erik

In the theme of "All About" low blood sugar, I'll throw this article into the mix. It is from the 60's and strikes me because the symptom cluster has solid crossover with dysautonomias. I have also read that those with POTS tend to respond more quickly to the rapid drops in blood sugar that follows a spike, causing hypoglycemia symptoms even where standard measure of hypoglycemia wouldn't be seen. Also, I think you all mentioned this, but a drop in sugar can (should) cause an adrenaline-like spike... and an adrenaline spike can eventually lead to another subsequent crash later (making a rough cycle that dysautonomiacs could fall in to easily from various causes). Here is the article: Relative Hypoglycemia as a Cause of Neuropsychiatric Illness HARRY M. SALZER, M.D. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2611193/ One can download entire as PDF or view pages piecemeal. Here is an excerpt related to associated symptoms: Psychiatric symptoms: depression, insomnia, anxiety, irritability, lack of concentration, crying spells, phobias, forgetfulness, confusion, unsocial or antisocial behavior, and suicidal tendencies. Neurological symptoms: headache, dizziness, inward and external tremulousness, numbness, blurred vision, staggering, fainting or blackouts, and muscular twitching. Somatic symptoms: exhaustion, fatigue, sweating, anorexia, tachycardia, cold hands and feet, obesity, chronic indigestion, bloating, abdominal spasm, muscle and joint pains, backache, muscle cramps, colitis, and convulsions. (I think I've had 90% of these symptoms... and 100% of the neurological ones on a pretty regular basis. Of course, they are "non-specific" as they say, meaning they can come from many different causes... but the crossover with dysautonomias is certainly interesting.)

I've been trying biotin for a couple months... just something along with various B-vites (those you would often find in an Energy Drink). For energy, it seems it might be slightly helpful... like "supportive" of the body, rather than "correcting" anything that is wrong.I don't seem to have a connective tissue thing so I wouldn't know if it helps along those lines. I also had mostly normal nails (guy nails, which means I don't really look at them that closely ... but with fludro on board things like hair & nails do seem to grow a bit quicker. Shoddy nails can also be associated with endocrine troubles, so that is another avenue to pursue if signs are there. I do tend to have darkness at the skin near base of a couple of my nails, but not so severe as would be expected for Addison's or whatever.

I think elevated Ang/AngII is an expected state if anyone is hypovolemic... however, it is supposed to trigger corrective actions which would then make it a temporary state (as in normal body regulation signals). So having high AngII seems expected for a population with low blood volume (and maybe even for a body condition simply mimicking that state?). It is the unexpected (paradoxical) lack of renin & aldosterone elevation that stands out as unusual in many. I think the chronically elevated AngII is suspected of having especially untoward impacts on circulatory regulation (although it is by no means the only thing interacting in that realm)... so AngII comes heavily into the "Flow" subgroup theories.

Now your grossing me out! Yes, witnessing baby poop up close is one of the best birth-control devices out there!

My POTSY jugs of urine keep for a few days before turning nasty... they're clear like water and don't "ferment" as quickly as normal-person urine. Being male, I have luxury of not stumbling to the bathroom constantly in dealing with my periodic POTS fluid dumping phases. Doesn't even taste that bad... if you accidentally mix up a beverage container for an "outgoing" container. Half-asleep brain-fog state is not good I keep them color coded and well segregated now! (Sorry, couldn't pass up a childish male opportunity to "gross out" the ladies

