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  1. Another good article, this one on a 1950s-era breathing technique for improving breathing in asthmatics that appears to offer help beyond drugs. A Breathing Technique Offers Help for People With Asthma http://www.nytimes.com/2009/11/03/health/03brod.html http://en.wikipedia.org/wiki/Buteyko_method http://www.ehow.com/how_2142970_learn-bute...ove-asthma.html www.buteykocenterusa.com/ http://www.thebreathingman.com/ The safety emphasis is training with a breathing specialist to check and reinforce proper technique.
  2. The shortage of novel 2009 H1N1 animal-human influenza virus arises from several factors. 1. This is a pandemic-type, not seasonal-type influenza. Seasonal influenza in humans is a relatively new occurrence, post-dating the 1918 Spanish Influenza pandemic, with bird-pig influenza genes slowly adapting over the course of years to humans, evolving into a nearly purely human-adapted virus in response to human immunity,. Successive mutations caused the emergence, in the mid-20th c,. of two new strains that became the predominant seasonal flu types we see today. The previously evolved and now seasonal-H1N1 disappeared for about 20 years, between 1957 and 1971. It re-emerged mysteriously, unchanged - a biological impossibility that has defied explanation. The 1968-1970 pandemic was a different strain, that went on to become immune-adapted as a seasonal influenza strain. The 2009 H1N1 strain is genetically different enough from the presently circulating seasonal-H1N1, that there is little protection from seasonal flu vaccines. People who were exposed before 1957 to the older version of H1N1 appear to possibly have immunity to it. Very elderly people who had been exposed to the pandemic-version in the 1920s were found recently to still have a very strong immune response to the reconstructed original 1918 pandemic virus. This reinforces the notion that exposure to strongly immune trigger influenza viruses causes the immune B-cell system to retain and maintain an antibody response for life. This helps us understand how pandemic strains can eventually become seasonal, as viruses must mutate in the game of virus-against-human immune systems, and thus evolve into less virulent and dangerous viruses because we have at least partial immunity to the previous viral surface protein mutations that allow binding to human lung and human intestinal cells. 2. Pandemic viruses have some important differences in their mode of action when compared against seasonal influenza strains. So they are not the same. It remains to be seen just how effective the present 2009 H1N1 vaccines are - that will take months to analyze the data. So why else was the vaccine 'late'? 3. Typically, seasonal influenza vaccines take about 6 months to select, generate and mass produce vaccines, from best guess estimates of last years influenza and strain studies of the most recent Southern Hemisphere strains in circulation. Multiple dominant strains of influenza in global circulation is a VERY recent phenomena. That tells us that something has changed to afford multiple strain emergences as pandemic viruses that crossed easily into humans and become adapted within a decade or less as seasonal strains. Purely animal influenza viruses that can infect humans, like the Bird Flu (H5N1) are VERY RARE. These are pandemic viruses. Before the advent of human adaptation of influenza viruses, they were all bird adapted strains (the original host of the virus). 4. The emergence of this 2009 pandemic virus caught global health officials by surprise. It spread very, very rapidly once it reached a critical threshold, in March-April 2009. It spread far more quickly than other 20th century pandemics (of which there were 4 in total), most likely due to air travel and the infectious ease of this virus. So, it emerged at a time when vaccine manufacturers were busy producing the 2009 seasonal vaccine. The virus had to be studied and individual samples tested to see if they could be cultured. 5. Culturing this virus was very difficult. Because it carries avian (bird) genes, it was good at culture evasion (traditional vaccines are still produced in duck embryos). Thus we have surprising emergence at the very end of the regular flu season of last year, exceptional virulence, unknown factors that causes fatality among seemingly healthy adults, an unusual infection rate among age-cohorts not typically made very sick by seasonal influenza viruses, and exceptional difficulty in culturing the virus, which is also rather monotypic - it hasn't changed despite migrating globally in just 2 months time, and infecting virtually every nation on the planet as of October 2009. A sixth problem is this: the cheap and quick lab test for H1N1 was found to be lower than 50% in accuracy. It has hindered case confirmation, and led nations to stop reporting cases this past summer, because of the rapid spread that made it less important to know exact numbers once it had moved through regions, and because of the difficulty in clinical confirmation of the virus. While it would seem prudent to use the anti-viral agents like Tamiflu in households where 2009 H1N1 virus is present and where one or more individuals are highly susceptible, a physician must also decide whether to use the spare existing supply ONLY for active cases. In other words, he will readily provide the drug IF one of the other sons becomes ill, but not before. This is typical where dose rationing is required due to drug shortages, at the start of a suspected major infectious illness wave of unknown duration.
