POTLUCK

Depression ( and mood swings) is a possible side effect of B-blockers.

I went to Mayo Neuro- Rochester ( not POTS clinic) and within 5 minutes they had not figured out what was wrong with me, and when I left they had not figured out what was wrong with me. That being said the Mayo- Rochester adult program for POTS does seem to have a lot of strengths from what I found out. jenglynn I agree with you, and in addition I think that if your HR changes by 30 points from lying to standing or is above 120 standing and there is not a clear diagnosis otherwise, then you have POTS by definition. I think that everyone on this site has a reason for it. Pots is a definition ( somewhat arbitrary ) and not an etiology. And I strongly agree with you that they need to be looking into etiology for everyone. I am very glad this program helped this child. Much like Dr. Levine's controversial ideas on exercise, it seems clear that lack of exercise is not normally the etiology for POTS but may often help. The analogy that comes to my mind is physical therapy for a fracture and forcing yourself to use it more. This may often be beneficial, but it seems like it might need to be considered if it is always the right thing to push someone to walk on their fractured leg.

A lot of info on these subjects in this article. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022475/ Including.... Oxidative Stress Theory Martin Pall (2007) has suggested that oxidative stress might help explain the pathophysiology among patients with ME/CFS. According to Pall’s theory, when NMDA receptors on neurons are activated by a virus, bacteria, mold, toxin, microbe or allergy, they trigger nitric oxide production. ---------------------------------------------------- Other aspects of the circulatory system also seem to be involved in ME/CFS. In response to postural stress, 81% of patients with ME/CFS and no controls experienced ejection fraction decreases, suggesting left ventricular dysfunction in the heart --------------------------------------------------- Also, discharges of the type one associates with epilepsy were seen in the temporal lobes. In a later study, Duffy et al. (2009) found that factors derived from the EEG data were able to discriminate with nearly 90% accuracy patients with ME/CFS from healthy controls and from those with major depression.

Rama, This appears very interesting as histone deacetylase (HDAC) inhibitors that you were referring to with Valproic Acid in the article, seem to be newly emerging in treatment for a variety of inflamatory diseases, muscle disorders etc. One of the mechanisms of action appears to be by increasing eNOS activity. Apparently histone deacetylase decreases eNOS and inhibiting it thus increases eNOS.

Rama, I am not following you on this. If everyone may have decreased NET than what is the value of considering if I might have it? Second you mentioned the decreased stomach vasoconstriction thing in regard to alpha 2 receptors. Does this go with Dr. Stewarts Regular flow POTS? do you go by Dr. S. categories? Lastly you mentioned the neuropathic POTS, are you seeing this as a different entity from hyperadrenergic POTS, because at times you have suggested all POTS patients are hyperadrenergic. I suppose what I am asking overall is how are you subdividing POTS patients. To my way of thinking, some aspects of POTS are opposites- like patients who have low flow and patients who have high flow. Some patients can not stand long without passing out , and I have never passed out. I do not use the word presyncopal for this reason. It also seems to me that coming up with ways to divide things is clearly helpful with treatment, rather than simply trying meds. You appear to have done a great deal of research and are obviously a bright guy and I am wondering what your thoughts based on all of this are.

I am just wondering if anyone else finds that a warm bath decreases their symptoms. Consistently any time of day, a warm bath ( warmer the better ) will leave me feeling better, decreased brain fog, less dysphoric/lack of oxygen feel, think clearer. It always raises my HR ( Lying and Standing ) also. I was just wondering if this tells me anything about the type of POTS I have, and/or if this is common, or if some people have the opposite. I was never really a bath person, as a shower is easier, and I do not really think it is the relaxation, I think it is the warmth, as other relaxation methods do not necesarily leave me feeling better.

Rereading my post, I noted that although he did not feel the SCAD (ACAD) was causing my problems at the time he was certain I had an SCAD deficiency, prior to the genetic test. Now the acylcarnitine profile is also showing longer chains, as named above, so I do not think he would feel it is a SCAD ( Short Chain Acyl-CoA Dehydrogenase Deficiency ) but I donto know.