I think wareagle nailed it. I'd just add an example: when I stand up and still for too long I will start to sweat, shake, feel anxious (or just plain horrible), yawn, need to pee suddenly, get tingly & numb in spots, and a few other things I'm forgetting. Several of those are related to sympathetic stimulation being "ramped up" either erroneously (as in "too sensitive" or "amplified") or perhaps "appropriately" as a crude attempt to keep me conscious & functional. Subtler things should have happened to keep the blood flow stable and systems operating, but they probably fail for me in my style of POTS. Therefore, the body resorts to the big "sledghammer" to fix the problem and starts a cascade of signals... sympathetic stimulation and parasympathetic withdrawal. As others have made clear. The quick answer is... nobody knows. Remember, nobody even knows (with certainty) what each cause of POTS is!!! So no way to know what is being fixed if don't know specifically what is broken. Some things are known, others are just well informed theories (which fail often enough in science . I also like the "catch-all"... that since "anything goes" with dysautonomia it follows that "anything goes" with treatment. The other thing that I keep in mind is that researchers do not even know what causes high-blood pressure ("essential hypertension") yet. That condition affects millions and costs lives. I expect it gets some priority in terms of pinning down exact cause... to keep the "little guys" like dysautonomias from getting neglected there are rare disease organizations, which helps. But my personal hope is that things like POTS might actually cross over enough with "simple stuff" like hypertension that things get solved together. Clinically, In the case of things more like NMH rather than POTS... there seem to be cases where even NRI's (like Strattera) can reduce fainting. For some other folks, Strattera will actually induce POTS-like symptoms, since it ramps up norepinephrine activity (perhaps mimicking NET deficiency, one of the potential subtypes of POTS). Yet, SSNRI given to a subset of POTS folks can ironically also help with POTS. Also, many folks with POTS take stimulants, which enhance norepinephrine & dopamine activity and even have reuptake effect on these just like NRI or SSNRI. It seems that almost all the meds that POTS folks take are either known for creating the very symptoms they are treating or are seeking a delicate balance between pro & con effects. There are also known cases where a drug will respond very very differently in the context of known nervous system damage (as in MSA, parkinsons, or other known denervations). This means that although a drug might tend to boost something in the general public, and be though to create a problem symptom in general public, in a patient that lacks those nerves it will not have same overall effect!

Cool. So, I will probably pursue the saliva test kind of privately or with my GP... then based on the results I will know whether to press hard for endocrine specialist and more advanced stim tests. I am "timid" because it is lousy to ask for some special test and have it negative... especially in the context of having one of medicine's "mystery diseases"! Must tread lightly and tactfully... like Ninja patient!!!

seaboardbc, I am curious about this because I've wondered (and read in one obscure account) about a diuretic being used successfully amid conditions for which they are oft avoided. What is your style of dysautonomia, if I may ask?

Here's a rough transcript related to POTS mention. 00:19:30 or so on episode time: (Patient wakes up & talks about heart attack & "head trauma" with fiance... he lies to her about what the head trauma was... it may have been related to his "straightening out" treatment... discussed later by docs) (Patient sits up & faints) Fiance: He's having another heart attack? Thirteen: I don't think so, his heart rate seems normal. (Taking pulse on neck) Taub: Are you OK? You weren't discussing wedding plans were you? [subtext: Investigating psychogenic cause for syncope... missing fact that patient just lied about intense personal conflict subject... which is in fact potential psychogenic cause] Patient: No, I guess I just... (faints again while sitting up again) Taub: (continues sentence for patient) ...Fainted. (looks around) ---------- cut to walking down hallway with House ---------- House: POTS. Postural Orthostatic Tachycardia Syndrome. BP plummets when he's upright, reverts to normal when he's lying down. Taub: He was lying down both times we took his blood pressure. [subtext: Implies reason it could have been missed before... since BP hadn't been taken sitting or standing yet] Thirteen: Retracted hypotension could have induced his heart attack, also explains the syncope... Taub: ...and his aphasia. He was upright, then you lay him down in the bed to test him... BP reverted to normal, voice came back, jabbing with the needle had nothing to do with it. Thirteen: POTS can be brought on by viral or bacterial infection such as mono. House: Load him up with fludrocortisone... (continues ongoing infidelity/trust theme/taunt with Taub)

