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About erik

  • Birthday 01/01/1970

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  1. I've heard of it used for kidney troubles. Gives a slower released fluid infusion. It would be interesting to know about it for POTS. (I believe there is still risk of infection, just way less than repeated IV or ports)
  2. I'm not familiar with a specific weight-range being associated with dysautonomia, but I have come across two things semi-related: I've seen "rapid weight loss" listed as a potential cause for POTS on some websites (as opposed to post-viral, etc.) Also Dr. Grubb was noticing many patients developing orthostatic intolerance/tachycardia (a.k.a. POTS) following gastric-bypass surgery (mentioned in this article here). Additionally, they were often helped by standard POTS treatments of fludrocortisone or midodrine.
  3. I have read that respiration is the short-term means of maintaining acid-base balance, and kidneys are long-term. Increased respiration eliminates more CO2 and thereby pushes blood more alkaline. Excess CO2 is the main "drive to breath" factor (a person will pass out from low oxygen before feeling much need to breath). IRRC, CO2 / acid-base levels, like temperature & other key autonomic senses, are measured in the hypothalmus. A mis-calibration or mis-response to these signals seems consistent with some of our general tendencies. I also vaguely recall that the kidney happens to do it's acid-base balance in a way that happens to affect blood volume, but I don't recall the specifics. The right circumstance could perhaps account for "shortness of breath" (an impetus to clear more CO2... aka, counter acidity), tendency to low blood volume (if the long term acid-base work of kidney happens to contradict blood volume sustaining activity). Also, note that acidity apparently alters potassium concentrations. As pH falls (more acidic), serum potassium will tend to go up. But for most folks, there isn't a persistent acid-base imbalance... instead a compensation is made (which means the problem could "pop out" elsewhere). Lactic acidosis is said to occur from hypoxia/hypoperfusion (shortage of blood/oxygen) to tissues. Hypoperfusion seems endemic to POTS, for one. Who knows, maybe this sets up a low-grade tendency toward lactic acidosis... and the compensations (usually successful) push the symptoms into shortness-of-breath and low-blood-volume for some.
  4. I just take a few over-the-counter potassium every so often, which is very small amount (3% of RDA each... perhaps by regulation?). I have not pursued a more intense or extended release potassium, though I had something once in the ER. I also take salt-tablets (thermotabs) with lots of water. I am seeking modest BP boost via water retention (which comes with kidney reclaiming salt via increased aldosterone) and it works for me. One might note that most receptor populations/tunings appear to adjust as well over time. This is said to happen in the kidney for people trying to do "low salt diet" for purposes of reducing essential hypertension. Even when they do succeed (which is very difficult), the kidney tends to just tune-up it's sensitivity and adjust to the new low-salt levels, defeating the whole exercise. The same may happen in the opposite direction too with salt supplementation, who knows. The entire picture of interwoven hormonal signals is a bit much to pin down 100%, even without dysfunction. When on fludrocortisone, I got used to taking potassium by necessity as it could go low on me. If any of the specific neuro-hormonal responses are lacking then the picture changes. Can't assume response will be either normal or abnormal... with POTS & the like, sometimes it seems like the "entire system" is off-kilter yet each of the pieces still tests pretty normal for most folks. If someone has an explicit malfunction like in the adrenals then it would need to be considered, of course... and one treatment or another could be very inappropriate. That's where a doc at least tries to guide things when possible.
  5. If you split a pill just be sure whatever variation of the drug you have is "splittable". Often the extended-release are NOT, so be sure what you have and ask doc/pharmacist. Otherwise, need to change prescription to a different dose or a splittable form.
  6. I saw this too. Maybe it was a Mystery Diagnosis episode... or something on Discovery Health??? They said it would be a rare case for the things to be connected, but that they turned out to be in that patient's mysterious case.
  7. Not suggesting to try it (since it is a key electrolyte especially for heart rhythm and must be treated with great caution), but when potassium goes high it is supposed to trigger aldosterone. The aldosterone steers the kidney to dump the potassium... and indirectly to retain salt (with which comes extra water). Aldosterone is like a "rudder" between K and Na/H20... while ADH/Vasopressin is like a "throttle" directly to water retention. To use this theory, one would want both Na & K present so that the salt is there to do it's water retention magic. Of course, this *assumes* a standard working renin response to K and focuses on just one of the influences on renin stimulation (albeit a key one). I've had low potassium (from fludrocortisone & running out of K supplements) and the ER was surprised I didn't induce serious heart trouble (I was lucky). One needs to be wary of either high or low (especially if already prone to arrhythmia)... it is really critical to heart function. Sodium variations seem less critical in short term stuff, and I think the body treats it as such.