" I may have a FOD as well, did the lab result say which ones you may have? they should as every elevated acylcarnitine is linked to different disorders a change in diet and carnintne may help (the script version) " I can not tell you which FOD, the automated lab result did not suggest one. ( I have had elevated CK, over 10 of them, almost always comes out 2-4x normal, and ammonia runs higher than normal range, and slightly decreased free carnitine) I saw a mitochondrial genetics doctor last spring. ( I did not know I had POTS at the time I just knew something was wrong cognitively, and DM, Hypothyroid, TLE are all common with mito disorders plus the lab abnormalities above are common indicators.) The doctor tested the above along with lactate (normal) and Acylcarnitines ( his report said "mild elevations of short-chain fatty acids on acylcarnitine profile." ) He tested for SCAD gene. He did not feel it was the cause of my problems, but did not know I had POTS then either. He said it shows if you have it 80% of the time. I tested negative. I recently had another acylcarnitine profile, just before my tilt test This acylcarnitine profile showed additional mild but bove normal, elevations of C-2, C-16, C16:1-hydroxy, C18, C18-hydroxy. I wrote to him and he suggested an appointment and to have a skin biopsy and in vitro fatty acid oxidation probe. I called for appointment. I do not know anything about these tests and what they entail. If I may ask have you had either of these tests, and what results suggested "an issue not processing ketones" if you do not mind my asking? Feel free to PM also. I wanted to have my results on here in case anyone can tell me anything about these things. Oh, and you mentioned the Carnitor, I am on it 30ml/day. He put me on it in the spring. Thank you Shoegal, and everyone for the info. and thoughts.

I do not know much about it. My catecholamines are PND. ( Done on 140mg Inderal-best I could get done as hard to get someone to order it. ) Will they suggest one way or the other? Is there testing for it? Net deficiency is the thing discovered by the Vanderbilt people & published in NEJM around 2000 isn't it? I thought they only found a handful of people with it, and it did not pan out to be a big cause for POTS??

Rama, Thanks for the info. The answer to your question about the VPA is it all went together and cured me 20 years ago. ( see my profile also. ) 20 years ago I developed this terrible dysphoric condition with cognitive problem so severe that my IQ test showed a performance IQ borderline MR. I remember not being able to tell the doctor what was missing on the picture of a frog that he later told me only had 3 legs. I suggested the background was missing and could not think of anything else. One of the doctors I saw after months of this, diagnosed me with TLE and sent me for BEAM (Quantitative EEG) which also confirmed it. I later had a repeat BEAM by another doc and have had several EEG's showing TL epileptiform discharges. Anyways, this doctor rapidly tried a number of things he uses for these TLE patients (mostly antiepileptics, some DA agonists etc.) The combo that worked was ( Selegiline, VPA, T4-for hypothyroid he found and sent me to Endo for, and Inderal 60 BID to get rid of the tremer caused by VPA ) I got completely better, within a few weeks to months, and stayed better till Dec 2009. I often wondered if I should stop the meds as I had no idea if they were even doing anything. I took the exact same meds for 20 years and was perfect. ( Top grades in school, running, hiking ) ( primary doc increased Inderal to 80BID for mild HTN ~2007 ) Then Thanksgiving weekend 2009, a stressful one, after a 10 mile hike, that evening I noticed some "dizziness", noticed it all day the next day, ended up getting checked out at the ER and the only thing wrong was elevated CPK-it runs 2-4x norm. They of course said your fine, drink lots of fluids. The "dizzy" feel is very similar to the dysphoria of 20 years ago, goes with working memory problems or "brainfog" and other "cerebral hypoperfusion" type problems. The only thing that helped was direct sunlight. I spent the last 2 years trying to figure it out via many doctors ( Mayo Neuro etc., ) research etc. Late in 2011, I tried going off meds, one by one, tapering slowly off Inderal resulted in HR ~80-105 Lying and over 140 Standing and bouncing alot. We ( myself, cardio. more than endo., primary ) thought it might be withdraw from Inderal, might be POTS, but it did not get better, if anything worse with time, eventualy had tilt test end of Feb 2012 and DX POTS. So the answer to your question about VPA is I got completely better on it 20 years ago but could not tell you which RX did it. Maybe, I had POTS then and the Inderal ( for tremor from VPA,) got rid of it. Clearly the TLE & POTS go together, but what is causing what, and what is the cure I can not tell you. ( As the article I posted on kindling shows the TLE EEG is very common with POTS. )

There are many very clear connections. The hypothalmus is a regulator for many of the bodies functions, and recieves feedback from many parts of the body, through many mechanisms. The article above has over 100 references making some of the connections. It seems to me that it is likely that most of the problems of POTS stem from just one thing, but that that thing is likely to be different in different people, with common pathways that result. There does not seem to be nearly as much research into POTS as other severe medical illnesses. When you consider the level of dehibilitation most of the people on this site have and the number of people who have this illness I would expect more. I suspect part of the problem is the effects are not as visible on the outside. It also frustrates me that there are so few doctors treating this illness and no algorithm for treatment for the primary care physician. A primary care can begin the basic testing with algorithms developed for most illness, recommend basic treatment and refer to specialists. Instead most doctors do not even know what POTS is. ( and as Claire's hysterical comic illustrates are not always even willing to google it .) Firewatcher did your doc really suggest your " hypothalamus is shot" as a possibility? That does not really suggest looking into things much.