Tough question! I'm tempted to say "nobody knows", and certainly I don't. If you can tolerate "rambling" here is a partial response (otherwise just ignore : There are the initial known effects of these drugs (synaptic reuptake inhibition in select locations)... and then there are the counter and cascading effects. Although they initially increase the duration of presence post-firing ("umph" is my word for it) of the neurotransmitter in the synapse (the primary "active region"... but not the only active region), the body can tend to respond with a down-regulation to things like this... so longer term result can be opposite/mixed. Also, folks are finding that not only are nerves populated with receptors for these and other messengers right at the synapse, but also in other adjacent places and even on adjacent "support" cells. Needless to say, there are many factors involved beyond synaptic umph. For example, the little pods of neurotransmitter are made more or less potent or populated by some stuff going on inside the nerve cell (and mitochondria)... and even the rate of migration of these little protected pods toward the synaptic surface where they get released is said to affects things. If less is "reuptaken" then there could be more "washout" or loss... and a tendency to depletion, but maybe not if the reuptake is simply delayed/slowed. Also, on the "receiving" side of the synapse (either the next nerve in the chain or the slower responding receptor that might be triggering production of some substance, like a hormone perhaps) can decide to make itself less or more populated with receptors! So even with more neurotransmitter umph... a down-regulation can push opposite. Whatever signals this down-regulation may or may not be localized... so it might be just that specific spot that gets down-regulated or perhaps whatever signals that is more global. Then there is the obvious! If the nerve doesn't reach threshold and fire, the neurotransmitter doesn't get spit out into synapse in the first place... so regulating the nerve threshold is hard to ignore. That is an "upstream" decision, most directly influenced by ion flows... a.k.a. key electrolytes, but indirectly by neuroregulators. Those regulators tend to be things binding to little channels through which specific ions flow... and acting as "valves" for this flow. Also, I suppose overall concentrations come in to play but maybe not often (just depletion or overt electrolyte imbalance???). One other (semi-new) curveball is that the gaseous neurotransmitters (nitric oxide & carbon monoxide) are now though to even travel backward UP the nerve in some cases (presumably a form of rapid feedback loop) in addition to their other localized signaling roles. Also, there are other localized messengers not constricted to nerves but "floating" or even "migrating" in bodily areas... such as kinins and friends. Long story short... for a "clinician" the only thing that matters is the end result in the patient. For a researcher, it almost seems too complicated to know "big picture" stuff... they just pin down specific pathologies mostly... then spin endless theories which may or may not be true (it almost doesn't matter, as in philosophy).

Although I can certainly reach "exhaustion" at times... I'm afraid my trend is like Rama. Crashes not usually correlated with prior activity levels. I expect in many/most folks they are related and people should pace themselves. After years & years of trying various approaches however, I still find myself rather "random"... except for the obvious triggers like dehydration, severe stress, etc. P.S. In my "road to diagnosis"... my first big suspect based on symptoms was Adrenal Insufficiency. To this day, I still don't know how that is tested for... and it seems that it only "half-exists" in medical world (as opposed to Addison's which is extreme form).

The theory of physical adaptations from psychogenic stimuli is nicely congruent with those who's POTS seems to emerge post trauma... not to mention the similarity with PTSD (for those in the subset of POTS who are similar to that... not everyone is). It could even be considered a positive adaptation because if one is in a traumatic environment, responding in accord is helpful. This is well discussed with all the "dissociative disorders". Problems come once you're back in "normal" environment but body is still in "adapted" mode, right? Perhaps the de-hyper-methylation step hast been neglected! I met a fellow who went to prison for a bit. Upon entry he was never good with remembering names & faces. After witnessing beating & murder "inside", he now has a photographic memory for names & faces and is very attuned to exactly who everyone is and what they are doing. This is "hypervigilance". He also has that "associative memory" that others have described here. It is an appropriate adaptation for some. It is likely backed by physiological changes. If he eventually seeks a simple suburban life and settles down with a sweet bride... perhaps this adaptation will no longer be healthy. In the subtler mental health conditions, it is an incongruity with surrounding & circumstance that defines "illness"... not any particular state.

