mine is very severe & all treatments till now have worsened my dysautonomia symptoms. If I can improve both with one magic bullet, maybe add a little salt back in due to the low BP side effect....I may be in business I am very anxious to hear how Danny does. What dosage did he start with? Any idea what a therapeutic dose will be? I plan to share all of this with my rheumatologist who's heading up my treatment.

Thank you for sharing this exciting new research!

Julie

[Lenna]

Lenna- I am so excited about the Losartan!!! I have recently been studying Dr. Stewart's categories & am convinced that I am a "low-flow" too. What has jazzed me up is that losartan is also being used as a treatment for Reynauds. Mine is very severe & all treatments till now have worsened my dysautonomia symptoms. If I can improve both with one magic bullet, maybe add a little salt back in due to the low BP side effect....I may be in business I am very anxious to hear how Danny does. What dosage did he start with? Any idea what a therapeutic dose will be? I plan to share all of this with my rheumatologist who's heading up my treatment.

Thank you for sharing this exciting new research!

Julie

Julie, wouldn't that be great if it could help with your Reynauds!

First, I want to say that so far Losartan has not been a "magic bullet" for Dan. He still has bad days and bad partial days. However, the "bad" doesn't seem to be as bad as it used to be. And there seem to be fewer bad days now. His dizziness is a little better, his energy is a little better, and his brain fog is much better. The past year has been very rough for him and this is the first improvement in a long time.

He's still evolving with the dose. His doctor doesn't really know what would be optimal, and we're having a tough time getting info from Dr. Stewart about it because this is still experimental. Dan started on 12.5 mg. each morning for 2 weeks; then he increased it to 25 mg. each morning and stayed on that for about a month. Now he recently started taking 12.5 mg. at bedtime in addition to the 25 mg. in the AM. I think he'll stay on that for at least a month before considering the possibility of increasing again. I doubt that he'll go any higher than 50 mg for a total daily dose. It seems to build up slowly, so he doesn't see the benefits of an increase for the first couple of weeks. I'm hoping that things continue to improve for him as he goes further with this.

The one downside is that it is creating havoc with his blood pressure, and so his doctor said that he MUST stay on salt pills to try and keep his blood pressure up. In light of what you were saying about salt, that might be an issue for you.

I'll keep you updated!

Lenna

[issie]

Okay, so I looked this drug up and it's a form of potassium. Potassium ups your aldesterone and aids in the balance of this system. I sent some of you the paper I wrote about how all this works. I questioned why the docs didn't just try to balance our potassium, magnesium and calcium levels (and other minerals) and work out what's wrong with the aldesterone/renin balance. This drug would work for us with the hyper POTS - because it lowers blood pressure and regulates it by potassium. Why not just try taking potassium? It would be a cheap try to see if it makes a difference. I've always said that I think humans are deficient in minerals. Our bodies make vitamins but not minerals. We probably don't eat right and that throws things out of balance further. We are not deficient in a pharmacitucal that's been concocted in a lab somewhere - we are deficient in minerals and vitamins - what our bodies are made up of.

Julie, I'm sorry that you are having to deal with heart issues on top of it all. But, I truly think that salt and florneff (Unless there is adrenal dysfunction) is the wrong way to treat this. We help one problem but create another one. As I said in my questioning of this - if you use salt it should be either sea salt or himalyian salt that has all the minerals in it. It helps to balance out the electrolytes better and helps the cells to function better. If you must do more salt - these are the forms to use. But, I personally feel that unless you are totally dehydrated - limit salt to a normal amount and don't salt load. When I'm bad, I must do a G2 one a day. My doc said to not swig it down - sip it and between drinking water. If you gulp it down it won't work. It takes time for the minerals to make the liquid be uptaken and you need water to go into the cells. I limit myself to one a day and if I'm real bad I use a Emergen C. Vitamin C is good for lots of things and Emergen C helps balance the electrolytes because of the minerals. It comes back to minerals. I think they are very important. But, it's the balance of them that is important.

[issie]

I know my aldosterone isn't low from salt, because I am one who doesn't use extra salt. So I'm wondering why the lower aldosterone to begin with? What in our body is miscommunicating and why?

Could be adrenal dysfunction/or kidney related.