The hypothalamus is in the temporal lobe of the brain, and head trauma often results in Temporal Lobe Epilepsy, and 81% of CFS/ME patients and zero controls had decreased ejection fractions suggestive of dysautonomia, and 90% could be identified by there temporal lobe epileptiform discharges and Temporal lobe epilepsy and they believe that CFS/ME dysautonomia is likely related to the kindling effect of these epielptic discharges. This connection is here... http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022475/ I may go back to trying antiepileptics for this, as whatever I had 20 years ago that resulted in Dysphoria/cognitive problems and was diagnosed on EEG as TLE got better on antiepileptics, then after 20 years in 12/09 this similar condition with a postural HR change came about. My original TLE doctor by the way believes TLE is a mitochondrial problem, and uses many of the mito supplements in treating his TLE patients.

Rama, Blocking the Ang II type 1 receptor, increases the type 2 receptor effect while decreasing the type 1 receptor effect, resulting in increase No I believe, but have no doubt you already know that. Schorobi, Bumped it up to 75mg a day and can't even tell if it is doing anything. I think 100 is the max recommended dose. But I agree caution is a good idea for many, as your own story clearly illustrates. best,

Even with Inderal 140mg a day alone it does not go that low.

OK, Melatonin is supposed to attenuate postural muscle sympathetic nerve activity, but it also reduces NO. In my case I take a low dose melatonin at night, because Propranolol blocks melatonin and I am on a very large dose. ( Inderal LA 80AM, 60PM ) Is it common for POTS patients to take doses that high? I tried to cut it to 60/60 the other day as my HR seemed low in the morning and I was hoping the Losartan was having an effect, but the HR went to a standing 115 by mid afternoon, just by lowering it to 60 once. ( That should not make much difference as it should be at a steady state but it did. ) What does fish oil do? how could that be used as a test? It seems someone should be seperating patients with an algorithm like doctors use to treat most illnesses. "POTS" is really an arbitrary definition of your HR going up 30 points or a HR over 120, and there can be infinate reasons for this. I suspect mine is compensatory as the dysphoria/smothered feeling/lack of oxygen feeling/brainfog/cognitive problems, which are really all the same, gets worse when the HR goes lower on Inderal and better when the HR goes to 100 or more. Also the blood pressure never drops off. A low BP for me is below 120 systolic or 80 diastolic, and without meds it does not go that low.

That is great Jangle, I am glad to here you are seeing positive initial results. I have found long acting meds often do not act long enough for me. I take the Inderal LA twice a day instead of once yet still see a decrease in my HR in about 3 hours that climbs back up before my next dose. ( drops in 3 hours and rises back over 20 points both lying and standing ) Therefore, I asked the cardio if I could take Losartan BID, which he saw no point in, but said "fine just cut it in half " which I do. I went to 75mg total today but still can't say I am better or worse. Of course, I never like rainy days and it rained all day here in CA. I think my blood pressure may a little lower but I don't like that the systolic seems to have come down more than the diastolic, as I prefer that difference to be high, but maybe the diastolic will go down later. Anyways, fixing the metrics does not necessarily fix me. My BP runs high both lying and standing even on 140mg a day of Propranolol so it does not hurt if it lowers it a bit.

That was hysterical. Thank you

My doctors have not really said how severe my symptoms are but many did not seem to take my symptoms seriously. However, I have only seen one POTS doctor and have not been to Vand/Cleveland/Mayo-dysautonomia. I did go to Mayo Rochester Neuro but they did not figure out I had POTS and I had not been diagnosed with it at that time.

Does a dehumidifier put out large amounts of negative ions?

