firewatcher

As a preface, I used to work for a Chinese medicine practitioner who decocted his own Chinese herbal medicine from reputable, clean-sourced, Chinese herbs, which are very hard to get. As much as I hate to say it, I seriously doubt that you will find ANY doctor (m.d.) that knows even the slightest thing about Chinese herbs (other than aristolochic acid nephropathy) and every MD will tell you to stay as far away from Chinese medicine as you can. Talking to the Chinese medicine practitioner will not help either, they won't know much about the drugs. Pre-prepared Chinese herbals (pills and powders, etc. from bottles with labels) may be adulterated with pesticides, heavy metals and pharmaceuticals. Very few brands have strict standards (or any.) Just because something is "natural" does not mean that it is not also dangerous. I would NOT mix Chinese medicine with regularly used drugs. If you want to try Chinese Herbal Medicine it can be very effective with fewer side effects, but it will be hit and miss. Much of it depends on the skill of the herbalist, the potency of the herbs and the correctness of the preparation. I would compare the effect to more of a "firm nudge" to your system and less of a "sledgehammer" like drugs. Just a warning, they are going to smell nasty and taste worse! But sometimes, they do work incredibly well! You can research the individual herbs at rootdown.us, where you can put in either the Chinese or the Latin name and then go to PubMed or drugs.com and check for interactions....however, the synergy (combined action) of two or more herbs will change the mechanism of action and may either increase or decrease the interaction or potency. ASK the herbalist for a list of what herbs are in your "tea," if they won't tell you what they are (include the Latin name!--it will be on the bag where they were bought bulk) Don't take them and DON'T go back. Many Chinese herbs are spelled almost identically in Chinese pin yin (the English phonetic) and one letter difference can be a completely different substance.

Clin Auton Res. 2013 May 25. [Epub ahead of print] Gastric emptying in postural tachycardia syndrome: a preliminary report.Park KJ, Singer W, Sletten DM, Low PA, Bharucha AE. SourceDepartment of Neurology, Mayo Clinic, Rochester, MN, USA. Abstract PURPOSE:Autonomic neuropathy is widely recognized to be associated with upper gastrointestinal symptoms and abnormal (i.e., rapid or slow) gastric emptying. While patients with postural orthostatic tachycardia syndrome (POTS) may also have gastrointestinal symptoms, our understanding of gastric-emptying disturbances in POTS is very limited. The objectives of this study were to evaluate the relationship between gastric-emptying disturbances and gastrointestinal symptoms in patients with POTS. METHODS:We retrospectively reviewed the medical records of 22 well-characterized patients with POTS and upper gastrointestinal symptoms in whom autonomic (i.e., postganglionic sudomotor, cardiovagal, and adrenergic) functions and gastric emptying were evaluated using standardized techniques and scintigraphy, respectively. Medical records were reviewed retrospectively to assess clinical features, gastric emptying, and autonomic functions. RESULTS:Over 70 % of patients had nausea and/or vomiting, which was the most common GI symptom; other common symptoms were abdominal pain (59 %), bloating (55 %), and postprandial fullness/early satiety (46 %). Over one-third of patients had abnormal [i.e., rapid (27 %) or delayed (9 %)] gastric emptying. Gastric-emptying disturbances were not significantly associated with GI symptoms, autonomic symptoms or autonomic dysfunction. CONCLUSIONS:Over one-third of patients with POTS and gastrointestinal symptoms have abnormal, more frequently rapid than delayed gastric emptying. These findings need to be confirmed in a larger cohort of patients. PMID: 23708963

I have used pseudoephedrine HCL for 4-6 weeks now. It has helped my symptoms as well. I can't take it every day because of tolerance and insomnia issues. The 12 hour does not work as well as the original formula for me, and causes worsening insomnia issues. I take a normal dose for congestion, every other day. I find that it helps tremendously for the orthostatic grey-outs, fatigue and brain-fog and does not spike my HR or BP.

I get this too, not constant, but frequent. So far, there has been little that has helped. Lyrica and gabapentin have helped, but gave me side effects. The allodynia is often caused by central sensitization, a change in the nervous system's pain response. This doc, C. Woolfe, has more information on this stuff than any other doc I've seen. He's a pediatric neurologist in NY. I have not seen him, but I'd like to. http://www.childrenshospital.org/cfapps/research/data_admin/Site2875/mainpageS2875P0.html