[ramakentesh]

There are many steps in the Renin/Angiotensin/Aldosterone process which regulate blood pressure and fluid volume in the body. One of these steps involves the conversion of Angiotensin II to ACE 2. If you have too much Angiotensin II because the conversion to ACE 2 isn't happening, then your blood vessels will be too constricted.

Most people with POTS have the opposite problem - their blood vessels are too dilated. That's why the first medications they're given when they are diagnosed with POTS are vasoconstrictors like Midodrine.

Another thing that helps most POTS patients is drinking lots of water and taking in lots of salt. However, if the RAA chain of events is disrupted by the inability of Angiotensin II to convert to ACE 2, then you will have low blood volume regardless of how much you drink and how much salt you eat.

Dr. Stewart in NY has given a name to the subset of POTS patients whose blood vessels are too constricted and whose blood volume is always low. He calls this "Low Flow POTS". Low Aldosterone and low Renin are also typically found in people with Low Flow Pots

I think about half of low flow (Hyperadrenergic) patients have impaired angiotensin II catabolism. You can asks the doctors yourself. Sometimes they reply.

While you have peripheral vasoconstriction in this form of Low flow POTS you also usually have vasomotor nerve failure from parasympathetic withdrawal. elevations in angiotensin II reduce the availability of nitric oxide neuronally at the nitrergic receptors, decreasing parasympathetic activity while potentiating norepinephrine transduction.

The other half of Low Flow are yet to be catagorised - some may have reduced cAMP activity, increased TPR only or NET deficiency. If I had postural hypertension I would be getting my angiotensin II levels checked though!

Increased angiotensin II levels can also occur due to chronic inflammation from systemic autoimmune illnesses like RA because inflammatory markers can affect either ACE 2 activity or upregulate angiotensin II receptors.

Any shift in the sympathetic/parasympathetic balance can also affect cerebral autoregulation.

I would hope that now days the first medication of choice would be mestonin rather than midodrine.

[Sarah4444]

I have been told I have hyperadrenergic POTS, but I don't have hypertension. However, I think I may have postural hypertension - sometimes. My bp is about 90/60 lying down and more like 120/80 standing, at first, then it seems to fall. Other times, it falls when I go from supine/sitting to standing.

The last doctor I saw told me that I can't have hyper POTS, as I don't have absolute hypertension. Can I still be one of the low flow people? How do you figure all this stuff out?

[heathmcev]

I have been told I have hyperadrenergic POTS, but I don't have hypertension. However, I think I may have postural hypertension - sometimes. My bp is about 90/60 lying down and more like 120/80 standing, at first, then it seems to fall. Other times, it falls when I go from supine/sitting to standing.

I would love to know about this too. I am also Hyperadrenergic with hypovolemia & orthostatic hypotension. I asked my pots specialist how hyper pots & OH can happen together and he just said "it's more complicated than that"... he didn't bite when I pressed further for an answer...

[juliegee]

I have been told I have hyperadrenergic POTS, but I don't have hypertension. However, I think I may have postural hypertension - sometimes. My bp is about 90/60 lying down and more like 120/80 standing, at first, then it seems to fall. Other times, it falls when I go from supine/sitting to standing.

I would love to know about this too. I am also Hyperadrenergic with hypovolemia & orthostatic hypotension. I asked my pots specialist how hyper pots & OH can happen together and he just said "it's more complicated than that"... he didn't bite when I pressed further for an answer...

Gulp- I'll bite. Just keep in mind that it's my uneducated dumb self talking I have the same pattern of BP. This is the way I understand it. It's all about maintaining homeostasis. Because of the hypovolemia, your BP drops upon standing. Your heart rushes to the rescue and elevates the HR temporarily pushing that BP up for a while (maybe seconds or minutes) until it ultimately fails because it cannot maintain the stress. Keep in mind that the drop in BP is also a form of homeostasis- syncope will land you on the floor and your heart can finally relax as blood can finally get to your brain & viital organs.

If you are like me, your BP will be quite low when you are supine or sitting as your heart is fairly relaxed. The hypertension may be quite brief and is only in response to standing.