Issie, Thank you for the complement. My performance IQ was low 70's at that time. And no I do nto believe it reflects my real IQ I believe it reflects how severe the symptoms were at the time. ( Maybe I had cerbral hypoperfusion that was not being compensated with an increase HR.) The thing is I have not purposely been doing things for over 20 years to boost my NO levels. I did not even know what NO was. The doctors just gave me those drugs for a DX of TLE 20 years ago and I stayed on them with no symptoms and no problems till December 2009. I am just noting on looking back that many raise NO. The TLE DX was based on EEG ( epileptiform discharges in the TL that the article shows most POTS people have, ) and symptoms ( that are similar to my symptoms now - lack of oxygen to the brain feel/dysphoria/cognitive problems/working memory problems.) It is only in 2012 that I have recieved the DX of POTS when I went off one of those RX from 20 years ago ( Inderal 80 BID) The list of RX 20 years ago is on my profile. I am just thinking now that maybe those RX from 20 years ago had things balanced for me, but the DM 2 decreased the NO further. Honestly, I am just looking for an answer to what changed in 12/09. The HR that increases on standing does not seem like a cause of symptoms that appear to be cerebral hypoperfusion, because increased HR would give my brain more blood, not less. Thus, it seems more likely it is a compensation mechanism. I do not think it is compensating for something physical, like a deconditioned heart, because I was an active runner and hiker before Dec 2009. I had done a 10mile hike with a 3200 foot gain during the day on the evening I first noticed a mild "dizzy" feel. So I am just trying to figure out what happened. I did not know I had POTS till this year. And my symptoms and tilt test were without meds. If it was too much NO than I would think stopping the meds would have fixed it. I can not say I am certain on anything though. Thank you for the thoughts. Jangle, I asked the doc if I could be agressive with the med. I started 12.5, went to 12.5 BID and now am at 25 BID in less than a week. I'm off work and need to get back! ( I am disapointed my Angiotensin came back low today.) Good luck with the Losartan!

Is she on Dinet? I have enjoyed her site. Tell her thank you for the site. She seems quite bright and offers info. on her site on everything from ABC News Diane Sawyer POTS to research articles.

http://potsgrrl.blogspot.com/2011/09/what-is-sjogrens-syndrome-and-how-can.html I have read a lot in her blog and she is very knowledgable. I am guessing she is on Dinet as I know she has mentioned it. I Just remember link to Sjorgens

Jangle, ( this is off the Hyperadrenergic topic but following on your amygdaloid states article ) The connection as referenced below of " discharges of the type one associates with epilepsy seen in the temporal lobes " seen in 90% of CFS, dysautonomic symptoms shown in 81% of CFS. There is a large connection between CFS and POTS and TLE. ( Note this article is very long and complex, with a lot of references, but see the last section and particularly last line under the blue Neurology section ) ( The Autonomic Nervous System section has the CFS/POTS connection) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022475/ My Mom has the TLE diagnosis also, she has a CFS diagnosis and she has a lying to standing HR increase of 26. I was given the TLE DX 20 years ago and was treated. The TLE symptoms were essentially dysphoria and neurocognitive problems. My performance I Q tested at borderline mental retardation level 20 years ago when I had symptoms. There were never convulsions in myself or in my Mom. The medicines relieved it and I was stable for 20 years. Several of my meds like Selegiline and VPA increase NO http://www.ncbi.nlm.nih.gov/pubmed/9721939 and as noted here http://www.ncbi.nlm.nih.gov/pubmed/19703427 it is suggested that NO would play a role in the mechanism of antiepileptic effects by VPA treatment. This article suggests a dual pro and antiepileptic role of NO http://www.ingentaconnect.com/content/ben/cnsnddt/2011/00000010/00000007/art00006

Jangle, Good luck with the Losartan I read the abstract of the above, and will read the full article later. What do you mean by "simulates presyncope severely." I just learned you cannot click on someones profile or you lose what you have written, as I clicked your profile to see if you had anything that would explain the phrase, and had to rewrite everything above as it was gone when I clcked back. Rissy2D-Thank you for the articles, and yes any elevated sugars can be harmful, although Jenny Ruhl presents a tremendous amount of literature showing damage begins above 140 & 150. Other than a few months my HgA1c is consistently below 6.0, so I am only suggesting less chance of nerve damage, not that it is ruled out.

Hi, I can relate to how you are feeling. I just posted "Labs:Angiotensin 2,Aldosterone, Renin" with the same idea, labs do not come back to support the type of POTS you think you have. I can feel my adranaline surge when I get the labs. My WBC's are by the way, always the opposite of yours, just slightly below normal range, my Mom's are too. Of course the doctors just say, " Oh, looks like that is just where you live." It's where I live. My Free catecholamines are pending but they were drawn on B-blocker so may not mean much anyway. Definately finding it hard to relax since getting these labs back. Stressors are just like standing they just have much more impact than they should now. What happens to your BP from lying to standing? Anyways, sorry to hear of your disappointment. I do not know you well, like I am sure many of the others do on here, but since I could relate to how you felt thought you might not mind my commenting.