I don't think they measured the guy's pulse, but maybe I missed it. Seemed more like "severe OH" on the surface at least... but anyway it is just TV (or perhaps it happened too quick for me to catch). I can say that I will not be telling many of my buddies that I have POTS now... thanks to the intertwining with a weird gay/not-gay dilemma in what is probably now the most "famous" mention of the condition. Oh well, thanks Hollywood. I'm sticking with the old name, "Soldiers Heart". Will get razzed less with that.

Yeah, I think I read that the most common link is "peripheral neuropathy" caused by the diabetes... then the little nerves out in the legs and such to control vascular response become compromised. So then the chain of events needed when one stands up gets faulty. This might be one of the more common ways a regular doctor encounters our sorts of troubles.

I've never been able to decipher the "medical definitions" but your personal description matches my personal description too! The OH for me is like an "instant drop upon standing" whereas the NMH seems like the "steady escelation of sympathetic overstimulation followed by a crash" and near-syncope.

I haven't found that exact reference, but here is an example of how to link to a Google Book (if that is what you mean). One can't just bring up a given page on demand so one should pick a phrase on the target page and then search for that phrase... then once there sometimes there is a "LINK" button in the upper right that generates something like this: http://books.google.com/books?id=3kw0gwdYX...ART&f=false It's tricky because they can't just put the whole book up "on demand" but sneak bits of it out as a teaser. This trick kind of gets around that for specific stuff. I searched for "QTST QSART" and found a similar sort of thing. Maybe can do this trick for something on Page 335 of Harrison's??? Not sure, sometimes these things don't work!

Nice idea. As a backup plan, in case the logo's don't get the message across you could consider moving to a neighborhood where most people are drunk, stoned or in need of medical assistance and such behaviors are commonplace and just ignored by people! These things change over time, but there were neighborhoods like that here and there in the old days at least! Maybe not where you want to live though

I've done best in recliner (slight head-up angle) while sleeping. Noticeable enough that I developed this habit (compulsion) long before ever hearing of POTS or that such a thing could exist. I run the risk of passing bad information here, but I recall reading that the body's aldosterone production increases drastically when upright. Aldosterone tends to tell kidneys to hold salt/water and build blood volume. Those of us that take fludrocortisone are basically taking a synthetic aldosterone to boost this effect. I don't know, but perhaps the slightly upright position gives a slight trigger to increase aldosterone (like standing does). Don't quote me on this! Just what I recall off the top of my head. They might put you on fludrocortisone for O.H. too since its a blood volume building inducer/retainer.

My "extremities" get mildly "tight & numb" feeling at various times. My calves & feet are most prone. My forearms will do so even if they aren't part of my exercise (for example if only working legs). I think it is part of (what is for me very mild) vascular constriction weirdness and maybe just part of POTS stuff at times. If I recall correctly, the body typically puts out mild generalized "constriction" message during exercise and then signals localized "dilation" in areas being worked. It seems sometimes the localized dilation isn't quite happening but the mild constriction is... or vice versa if I go faint unexpectedly. I think flakey vasoconstriction of the very mild variety like I have is probably part of the game with POTS or perhaps other dysautonomias. I know I don't personally have extreme enough responses to qualify for Raynaud's or something like that. Just mild weirdness, mostly a mild discomfort (though I have wondered if it inhibits performance & recovery from exercise).