  3. >Like our group of disorders, autism has subtypes, and likely multiple pathways to the cause the symptoms of disorders. More in common than you think. Some of the liver and brain metabolic pathway dysregulation seen in Autism appears to be present in POTS. Agreed on the idiocy of applying secretin - it's using a hammer to flatten a pin. Two thumbs up for Offit, who has been demonized, threatened and humiliated by overzealous parents who firmly believe that vaccines are the cause of their offsprings autism. Nope. The cause is much more interesting, having to do with piss poor methylation status in Mommy and Daddy, especially when they had their fun teen years of alcohol, drug use, smoking and abysmal dietary and sleep habits. Those are the years when eggies and spermies are environmentally mapped, that is, the health status of the adult is translated into fine tuning of gene silencing, gene regulation and expression. That's epigenetics. It's a pattern that is thought to be 'heritable' for a span of a few generations, before the changes are either 'fixed' or 'lost' due to changing health status within families. Daddy especially is culpable - after all, when he produces his little spermies, during maturation, they undergo methylation stripping (de-silencing) and then resilencing, according to his genetics but also his health status. He produces his sex cells over the course of his life. Older daddies who have been bad actors (made poor health style choices for many years) are a prime cause of heritable disorders in their children. Not that they would admit it. Mommy is also culpable, for maternal methylation patterns are often dominant in key metabolic gene families (eg.., entire chromosomal regions) and in innate immune response patterns. Mommy, however, has one shot for programming her eggs, when she is still a teenager. Mommy further 'edits' neonatal development during pregnancy, reinforcing gene expression changes by her gestational health status. How many teens do you know that are careful with their diet, sleep habits, get enough exercise and fresh air? Do you see where I am going with this? While parental health plays a role in methylation and antioxidant pathology, so does offpsring early nutrition, and also environmental exposure, sleep hygiene, and parental stress levels. The fact is this: environmental exposure to mercury (air and soil pollution) and arsenic (drinking water and food) is much, much more likely to interfere with building precious methylation pool stores, with critical intracellular antioxidant formation, and with oxidiative stress tolerance than is the preservative in a booster vaccine series. The chemistry is compelling and quite interesting. Why children? Children, especially in the critical period, age 0-6 when 85% of brain development occurs, have many times the metabolic free radical production level of adults, because of the significant developmental growth rate, and in the important staged and methylation driven turning on and off of genes. Both the methylation and antioxidant pool get sucked down to critical levels, if (a) parents are lax with their kids diets and lifestyle. ( kids and parents live in polluted environments, and ? kids have less than stellar parental social conditioning. Thats the other really interesting bit about epigenetics. While parental gene influence can predispose offspring to faulty genes, gene regulation and gene products, there is considerable 'fine tuning' that occurs during development, in an amazing suite of effector molecules, that bind to 'noncoding regions' on genes and operate up- and down-stream of the target gene position in the chromosome. These effects also affect post translational modification: the alteration of gene products by additional chemistry steps that can change structure and function. The segue to ANS? Many of the same base mechanisms, epigenetics, lifestyle factors, health/fitness status, chronic stress loading and environmental exposures during progressive life stages are operators in the full blown expression of weakly heritable symptoms.