  8. Dr. Bombay is cool, though I think Miss Often might better solve some of my personal problems... or at least distract me from them.
  9. At this point it is just rumor, but I have heard that the FDA is considering yanking approval for blood-letting unless the technique can be put through the final round of studies documenting its clinical benefit. Not sure how it works when a key party of interest is foreign based (Transylvanian), but if they cannot lobby this issue perhaps the Chupacabra can speak up more locally... I'm betting we won't here much in the way of vocal support from leeches. Anyway, the rumor is that a public protest is planned for October 31st... so if you are so inclined, dress appropriately to protest this decision!
  10. Yeah, it is not tasty! I tolerated it too and it seemed a little helpful, maybe a little calm-focus influence on the mind. I might try another batch some time (I bought a "bulk" supply). I haven't tried the other "racetams", but some others are out there as spinoffs of Piracetam. I haven't had adderall or ritalin so I can't comment on where it falls compared to those.
  11. Well, the exact terms may vary, but on my record is a diagnosis & billing-code of 337.9 (various autonomic codes specified here) and generally if insurance is willing to shell out money, then you can be pretty sure that "something" exists medically! Also, this "fpnotebook" outline is titled "Autonomic Dysfunction Aka: Dysautonomia, Autonomic Neuropathy, Chronic Autonomic Neuropathy". On my record is the abbrev. "AUTONOMIC NERVE DIS NEC" which is included near the bottom of the page in a list of related terms or synonyms of the family of autonomic dysfunctions. Family Practice Notebook entry for Dysautonomia
  12. Anybody know details on the nature of the dispute? It appears the drug manufacturer claims they did the necessary studies and the FDA deemed them unconvincing or missing? Would it happen to be something like a dispute over whether "surrogate markers" are sufficient evidence in lieu of "clinical indicators"? In other words, I suspect there is ample evidence of BP elevation after midodrine administration... but perhaps the FDA is insisting on scientific evidence of specific patient symptom improvement. I hope this is not the nature of the dispute, because for O.H. or O.I. it sure seems to me like a "surrogate marker" can be take as supportive evidence.
  13. Hmm. As a long shot, one can hope one/some of the generic manufacturers sponsor the "phase 4" studies and thereby gain/share a 3 year exclusive period. That at least gives some incentive to try a study (or "find" supportive data somewhere). That 3 year exclusion is not available to the original company (who apparently already had their original 5 year exclusive period). It's not a huge market but at least they'd have a lock on it and might stand to profit overall. After that 3-year period, back to having generics (which aren't very cheap anyway) and continued availability. Only thing better would be if the FDA magically "looked the other way" and ignored these regulations designed to protect us all. (It would be cool if Shire had some helpful info that they could sell to one of the generic makers to jump start their trial). The "expanded access" or "compassionate use" status sounds very burdensome... and insurance coverage would be lacking... and who knows how liability insurance looks on such actions by a doctor!?! Sounds like "orphan status" doesn't change the requirement for the same approval process, it just opens up tax benefits and/or outside funding for the study (provided fewer than 200K folks in the US have the condition... which is not the case for "OI" in general, but it is reportedly the case that only 100K patients are prescribed midodrine specifically).
  14. I haven't taken midodrine (was just getting to the point of asking to try it) but I refer to pseudoeffedrine as my "poor man's midodrine" which I have used in the past in an attempt to do something similar. I am unsure how much CNS interaction it has or how well it would fill in for midodrine. I get a bit palpy on pseudoeffedrine. There is also phenylephrine, a substitute for pseudoeffedrine that is said to do it's thing "indirectly"... presumably by norepinephrine release/activation... whereas I think pseudoeffedrine is credited with being a direct alpha-agonist more akin to midodrine. Both are over-the-counter, though typically you have to sign for pseudoeffedrine due to illicit-drug precursor prevention efforts. Welbutrin (buproprion) might offer potential BP increase and fall short of full on stimulants (still lending itself to insomnia for some folks though). ProVigil might do this indirectly a little too but not sure how much it's known for that. The SSNRI's sometimes boost BP I think. All these less direct options get tricky and are probably quite "trial & error" like everything else.
  15. Dreaming. I know I'm inconsistent and can't promise or endeavor to do much overall... so as I contemplate some ambition or envision the future, rather than feeling hope or excitement, I feel fear & loss. It is an odd "mourning"... not for something lost, but something that will never be. (This is a "bad attitude" thing on my part, I know, but you did invite "venting", right?)
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