ramakentesh

Very common to have either inflammatory autoimmune conditions or autoimmune conditions with POTS. I have Ankylosing Spondylitis and POTS that cycle between each other. Thankfully my POTS is episodic although my general fatigue levels arent. Current theories are as you say - autoimmune or cytokine mediated lesions on small fibers causing impaired small vessel venous return or more recently autoantibodies blocking/binding to alpha 1 adrenoreceptors impairing venous return or causing a sympathetic response to compensate. the confusing this is that in both scenarios the sympathetic response can compensate for the blood flow abnormalities creating a mild hyperadrenergic state, or fail and leave you dizzy and very fatigued. Hashimotos is common, chrohns, RA, Sjogrens. There is a study right now evaluating whether POTSies with EDS have the same alpha 1 autoantibody levels as POTS post viral onset or POTS with comorbid autoimmune disease. POTS in a setting of comorbid autoimmune disease is now presumed to have a similar etiology. It may wax and wane in some.

Excellent thanks. I tried it for the first time yesterday and today at 100mgs and it was interesting. Definately increased my energy, my standing time and I did not a higher tachycardia but I felt relaxed. lasted a long time too - from about 1pm to 7pm which is amazing. Today much less response. As a side effect I found myself having to stop from getting aggressive with people that were talking to me. It was like I was so focused that people talking to me annoyed me because I just wanted to think about what my mind wanted. I dont know it was kinda weird. Other thing was I woke like Id been run over by a truck today. Really thirsty, out of it and kinda dopey. It must have dopamine action because everything I look at looks so amazing or something. Weird. Also food tasted much better than normal. I drank coffee with it and that pushed me over the edge I think.

caffeine is a vasoconstrictor not a dilator

Prognosis data is interesting and somewhat alarming but largely mirrors the info on this site.

I range from 100% well to quite disabled at times. I had a period of complete remission for 3 years at one stage.

Volume status via volume loading, salt, florinef or licorice Adrenergic vasoconstriction via vasoconstrictors - midodrine, phenylephrene, pseudoephedrine, synephrine, caffeine, dihydroergotamine, etc

Anyone else find their med sensitivity went away after long term florinef - I bet There are a few.

True but at least it didn't make it worse. Thanks for your info.

Dihydroergotamine - a selective veinous vasoconstrictor.

Its autoimmune or steroids increase your blood pressure.

There was even a company trying to capitalize on the study to sell their product and two of the researchers had to contact them. By reducing sympathetic vasoconstriction vitamin c in large doses did not improve symptoms, merely local vessel blood flow.

This study has often caused confusion. Intravenous vitamin c improved the regional local blood flow by vasodilatong but in all patients tested it actually made standing tolerance far worse. Please email Dr Stewart to confirm. this is the danger of applying selective medical research to patient interpretation.

If blood volume was the only problem then florinef would cure pots.

You beat me! Blocking autoantibodies against alpha 1 vasoconstrictor receptors causing elevated norepinephrine release in the face of orthostatic vasoconstriction failure but the increased NE is felt by other receptors fully causing tachycardia and other symptomatic effects of sympathetic excess. Beta 1 receptor activating autoantibodies also implicated. replication studies on way!

they think increased sensitivity of the sinus node to beta receptor stimulation from beta 1 receptor supersensitivity. there are several theories as to why, none proven.

I used to be kind of like this until I was able to increase my blood volume with florinef. From then all meds work as they should without any major problems. it appears low blood volume can interfere with vasoconstrictors and other meds.

what davecome said!

The most interesting thing about people with low blood volume in POTS is that treating it rarely totally corrects the underlying problem, suggesting it is an epiphenonema rather than a primary cause in most.

great and informative post. thanks.

Hi Macca, I think i know who your doctor is - I live in the same city. Ive taken DHE for many years for POTS. its helpful and pretty well tolerated. My only problem with it is that the first dose works great for about 40 minutes and the second dose almost does nothing. I upgraded to other meds in the end. As a fellow aussie feel free to PM me to discuss in more detail. cheers.

Happens to me as well. I believe it because the POTS body overcompensates for variations in blood pressure, constricting overly in response to hypotension. You may find that meds like midodrine will make you feel better AND LOWER your standing BP. This is what happens to me.

Midodrine can actually sensitize alpha 1 receptors over time and allow for norepinephrine stores to be increased in sympathetic presynaptic vessicles, both of which would or should result in overall improvement to orthostatic intolerance syndromes. I know of patients who after taking midodrine for a long period, wheened off and were normal. So they did not become dependent and in fact improved behind the scenes while on it. For me personally midodrine and phenylephrene dont really help that much with fatigue alwasy but definately with dizziness. The only med that has touched my fatigue is pseudoephedrine but Im not a hugely tachy POTS patient so I can tolerate it ok.

Recent evidence suggested that those with EDS often have abnormal QSART suggesting a possible neuropathic basis for their pots along with increased venous elasticity which has never been demonstrated.

I think they will solve the primary etiology of POTs eventually.

that article is discussing a few well known and potential norepinephrine transporter inhibitors. Only one or two of them are dietary and I doubt they are anywhere near as potent as the chemical ones listed at the start of the article. Not seeing the histamine connection at all - histamine's effects are mainly microcirculatory whereas norepinephrine transporters occur on large sympathetic synapses, in some immune cells and in the brain stem. Norepinephrine's effects in the brain are the opposite to peripherally. In the brain it acts as an alpha 2 receptor agonist suppressing sympathetic outflow so cerebral gaba would work in synergy with norepinephrine rather than suppress it. gaba is mainly a central neurotransmitter whereas norepinephrine is used in the entire central and peripheral sympathetic nervous system.