Neurology. 2013 Apr 24. [Epub ahead of print] Low-dose propranolol and exercise capacity in postural tachycardia syndrome: A randomized study.Arnold AC, Okamoto LE, Diedrich A, Paranjape SY, Raj SR, Biaggioni I, Gamboa A. SourceFrom the Department of Medicine, Division of Clinical Pharmacology, Vanderbilt University, Nashville, TN. Abstract OBJECTIVE:To determine the effect of low-dose propranolol on maximal exercise capacity in patients with postural tachycardia syndrome (POTS). METHODS:We compared the effect of placebo vs a single low dose of propranolol (20 mg) on peak oxygen consumption (VO2max), an established measure of exercise capacity, in 11 patients with POTS and 7 healthy subjects in a randomized, double-blind study. Subjects exercised on a semirecumbent bicycle, with increasing intervals of resistance to maximal effort. RESULTS:Maximal exercise capacity was similar between groups following placebo. Low-dose propranolol improved VO2max in patients with POTS (24.5 ± 0.7 placebo vs 27.6 ± 1.0 mL/min/kg propranolol; p = 0.024), but not healthy subjects. The increase in VO2max in POTS was associated with attenuated peak heart rate responses (142 ± 8 propranolol vs 165 ± 4 bpm placebo; p = 0.005) and improved stroke volume (81 ± 4 propranolol vs 67 ± 3 mL placebo; p = 0.013). In a separate cohort of POTS patients, neither high-dose propranolol (80 mg) nor metoprolol (100 mg) improved VO2max, despite similar lowering of heart rate. CONCLUSIONS:These findings suggest that nonselective β-blockade with propranolol, when used at the low doses frequently used for treatment of POTS, may provide a modest beneficial effect to improve heart rate control and exercise capacity. CLASSIFICATION OF EVIDENCE:This study provides Class II evidence that a single low dose of propranolol (20 mg) as compared with placebo is useful in increasing maximum exercise capacity measured 1 hour after medication. PMID:23616163[PubMed - as supplied by publisher]

I smell ammonia, not a burning smell. It started with ragweed season for me. A sinus infection can cause phantosmia (phantom smells) as well as epilepsy and migraines. I have vasomotor rhinitis, so I can get transient sinus infections. There are so many crazy things that can cause this, I figure it is one of the ones I've already been diagnosed with and just roll with it.

My insurance company also gave me a nurse "case manager." She calls and checks in every six months or so, just in case I have any questions...the problem is that she's never heard of two of my conditions and I end up educating her! Call them back and educate them. Occasionally, they can be a good resource for finding doctors. One of the nurses that I've had like this actually called several docs and asked if they treated POTS, she promptly called back and told me that they didn't. Good try though. Let us know what they say.

better explanation: http://pharmrev.aspetjournals.org/content/60/2/210.full

Basic Science Reports Chronic 17β-Estradiol Replacement Increases Nitric Oxide–Mediated Vasodilation of Guinea Pig Coronary Microcirculation Loren P. Thompson, PhD; Gerard Pinkas, BS; Carl P. Weiner, MD "The incidence of coronary artery disease is lower in premenopausal women than in age-matched men.1 2 After the menopause, the risk of coronary artery disease rises to levels equivalent to those of men.1 2 3 4 Epidemiological and clinical evidence suggests that estrogen is cardioprotective, because hormone replacement therapy reduces the risk of coronary artery disease in women.2 5 6 7 However, the mechanisms by which estrogen is cardioprotective are incompletely understood. Although estrogen lowers LDL cholesterol and increases HDL cholesterol,3 4 these changes account for only 25% of its cardioprotective effect in women.3 4 The remaining 75% is accounted for by alternative mechanisms. Estrogen may be cardioprotective by enhancing vasodilation of the coronary circulation. Functional estradiol receptors are present on both endothelial8 and vascular smooth muscle cells.9 10 Acute infusions of estradiol increase coronary blood flow in the open-chest dog11 and the nonpregnant sheep.12 13 Several mechanisms have been proposed to mediate the direct effect of estradiol on the vasculature, including membrane-altering properties and/or calcium channel blocking,14 stimulation of the NO/cGMP pathway, and activation of K+ channels of the coronary vascular smooth muscle.11 15 16 Although it is important to understand how estradiol relaxes vascular smooth muscle directly, it may be independent of the genomic effect chronic estradiol administration has on the coronary vasculature. Chronic exposure to estradiol has been shown to upregulate gene expression of endothelial NO synthase17 18 19 20 and thereby can increase NO production...."

And another article on ACE, angiotensin II, immunity, fertility and BP: http://www.sciencedaily.com/releases/2012/09/120908081615.htm

http://www.sciencedaily.com/releases/2012/09/120908081613.htm Perhaps this is a link between EDS, autoimmunity and POTS....

