erik

That's uncanny. I've not had singulair (just albuterol inhaler at times), but I happened to wake up in just that state the other day (except headache was less than migraine level... or who knows, perhaps I might have those painless migraines since migraine does run in my family). I couldn't pinpoint a cause but it was horrible and tapered off over a couple days. Certain head motions were worse than others. Initially most any movement triggered the spinning, then eventually it got to where mostly just leaning back (or simply lifting head from downward gaze) was the worst (and that was last to fade away days later). I was stumbling enough to look like a drunk about to pass out, slammed into a few walls and had to walk very cautiously and deliberately to get around. I can't figure anything specific to pin it on and so far this has been a fluke event for me (though it's similar to problems I've had, just 20 times worse suddenly). I hope it stays that way, it was nasty.

I yawn a lot and even when I ought to be rested. Yawning is also one of the things that hits me when I stand still for a while... along with other symptoms like lightheadedness, et al. I just figure it's an intuitive response that is trying to increase blood flow to the brain. Not sure if that's an official medical explanation but it seems to fit. I yawned excessively while I was being fired once. It was noticeable enough to my boss that they mentioned it to a former co-worker who told me about it. I guess they thought I was being a jerk and act unaffected or something... when in reality I was mostly just in a lightheaded daze. I think people misinterpret a lot of little things like that, such as your date that though you were disinterested! Hmm, that gives me hope that perhaps some of the ladies I managed to bore were actually just oxygen deprived and not truly disinterested in me... perhaps some were oxygen deprived enough to forget to call me back... I best call a few back and give them a second chance, just in case

Welcome to official status! I suppose it is a mixed blessing but it is always nice to have a more tangible and pinned down explanation and have acknowledgment and treatment options opened up from professionals. I wish you the best. I was just given official POTS diagnosis recently too.

I've had 'em since about 20 yrs old. Generally do OK but did have one swell up huge once (after a chiropractor shock/ultrasound treatment to lower back that also resulted in little tumors a week later). I didn't realize Hemorrhoids could throw clots. I will definitely have the thing taken care of if one swells up huge again. I wonder how long a generated clot could hang around afterward... I had an unexplained hemoptsys (coughing blood) several years later. One cause can be pulmonary embolism (blockage in lungs from something, such as a clot). I'd figure clots don't usually linger that long, but maybe they can??? or perhaps the roids were acting up at that time too and I just ignored it as best I could, I don't recall.

They do say there is PDE5 out and about, other than in the areas that Viagra is prominent in, it is just said to be in much lesser activity or level. It seems a long-duration version like Cialis would match these non-ED goals... is there something wrong about Cialis? It seems to be PDE5 inhibitor just like Viagra. I think it is credited with being even more selective... avoiding problems in the eyes and such, at least slightly less likely to cause trouble there than Viagra. I am personally optimistic that in the quest for the "next Viagra" developers will stumble accidentally upon cures for POTS, and perhaps hypertension too. I've been tempted to try vinpocetine but as always it is hard to tell what all the risks would be. It's said to be selective for PDE1 and is credited with some generalized effect (as well as cerebral). Beyond vinpocetine there seem to be quite a number of things in this genera. I've wondered about Horny Goat Weed as well, which is usually marketed for "male prowess" stuff but could have some POTS interaction. I almost bought some when it was on sale, but didn't want to have the cute GNC clerk have to unlock the "special cabinet" for me and all that. But really I kind of figure at least some of these things have been contemplated by the "autonomic experts" out there. I wouldn't have a chance to know unless they published something easily searchable about "what they contemplated" as opposed to things that made it to experimental trial and a regular publication. And of course, with human experiments one is likely to be more selective with what one bothers to test out... giving hamsters a cocktail of ADH/Cialis/HornyGoatWeed/Vinpocetine is a bit easier to get past the review boards! I did try yohimbine (for energy & diet purpose, not for "male prowess" which it is also said to support), despite it being quite "wrong" adrenergically. At the modest dose I tried, it did not give me anxiety or physical symptoms (not beyond my normal range at least). I'm sure it might at higher doses or in other folks, though. It is said to do that (and this was even tried as a form of therapy, used as a tool inducing "physical" anxiety sensations). There was this one exercise related amino-blends that I got for free which surprisingly did seem to work for me. It was the kind of thing that is supposed to support you in numerous ways including dilation (N.O. induced vasodilation is often cited by exercise supplement ads). I love the simplicity of the "you're tired because your muscles aren't getting enough blood" theory. It probably isn't the fabled "whole story" but it is a great fundamental thing to address. In that vein, there are hundreds or thousands of mild vasodilators marketed to "exercise" support that might be slightly beneficial and avoid overt O.H. if one is on that cusp.