  4. Sitting, 50-60 bpm Standing, 60-70 Supine, as low as 25-50 Bradycardia is more my thing. It used to puzzle me when doctors when comment on how 'fit' I was (when I wasn't exactly a poster child for daily workouts other than walking). My Mom also has this condition. Tachycardia didn't set in until my ANS/POTS symptoms emerged and dramatically worsened in a relatively short period of time, mid-30s. Even with a prolonged period of careful symptom management, if I am under a lot of stress, or haven't been keeping up on fluids, or diet slips cause insulin/epinephrine to surge, my supine heartbeat rate can be as high as 100 for several days, when checked first thing in the morning, upon waking.
  5. Need to correct this misconception: Tamiflu does not prevent you from contracting H1N1 when exposed. What it does is slow down and hinder viral replication, shortening the duration of illness and maybe reducing carriage (viral shedding after symptoms begin to subside). Your doctor was absolutely correct to tell you 'no'. Regional hospital supply is ok, but community hospitals and clinics are already running into problems with Tamiflu access. Supply isn't nearly as robust as many people think. It needs to be conserved for those who need it. Tamiflu (Children's formula, especially) - shortage in the news http://tamiflu-news.newslib.com/ Regarding vaccine access: The CDC and States have really dropped the ball on this one. They KNEW months in advance that the demand at the start of the Fall Wave was going to be higher than supply, but got overconfident on promises back in July and August, of expected production volume that was, even then, falling short because this virus is difficult to culture and 'grow'. In many places, clinics and pharmacies are dispensing these shots for as much as $50 a dose, for which you may stand in line for up to 5 hours. The working assumption is: your health insurance will cover it. Mine does not. They see vaccines as 'electives', and figure them into yearly deductibles. There is, as far as I can tell, absolutely zero intent by public health officials to sort the most susceptible from those who are least likely to contract Swine Flu (the elderly). In fact, senior citizens dominated the turnout at many 'free shot' community fairs through the nation in the last few weeks. The community health centers I contacted had absolutely no intent of rationing for the most susceptible - the limited supply was handed out on a first come, first serve basis. Their total supply was limited to less than one thousand doses. No repeats possible.
  6. Au contraire, there is an element of depression, as in neurochemical imbalances between excitatory and inhibitory neurochemistry that affects not just the brain, but the secretory organs of the body, too. That chemistry discussion has to wait a bit, yet. How about a little history? The History of Dysautonomia http://www.cvm.missouri.edu/neurology/Dysauton/history.htm http://www.dynakids.org/why_i_never_heard.jsp Timeline of Dysautonomia: http://www.google.com/#q=history+of+dysaut...03f3b2a1b734003 NOTE THE DATES. Far down the road, we will come back to the importance of these dates - it will be one of the last pieces of this complex puzzle to be laid out. Dysautonomia medical description and case prevalance suggests that is a relatively modern family of abnormal neurological and metabolic states, like type II diabetes.