Int J Gynaecol Obstet. 2012 Sep;118(3):242-6. Epub 2012 Jun 20. Gynecologic disorders and menstrual cycle lightheadedness in postural tachycardia syndrome. Peggs KJ, Nguyen H, Enayat D, Keller NR, Al-Hendy A, Raj SR. Source Paden Autonomic Dysfunction Service, Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, USA. Abstract OBJECTIVE: To assess differences in gynecologic history and lightheadedness during menstrual cycle phases among patients with POTS and healthy control women. METHODS: In a prospective, questionnaire-based study carried out at Paden Autonomic Dysfunction Center, Vanderbilt University, between April 2005 and January 2009, a custom-designed questionnaire was administered to patients with POTS (n=65) and healthy individuals (n=95). The results were analyzed via Fisher exact test and Mann-Whitney U test. RESULTS: Patients with POTS reported increased lightheadedness through all phases of the menstrual cycle phases as compared with healthy controls. Both groups experienced the greatest lightheadedness during menses, and a decrease in lightheadedness during the follicular phase. Patients with POTS reported a higher incidence of gynecologic diseases as compared with healthy controls. CONCLUSION: The severity of lightheadedness was found to vary during the menstrual cycle, which may relate to changes in estrogen levels. Patients with POTS also reported an increase in estrogen-related gynecologic disease. Copyright © 2012 International Federation of Gynecology and Obstetrics. Published by Elsevier Ireland Ltd. All rights reserved. PMID: 22721633 [PubMed - in process] PMCID: PMC3413773 [Available on 2013/9/1]

I should probably note that most fermented foods are not a migraine trigger for me, with the exception of fermented fruits like wine. Cheeses and soy sauce do not trigger my headaches like they do for many migraine sufferers.

I tried yogurt, but did not have good effects (so probably not that flora.) I started Miso a couple days ago, and will slowly be working up to a cup of miso soup (1 heaping tablespoon of miso paste in a mug of hot water) with every meal. It is a bit of an acquired taste: I've had some that tasted like a dirty dish-rag! This latest is pretty tasty, more like broth. I don't do supplement probiotics since I believe that the gut microbiome is more complex than a pill can produce. So far, so good on the headaches. I'll keep you posted as to my progress.

My neurologist diagnosed me with "Chronic Daily Migraine/Transformed Migraine," which is by far my most disabling symptom. Meds have not really proven effective for this or have stronger side effects than the headache. I've had acupuncture for over a year, which helps, but has not solved the problem. I am currently trying a "back door" route for my headaches that involves old foods and cutting edge science...alteration of the gut flora. My current attempts are with Miso which contains kojic acid: Chem Pharm Bull (Tokyo). 2010 Oct;58(10):1353-61. Kojic acid derivatives as histamine H(3) receptor ligands. Sander K, Kottke T, Weizel L, Stark H. Source Johann Wolfgang Goethe University, Institute of Pharmaceutical Chemistry, Biocenter, ZAFES/CMP/ICNF, Frankfurt/Main, Germany. Abstract The histamine H(3) receptor (H(3)R) is a promising target in the development of new compounds for the treatment of mainly centrally occurring diseases. However, emerging novel therapeutic concepts have been introduced and some indications in the H(3)R field, e.g. migraine, pain or allergic rhinitis, might take advantage of peripherally acting ligands. In this work, kojic acid-derived structural elements were inserted into a well established H(3)R antagonist/inverse agonist scaffold to investigate the bioisosteric potential of γ-pyranones with respect to the different moieties of the H(3)R pharmacophore. The most affine compounds showed receptor binding in the low nanomolar concentration range. Evaluation and comparison of kojic acid-containing ligands and their corresponding phenyl analogues (3-7) revealed that the newly integrated scaffold greatly influences chemical properties (S Log P, topological polar surface area (tPSA)) and hence, potentially modifies the pharmacokinetic profile of the different derivatives. Benzyl-1-(4-(3-(piperidin-1-yl)propoxy)phenyl)methanamine ligands 3 and 4 belong to the centrally acting diamine-based class of H(3)R antagonist/inverse agonist, whereas kojic acid analogues 6 and 7 might act peripherally. The latter compounds state promising lead structures in the development of H(3)R ligands with a modified profile of action. PMID: 20930404 [PubMed - indexed for MEDLINE]

Zap, I take a baby dose of Propranolol (20mg) and only in the morning. The melatonin is a baby dose too (1.5mg) and it is (according to my doctor) supposed to be taken 12 hours before your targeted wake-up time. I take mine at bedtime only because that is what works for me. My son was recently diagnosed with DPSD (delayed phase sleep disorder) too and he takes melatonin at dinner since he has to get up at 6 for school. Lack of sleep was awful for my migraines, it is a well known trigger. Good luck with the peace part!