Julie

[issie]

I also think that hyper POTS is related to the norepinephrine release - too much of it. I have both high and low bp's. But, if I understand it correctly it's the amount of norepi. your body releases in relationship to the postural positions of your body. Norep. is an adrenal type response along with epinephrine that gives that fight or flight response. It is connected to how your body responds to stress. I don't handle any type of stress well.

[ramakentesh]

It depends where you are diagnosed, but in nearly all cases Hyperadrenergic POTS is characterised by an excessive sympathetic response to standing - that is increased blood pressure and postural hypertension, increased norepinephrine levels (although this is NOT a defining characteristic) and increased MSNA nerve firing rates similar to essential hypertension.

* NET deficiency may cause increased peripheral resistance and postural hypertension. In this case MSNA may still be decreased however - that is, increased peripheral, decreased central.

* Increased Angiotensin II also seems to caused postural hypertension in adult cases, whereas in children due to the reduced cardiac output from low blood volume.

* receptor hypersensitivity - either alpha or beta 1 hyper responses or reduced beta 2 activity.

So in short - hyperadrenergic POTS is not just caused by norepinephrine, although in some cases angiotensin II does mediate increased release of norepinephrine and NET deficiency may result in increased plasma levels, although this is often not the case paradoxically.

Also the postural hypertension found in POTS is nearly always seen in certain patients not only in response to standing but also to any psychological stimuli that evokes the flight or fight response.

However most POTS patients are characterised by an exaggerated sympathetic response to psychological stimuli.

[issie]

It depends where you are diagnosed, but in nearly all cases Hyperadrenergic POTS is characterised by an excessive sympathetic response to standing - that is increased blood pressure and postural hypertension, increased norepinephrine levels (although this is NOT a defining characteristic) and increased MSNA nerve firing rates similar to essential hypertension.

* NET deficiency may cause increased peripheral resistance and postural hypertension. In this case MSNA may still be decreased however - that is, increased peripheral, decreased central.

* Increased Angiotensin II also seems to caused postural hypertension in adult cases, whereas in children due to the reduced cardiac output from low blood volume.

* receptor hypersensitivity - either alpha or beta 1 hyper responses or reduced beta 2 activity.

So in short - hyperadrenergic POTS is not just caused by norepinephrine, although in some cases angiotensin II does mediate increased release of norepinephrine and NET deficiency may result in increased plasma levels, although this is often not the case paradoxically.

Also the postural hypertension found in POTS is nearly always seen in certain patients not only in response to standing but also to any psychological stimuli that evokes the flight or fight response.

However most POTS patients are characterised by an exaggerated sympathetic response to psychological stimuli.

So, I ask again - what is the standard form of treatment for this response? What if the response is from high Angiotensin II AND low blood volume? Since noriepinephrine can be dervied from dopamine - in that chain - could this have something to do with this response? My dopamine levels came back low. (Before my POTS diagnosis - I was wrongly diagnosised with Parkinson's. Treatment didn't help, but made me worse. My guess is - it upped the noriepinephrine levels even more with the increase of dopamine.)

I for sure have exaggerated response to any type of stimuli - even florescent lighting causes issues. Stress is a big factor in whether or not my POTS is better or worse.

[Lovebug]

So, I ask again - what is the standard form of treatment for this response? What if the response is from high Angiotensin II AND low blood volume? Since noriepinephrine can be dervied from dopamine - in that chain - could this have something to do with this response? My dopamine levels came back low. (Before my POTS diagnosis - I was wrongly diagnosised with Parkinson's. Treatment didn't help, but made me worse. My guess is - it upped the noriepinephrine levels even more with the increase of dopamine.)

I for sure have exaggerated response to any type of stimuli - even florescent lighting causes issues. Stress is a big factor in whether or not my POTS is better or worse.

That's interesting....What does fluorescent lights do to you and do you know why you have a reaction to it?

[issie]

That's interesting....What does fluorescent lights do to you and do you know why you have a reaction to it?

They mess up my autonomic response - I will get really anxious and I get tremors. Wal-Mart lighting will do it to me. Doctors wondered if I didn't have some type of eplisey - but I tested negative for that. I just wear my sunglasses when I'm in those type of lights - or if I start to feel "that" certain feeling coming on. I know - it sounds strange - but for me - It just is one other thing to deal with.