  7. Reasonably good definition of hypoglycemia: http://en.wikipedia.org/wiki/Hypoglycemia Whipple's Triad, and it's application for diagnosis: http://en.wikipedia.org/wiki/Whipple%27s_triad Evaluation and Management of Adult Hypoglycemic Disorders: An Endocrine Society Clinical Practice Guideline http://jcem.endojournals.org/cgi/content/abstract/94/3/709 In my case, a glucose tolerance test induced hypoglycemia causes classic adrenergic symptoms - no sweating, but exceptional nervousness, coldness and shaking, drop in blood pressure, tachycardia, staring, mental fog. Where there are symptoms in the absence of a significant drop in blood glucose, a vague diagnosis of Idiopathic postprandial syndrome is applied. http://en.wikipedia.org/wiki/Idiopathic_po...andial_syndrome The second reference: http://www.uni-duesseldorf.de/MedFak/insul...an_hypo.htm#APS provides an interesting answer: abnormal epinephrine response. Despite normal concentrations of blood glucose patients face unspecific symptoms (sweating, tremor, palpitations, anxiety, nausea) caused through autonomic adrenergic counterregulation. The adrenergic tone elicits the symptoms and simultaneously avoids hypoglycemia through biochemical mechanisms (action of epinephrine / adrenaline The 'shock response' effect (termed 'biochemical centralization, analgous to blood volume conserving action observed in traumatic shock events) is described here: "Stress-Hyperglycemia" during the postaggressive metabolic state essentially means the physiological adaptation to jeopardized cerebral blood flow in order to meet the fuel needs by the brain. This is achieved by a biochemical centralisation of the glucose metabolism analogous to the hemodynamic centralisation of the circulation during shock (cardiogenous, hemorrhagic, hypovolemic). Metabolic centralisation physiologically resembles a glucagon-mediated "endogenous infusion of glucose". Glucohomeostasis http://www.uni-duesseldorf.de/MedFak/insul...physiol.htm#top This latter case, where patients report and physicians observe symptoms consistent with hypoglycemia during a GTT, but the blood work fails to show significant deviation from normal blood glucose rise and fall, is why many inexpert physicians will say..."I don't believe in hypoglycemia". In other words, they don't know what's going on, and in the absence of testing for epinephrine surge, they write it off as psychosomatic, or anxiety disorder. If we have a significantly altered blood volume after eating, such that blood flow to the brain is compromised, the hypothalamus lets loose a surge of ACTH and epinephrine, further reducing blood flow to the extremities. Why would blood volume change? Your body sends blood to the intestinal tract for nutrient absorption. If you have low blood volume to begin with, this may trigger an exceptional drop in BP, with a hair-trigger epinephrine release response from the hypothalamus.
  8. Rule #1: the easy explanation won't work if the organ in question has been removed. Curious, I went looking again. I found this. http://www.scoliosis.org/forum/archive/index.php/t-1350.html Kinda sounds like the scoliosis - abnormal thoracic positioning - worsens the GERD/reflux - that would be your upper right quad pain. The right side weakness/tingling and numbness would maybe be a branching nerve pinch issue related to the scoliosis. When I see a thread of folks who have similar background (scoliosis, GERD, and tingling/weak/numb extremities), I figure that there is probably two problems with a related cause - in this case, spinal deformation causing diaphragm compression with nerve complications. Most unusual. Interesting case.
  9. Just maybe, you have shingles. You already appear to have aggravated inflammation condition (mild acne) - sometimes associated with periods of excess stress and often associated with blood sugar issues (causing excess triglyceride release from subcutaneous stores and affecting sebaceous gland activity on the face, upper chest and back). It's contagious. Normally, presentation is an isolated patch, but it can, in some cases, be widespread on head, trunk, arms, and lower extremities. Photos below (not for the squeamish / have nausea) http://www.lib.uiowa.edu/haRDIN/MD/dermnet/shingles.html
  10. Your symptoms fit the description for gallbladder disease - persistent flank pain, nausea, headache. Have your docs run a simple liver panel to determine if you have a blockage or chronic GB inflammation problem? Even if they have ruled it out, I would look quietly for a second opinion on it.
  11. When I first read this thread, my jaw dropped. 1. It's relatively old news (2007). 2. It's not like a major research center, one of the few treating autonomic system disorders, would publish fallacy. Autonomic Disorders and Mitral Valve Prolapse Center http://www.mvprolapse.com/dysautonomia.html http://www.mvprolapse.com/treatment.html Yeah, there is a blood sugar control issue here. POTS doesn't mimic hypoglycemia - hypoglycemia is part of the metabolic dysregulation, a pantheon of altered pathway states - the 'family' of autonomic system diseases. Autonomic disorders are *largely* familial rather than being caused by a viral infection. The viral infections, extended bed rest - that tipped the scales in favor of overt symptom emergence. The primary issues are genetic in origin, but not the way you're thinking. To understand dysautonomic states, we'll need to think about receptors - nuclear receptors. And epigenetics. And antioxidant status and it's maintenance. POTS and an assortment of other autonomic disorders are very likely to be epigenetic in origin - a problem of silencing of genes (many of them regulated by key nuclear receptors) that are turned on and off as you progress through key organism developmental stages. The nifty part is this: we have amazing neural plasticity. We can, to an extent, manipulate nuclear receptors and antioxidant status by diet, lifestyle, supplements - and by understanding the role of methylation status in human health and reproductive fitness. You've already got the important bits embedded in many, many threads here - technical material and lots of observational reporting. We should start connecting the dots.