Besides the two diabedes insipidus cases (I guess nephrogenic might cause high ADH if the kidneys are unresponsive & central is a lack of ADH)... someone with SIADH could be in a troubling pair-bonding predicament! Perhaps having "inappropriate" ADH secretion might lead to "inappropriate" pair-bonding... intriguing In the theme of "boys only topic" I have been wondering (silently) if the phenomenon of "AM tumescence" (rhymes with "scorning should") can tell us anything about why the AM hours can be more orthostatically challenging for some. Is this indication that there is a generalized vascular dilation going on, that there are key hormones fluxing pre & early day, is it a sign of general blood flow changes that could be in effect, etc? Yet another data point to consider when looking for a correlating factor between symptoms and other processes. It also seems like a cross section of men with autonomic problems may have tried drugs like Viagra and similar over the years (just by chance but also because autonomic problems can cause ED). I wonder if they happen to notice either a significant orthostatic problem or perhaps instead a huge help from those drugs (along the lines of the benefit to Raynaud's that has been studied or the avoidance of fatigue via increased blood flow to muscles). Unfortunately one is likely to be distracted from such observations but perhaps some of the guys did happen to notice side benefit? I would be particularly curious about Tadalafil (Cialis) because it has a really really long effect duration (36 hour window of opportunity by some accounts, so to speak)... so it seems one might notice either a really positive or negative effect throughout such an extended drug duration. Any of the guys happen to bump in to this drug and notice a big benefit or bad POTS crash related to it?

It seems like the writing project has been going well. That is certainly a lot of writing! Sounds like fun. In looking at propranolol and topiramate it does seem they will share metabolism by a particular liver enzyme (CYP2C19) so they can interact in that regard which just means that dosing of each can affect the other. This might explain needing to rework a balance of things after prior adjustment. I don't happen to see oxycodone sharing any direct metabolic interaction, but in some folks it could contribute to orthostatic trouble (but that would vary of course). The details are complex details beyond me, but they do say drugs that inhibit that enzyme (which topiramate is said to do to a weak extent) can change the propranolol effects (and potentially enhance side effects). This doesn't mean a "bad drug interaction" situation, just that extra adjustments between the two make sense. Hopefully that can all be worked out soon, between your adjustments and doc feedback and such! Merry Christmas to you too. I wish you better luck with the mall folk. I think many tend to be pre-occupied (self absorbed) but also people are just generally apprehensive about helping others out depending on the circumstances. I know my mind gets wrapped up in the complications of possibly offending someone just by offering help, or overstepping bounds or whatever. Then again my mind gets wrapped up in a number of ways and I may just be making excuses for rather rude people!

Separate from the tylenol, the exercise & soreness itself could prompt some reactions. Exercise tends to bring a blend of stimulation & exhaustion that could take some getting used to especially in a body that reacts to things in unusual ways.

I know reading is a challenge for me and has been since I was young. It tires me out very quickly and requires extreme effort to stay focused. Hard to say if it's directly tied to my autonomic challenges (which sound similar to your daughter's) but they're definitely not going to help any, that's for sure. They do say that high "inattention scores" (like ADHD) are more prevalent amongst POTSies. I've had some luck with nuVigil (like ProVigil) to help with mental focus. Something along those lines might be worth considering depending on what further evaluation turns up. I wouldn't be surprised if autonomic troubles are associated with such cognitive troubles... certainly "brain fog" is well acknowledged in the family of symptoms we tend to get.

Hard to imagine the baroreflex stuff wouldn't be at least a part of the problem. Maybe rapid changes are worse than effective altitude too.

One thing I have noticed is that I have bonded & have a love/hate relationship with my key exercise devices over the years... and also happen to refer to them as "she". I know that exercise induces a rapid increase in ADH/vasopressin to promote water retention. Perhaps that explains this particular bonding behavior? I know that I would feel very upset with someone else taking my bike for a spin and might even respond aggressively, even though I have to spend ample time & money on her to keep things rolling along smoothly. Perhaps this is indeed a low level chemical response to some exercise induced vasopressin?!? When it comes to consummated relationships, there is the "Coolidge Effect" (perhaps to be renamed the "Pro Golfer Effect"?). It is a scientific notion and is sure to battle with any vasopressin pair-bonding going on.