It is said to be a back & forth (two direction) interaction between POTS & anxiety/stress... with either making the other worse. I'm not sure how to state this appropriately, but I have wondered if it might be enlightening for a person without insight into POTS who is inclined to say "it is 100% in your head" to perhaps voluntarily be given a shot of norepinephrine inducing agent that raised their level suddenly to the levels that some of us endure often enough! I think some of the skeptics might change their tune pronto! There are experimental procedures where anxiety inducing meds are administered in order to measure how well a particular treatment then blocks them... so this is not a totally inhumane thing to consider! It is done safely (voluntarily) in research circles. Of course, as the person goes in to panic mode... everyone around them can say repeatedly "come on now, it's just in your head, right?" I am not so cruel, but it is intriguing thought On the other hand. If you have either dysautonomia, anxiety, both... or any chronic illness. It behooves you to address whatever you can as best you can. This means one doesn't get to ignore anxiety/stress issues simply because there is a more physical condition going on. One kinda has to take it all on as best one can. Treating anxiety will help POTS. Treating POTS will help anxiety. Treating both (and being vigilant about both) is probably wisest approach. Any chronic illness pushes "depression" buttons. It's just an extra challenge in our worlds.

Fludro is technically said to be "high potency" glucocorticoid and "ultra high potency" minercorticoid. So while it is technically both, one is taking a very small dose and the glucocorticoid factor is pretty low, especially compared to something like predisone and the others in that class. Note that doses are in micrograms, which keeps the gluco aspect at bay for most folks so for practical porpoises like us, it isn't a gluco. Some might be sensitive enough that they get some of those things though... for example, I get mood effects for a while when taking it, which is not typically thought to relate to kidney regulation (mineralcorticoid) but is very typical of glucocorticoid hormone impact. I have not personally heard it to be considered "immunosuppressive" at the low 50-200 microgram doses we tend to use... but the standard drug information printouts still have that standard "steroid" information on them.

I've only hopped on one for a minute or so. They have a neat feel to the way they "float" you around and respond. There is one saving grace to the standing-up issue... one is at least leaning fore-aft-side-to-side, so your calf & leg muscles are actually a bit active even though you are upright. For folks with mild cases like me, this might work out ok. If you can walk 'n' chew gum at the same time... perhaps one could Segway and do the leg/buttock flexing countermaneuvers at the same time and stay conscious/safe on one! The "touristy" places that offer tours on these will apparently let you do a trial ride for free to see if you feel safe using them. Might be a way to sneak a ride. They make me want to dress up in a DEVO outfit though! Are we not men? We are Devo!

This describes me at times. Zoned out... perhaps even something loosely akin to the "thousand yard stare". Beyond that, I've had couple of "catatonic" episodes... one involved remarkably low Potassium levels (documented). Besides the "detached" state, some phases of "emotional lability" seem associated with POTS to me... though not every doc will buy in to that.Somewhat different, but also in the genera of making one feel "unreliable"... I can reach a fatigue level where I get what feels like flu symptoms coming on (maybe this is more CFS side rather than POTS???). This can even include great discomfort and night-sweats and such... but lacking typical POTS heart rate things. I seem to have had great luck lately with steady moderate stream of salt, potassium, magnesium & water... then rest for a while. For me personally, this may be somewhat useful in staving off and treating these things. I do not yet have them, but I will probably try out some "slow release" versions of those key minerals and see if that is even better (or at least more convenient than popping pills every few hours). Besides getting things measurably out of whack (electrolytes and such)... I think we folk tend to have tighter ranges of "normal". Meaning even a normal reading might be personally a bit out of range for us in some of these key items like electrolytes & sugar. I believe the glucose sensitivity is a medically (research) documented aspect of POTS/dysautonomia. The rest just "seems to be the case" to me personally.

Would be cool if there were a "canceling additive" or some treatment other than complete long term avoidance. Is such an inconvenient & expensive thing both to do a trial run & to deal with if diagnosed. Something like "beano" for Celiac

In most cases, the worst they can do is "say bad stuff" to you. You are aware of yourself and your condition and are an adult and will certainly be able to handle this. In some situations, a bad doc can throw a wrench into things horribly... but it sounds like in your context this is not the case. At worst it will be "a very bad aggravating day"... with appropriate fallout from that, but not a chance of worse. Does this seem like the case? People aren't trying to have you "committed" or anything right??? P.S. (I may be repeating) but there is probably a good chance a therapist will recommend using something like this forum... so the answer to your post topic question might be "both"