  12. >Exercise increases the bioavailability of nitric oxide which in a subset of POTS patients was found to be inappropriately low causing increased orthostatic sympathetic activity. Exercise improves the release, uptake and turnover of NO in the peripheral vasculature. Inappropriate mopping up of that nitric oxide signal is an important issue, as it points to the associated problem of cleaning up energy metabolism free radicals that can cause aggregate damage in muscle and nervous system tissue. Think: low glutathione status. An aside: I've been reading this forum on an off for a while. You have a couple of members who have come tantalizingly close to the central metabolic pathway issues underlying the vast majority of autonomic system disorders, back in late 2006 and as late as 2008. For some reason, these clever members put out the critical pointers in posts meet with dead silence from the rest of you. I find that curious.
  13. >1. With POTS, do you think you will be able to do a long hike without making your symptoms worse? How well you cope physically with extreme periods of exertion will depend on: a. your present fitness level b. how well you understand and control blood sugar and breathing during extended periods of exertion, c. recent history of symptom severity, d. recent history of stress management, particularly acute mental stress episodes/events I've always found moderately-paced walks meditative, calming, and energizing - as long as I was careful to maintain my blood sugar levels and take regular breaks. >2. With POTS, does Xanax-type medication make your symptoms get a lot better or even go away? This is a GABA receptor modifier. Your positive response to a anxiolytic drug underscores the importance of GABA in dynautonomic disease. >3. With POTS, is it possible to work out 1-2 hours a day and feel fine during the workout? Well, again, this will depend on your fitness level. Generally speaking, the answer should be NO WAY! At about 1-1.5 hours into a workout, you're starting to seriously deplete energy reserves, and that can bring on a marked drop in blood sugar, and with it, release of epinephrine and extended release of cortisol. > Does cardio or weights make you worse? Will depend on your level of fitness, how you train, and most importantly, how you breath. Dollars to donuts, many of you who lift weights do not regulate your breathing correctly. That can worsen hypoxia, an attendant problem in dysautonomia, and cause irregular BP spiking and plunging. For me, the ticket out of POTS **** included vastly improving physical condition, slowly and with careful attention to nutritional support. However, early on in training, I would run out of energy easily, until I learned to pace my workout, and even break it up into shorter periods to get around blood sugar and blood pressure control problems. As I put on muscle and improved aerobic performance, I found that I was finally able to improve energy storage in liver and muscle, so that I was able to perform well above expectations in as little as 6 months and outperforming expectations in about a year. In order to learn how to work out correctly, I had to learn, and to do that, I had to join a physical fitness forum and read, read, and practice. >4. With POTS, on days where you feel bad even when sitting or lying down, does standing up and walking around make it even worse? Can't answer this because I don't know what you mean by 'feeling bad'. Sometimes, if I've had a really emotionally stress period and have slacked off on my exercise and diet, I will feel myself start to 'shut down' - I may feel cold and feel like I need to lie down. This is pretty rare, though. >5. With POTS, do stressful events or situations make your symptoms worse? Yes. Not only do stressful events make the symptoms worse, but the frequency of these events, over the course of months to years, has a direct role in sudden escalation of symptoms and their severity. How you cope with acute and chronic stress is very important to managing dysautonomic conditions. You can never be 'cured', but you can work towards extended remission.
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