Adrenals appear to excrete "C" upon "stress" stimulation... but body generally keeps it in tight margin elsewhere: Human adrenal glands secrete vitamin C in response to ACTH

Hmm. That might explain why I enjoy the movie Legally Blond so much. I knew there was a perfectly legitimate scientific reason. Hormones are complex to say the least! Nitric oxide is ubiquitous as a signaler, messenger, transmitter & modulator in the nervous system so the precise where & how can't really be ignored. Sometimes a study is focused on a subset of POTS folks too... like low-flow in regard to the neuronal nitric oxide synthase thing. When looking for inducers of "vascular permeability factor", I bumped in to this which shows estrogen influence (though they're looking at uterine specific action here, of course). In the context of POTS, such radical flux in endothelial & microvascular signals could be problematic, perhaps even if limited to selective uterine response or maybe it isn't that well contained always: ...rapid stimulation by estrogen correlates with estrogen-induced increases in uterine capillary permeability and growth Anectdotally, it seems like stable (& extended low-hormone phase) are helpful for some folks. It's on some POTS treatment option lists, IIRC. Are there some studies directly of that treatment? There have to be tons of impacts of any hormone regime, but this baroreflex specific study is interesting since that autonomic response is implicated for some POTS: Sympathetic Activity and Baroreflex Sensitivity in Young Women Taking Oral Contraceptives I can't tell for sure which baroreflex changes might be advantageous and which might not. In theory, if hormones can adjust something like that it could at least explain some variation and perhaps a reason stability (or a particular influence) could be helpful. Effect of estrogen on endothelial dysfunction in postmenopausal women with diabetes The study states flatly that estrogen promotes nitric oxide release. There may be some more detail available to that, for example: Prolactin and Estrogen Upregulate Carboxypeptidase-D to Promote Nitric Oxide Production and Survival of MCF-7 Breast Cancer Cells ...and to fight that... Nitric Oxide Synthase Inhibition by L-NAME Inhibits Tumor-Induced Angiogenesis in Mammary Tumors I wouldn't know if any of that has to do with neurons... from looking at what is said to regulate neuronal NO activity it seems it is different and general notions of NO may or may not apply. The endothelial vs neuronal roles are different, one being more of a messenger and the other a neuromodulator. All these substances play multiple different roles in different places (and NO is usually short lived & local intermediary). But it's interesting to see at least a detail of how estrogen interacts with NO in one locale.

Oh no. That is a serious ordeal. Any surgery is tough and that is an especially rugged situation. I don't know what to say other than to wish you continued recovery and as others mention, I hope it is faster than expected. Do keep us posted as best you can.

I'm trying to digest the details as best I can and will continue to re-read stuff but I am having trouble connecting some dots so far. #1 seems to indicate that only low-flow POTSies have low blood volume (normal & high don't). Just an interesting thing if I am reading it right. Renin activity was reduced & AngII increased in low-flow, and whereas others had Renin & AngII correlated, they were inversely correlated in low-flow (like a flipped relationship). I think this looks like the study about AngII in POTS on NYMC site, especially since the "Angiotensin II concentrations seem to follow a bimodal distribution" as they say. I may be recalling this very study, but I remember that #2 is consistent with #3, though I believe L-NAME is non-specific NOS inhibitor so presuming conclusion from #3 to hold we don't get added info from #2. #3 seems to match the study summary from the first post: It specifically implicates neuronal NOS (nNOS) as opposed to endothelial (eNOS). It seems to state that endothelial function is intact in terms of NO & NOS activity, but I might be misinterpreting it??? The nNOS vs eNOS inhibition via AngII thing is what I'm trying to understand causally.#4 is complicated & I'll need to re-review a few more times! The NOS inhibitor used was nitro-L-arginine (NLA) same as the non-specific inhibitor used in #3 but no nNOS-specific inhibitor was used. That might not have been necessary, I don't know... would it have been informative to use the same nNOS specific inhibitor as in #3? I think this study was subsequent to #3 but not sure. I'll have to see if I can wrap my head around the study with further examination. Is there a description of how AngII ends up inhibiting nNOS specifically? I have had easier time finding descriptions of endothelial & renal interactions but #3 study says it's nNOS and not eNOS. Am I mis-interpreting that or otherwise missing an obvious chain of events? I'll re-read but if you can describe the causal link for me that would be a cool shortcut! Are there AT receptors modulating the neuronal function... is it that simple? Where are AT receptors known to be located?

Do you have a study reference on the Angiotensin II cause?

What about men? If low-estrogen is bad then we are in dire straights!