Clin Sci (Lond). 2012 Aug 29. [Epub ahead of print] Diagnosing Postural Tachycardia Syndrome: Comparison of Tilt Test versus Standing Hemodynamics. Plash WB, Diedrich A, Biaggioni I, Garland EM, Paranjape SY, Black BK, Dupont WD, Raj SR. Abstract Postural tachycardia syndrome (POTS) is characterized by increased heart rate (ΔHR) of ≥30 bpm with symptoms related to upright posture. Active stand (STAND) and passive head-up tilt (TILT) produce different physiological responses. We hypothesized these different responses would affect the ability of individuals to achieve the POTS HR increase criterion. Patients with POTS (n=15) and healthy controls (n=15) underwent 30 min of TILT and STAND testing. ΔHR values were analyzed at 5 min intervals. Receiver Operating Characteristics analysis was performed to determine optimal cut point values of ΔHR for both TILT and STAND. TILT produced larger ΔHR than STAND for all 5 min intervals from 5 min (38±3 bpm vs. 33±3 bpm; P=0.03) to 30 min (51±3 bpm vs. 38±3 bpm; P<0.001). Sensitivity (Sn) of the 30 bpm criterion was similar for all tests (TILT-10=93%, STAND-10=87%, TILT30=100%, and STAND30=93%). Specificity (Sp) of the 30 bpm criterion was less at both 10 and 30 min for TILT (TILT10=40%, TILT30=20%) than STAND (STAND10=67%, STAND30=53%). The optimal ΔHR to discriminate POTS at 10 min were 38 bpm (TILT) and 29 bpm (STAND), and at 30 min were 47 bpm (TILT) and 34 bpm (STAND). Orthostatic tachycardia was greater for TILT (with lower specificity for POTS diagnosis) than STAND at 10 and 30 min. The 30 bpm ΔHR criterion is not suitable for 30 min TILT. Diagnosis of POTS should consider orthostatic intolerance criteria and not be based solely on orthostatic tachycardia regardless of test used. PMID: 22931296 [PubMed - as supplied by publisher]

My sleep doc told me that Propranolol destroys your body's natural melatonin, so YES, it can make your insomnia worse. I have a genetic circadian sleep disorder where I don't naturally fall asleep until early in the morning. Taking a BB first thing in the morning and melatonin at night has really helped artificially reset my body clock. I was stabilized using Western meds, but never got "better" until I started seeing an Oriental Medicine Practitioner and using Chinese herbal formulas. I've made more progress using them with fewer side effects than I ever did with pharmaceuticals. As far as finding peace...that you have to find regardless of your circumstance, for both the good and bad days (also, peace does not equal a cure! You can have peace in the midst of illness!)

Yes, I can still work. I have hyper-POTS, and have always had it (or was so young at onset that I don't remember.) I had been able to and did work full-time for many years doing a primarily seated job. I had a "POTS-crash" back in '07 and have been able to slowly work back up to a mostly standing part-time job in addition to raising two kids ( I was self-employed for many years and have taken time out to help a friend's business.) Much of what you can do depends on how you define "work." A 60 hour a week job hanging drywall or a 35 hour a week desk job.

One positive! The fitness expert I challenged on facebook (with quotes from the fulltext of the commentary) retracted and corrected her statements! I think she may have actually learned something about POTS in the exchange. Get noisy people! But be polite!

The 30 bpm jump in HR is described in BOTH deconditioning and OVERconditioning! You are supposed to use the morning HR surge to gauge if you have recovered from a heavy workout enough to go again.

Unfortunately, just one of several "fitness" experts blogging on this commentary. What is truly sad is that this is not what Dr. Joyner actually has said! He wants us to have fully monitored, supportive rehabilitation, not a "health club membership." He also mentions that our deconditioning is "secondary" to our illness, as opposed to obesity and type II diabetes which are "primary deconditioning" causing the illness. I've responded to one of the "fitness experts" on facebook, but she has ignored my posts. Good luck if you choose to spend your energy responding to this...

If you can afford a physical therapist or if insurance will cover it, I'd suggest you get one. It may save you some serious frustration and give you positive, genuine support.

In my case, they tended to occur simultaneously. The meds helped enough for me to get through the crash, and then I improved as my tone improved. My periods of "remission" occurred either at the same time as or because of improved physical tone.

That is great that you had no previous exercise intolerance. I've always had it, and still have it now. The explanations I've seen for puberty onset is the rapid fluctuations of hormones (testosterone, estrogen, growth hormone, etc.) causing "spurts" in growth that cause differing ratios of blood volume to muscle mass, as well as a rapidly shifting center of gravity. During puberty, the heart's size and pumping capacity also changes.