No & I don't know. I lean toward drug rather than herb, personally (or just inferring no general distinctions). Just mining for clarification about whether it induces it's alpha-agonism directly or via NE cascade (NE being key alpha-agonist, of course): End user can impose their own judgment on quality of info as well as my "reading" of the phrase, which I tagged as such.

This article says a few things about out of control BP, especially with standing & especially in combination with mast cell activation disorder (MCAD): http://www.nature.com/nrneph/journal/v2/n8...cpneph0228.html

Good point. Histamines, serotonin, bradykinin & LTE4 are mentioned here for hormonal permeability modulators. I guess MAST relates to pseudo-histamine effect (and kinins can mimic histamines). Plenty of other players in the game I would imagine. I can see myself as being a bit Aspergy... the use of the term "spectrum" for autism and other conditions is probably wise as folks can fall all over the map and perhaps the obvious cases are more of a confluence of multiple traits rather than any single one.

There is also this study on phases of BC pills and relation to baroreflex (which is potentially key to POTS). There are probably other subsequent investigations: Sympathetic Activity and Baroreflex Sensitivity in Young Women Taking Oral Contraceptives It is hard to keep all the vocabulary straight, so I wouldn't know if the study supports the notion of a beneficial baroreflex mediated change or if other hormonal effects are more likely. I don't know if NO/NOS stuff is being adjusted specifically in neurons via a hormonal activity... endothelial NO stuff is mentioned more often but who knows. Perhaps this study gives quick insight as to regulation of nNOS: Nitric Oxide Limits Pressor Responses to Sympathetic Activation in Rat Spinal Cord This is not the calcium ion effect happening later via cAMP (which NO triggers, and which the PDE inhibitors amplify)... this is more of a neuroregulatory calcium activity via NMDA-receptor influence. This Nitric Oxide page gives a great many more details on how NO is regulated:http://www.whatislife.com/reader2/Metabolism/pathway/no.html Some key things it mentions are NMDA & non-NMDA glutamate receptors (the NMDA regulating calcium, the non-NMDA regulating arginine uptake) and also calmodulin. It is unclear to me which of these things apply to which neurons... but the first "pressor response via NMDA" article seems to indicate involvement in the nNOS deficit implicated in the NYMC study. Perhaps something can be done other than just amplifying the cAMP to make up for NO deficiency? Of course, one can consider all the NO "sports" products & research too. Maybe some of that would come in handy?

Another study indicating systemic changes resultant from NET: Influences of Norepinephrine Transporter Function on the Distribution of Sympathetic Activity in Humans They get in to some great topics in their "discussion" section, especially how complicated things get with paradoxical effects. This closing paragraph is catchy:

I think the mottled look is considered a sign of pooling. Seems different things can result in that but they say POTS patients tends to lack arterial constriction response to orthostatic stress so flow isn't diverted in the simple effective manner it ought to be. Ironically it can also result from extra serotonin in blood or exaggerated platelet response to that hormone (which is also associated with "leaking", I believe... as are several other agents). The mottled look is also associated with autism/asperger's. Maybe we have autonomic asperger's?

Here's a cool overview article on Orthostatic Hypertension (maybe a repeat post, but what the heck). It mentions a number of familiar concepts: Orthostatic Hypertension: When Pressor Reflexes Overcompensate There is this on Butcher's Broom for OH (hypo), and if it helps underlying probs no reason it couldn't help for OH (hyper) though elsewhere there are warnings about combination with other drugs, as one might expect of any drug/herb: Ruscus aculeatus (butcher's broom) as a potential treatment for orthostatic hypotension, with a case report From their description it does induce norepi but in a localized end-stage spot... as opposed to something which enhances it up-stream or tells adrenals to flood the blood with it, etc. So norepinephrine is "technically" induced, but not in the manner one would tend to be "concerned" with. That's how I interpret it, at least

Fascinating for sure. N.O. is pretty ubiquitous in the body as signaler, secondary messenger, etc. As with any enzyme (such as NOS, NET, DAT) one has to ask what is regulating it. Is there a signal somewhere that is altering the production, transport, catabolism, etc. of that enzyme that is observed to be deficient or increased? Is it just a permanent genetic factor? It is interesting/surprising that this looks specifically neuronal in POTS... endothelial would have been a likely suspect too. Some interesting research tidbits: Effect of estrogen on endothelial dysfunction in postmenopausal women with diabetes. Impaired flow-mediated vasodilation in type 2 diabetes: lack of relation to microvascular dysfunction.