firewatcher

I agree with the observation that chronic caffeine messes with my POTS, but can be tolerated in small doses. I also get the crazy increases in symptoms with sweetener consumption though. I totally avoid all artificial sweetners, to the point of going without any drink, rather than drinking a diet anything. They trigger awful headaches in me. I think it is similar to the medication intolerance we experience, the body can handle the real thing, but put it into a molecule or "synthesize" it and our bodies simply overreact.

J Pediatr. 2011 Oct 11. [Epub ahead of print] Postural Tachycardia in Children and Adolescents: What is Abnormal? Singer W, Sletten DM, Opfer-Gehrking TL, Brands CK, Fischer PR, Low PA. Source Department of Neurology, Mayo Clinic, Rochester, MN. Abstract OBJECTIVES: To evaluate whether the use of adult heart rate (HR) criteria is appropriate for diagnosing orthostatic intolerance (OI) and postural tachycardia syndrome (POTS) in children and adolescents, and to establish normative data and diagnostic criteria for pediatric OI and POTS. STUDY DESIGN: A total of 106 normal controls aged 8-19 years (mean age, 14.5±3.3 years) underwent standardized autonomic testing, including 5 minutes of 70-degree head-up tilt. The orthostatic HR increment and absolute orthostatic HR were assessed and retrospectively compared with values in 654 pediatric patients of similar age (mean age, 15.5±2.3 years) who were referred to our Clinical Autonomic Laboratory with symptoms of OI. RESULTS: The HR increment was mildly higher in patients referred for OI/POTS, but there was considerable overlap between the patient and control groups. Some 42% of the normal controls had an HR increment of ≥30 beats per minute. The 95th percentile for the orthostatic HR increment in the normal controls was 42.9 beats per minute. There was a greater and more consistent difference in absolute orthostatic HR between the 2 groups, although there was still considerable overlap. CONCLUSION: The diagnostic criteria for OI and POTS in adults are unsuitable for children and adolescents. Based on our normative data, we propose new criteria for the diagnosis of OI and POTS in children and adolescents. Copyright © 2011 Mosby, Inc. All rights reserved. PMID: 21996154

10 months after 37 years.

tinks, I also had horrible constipation issues as a child. Another very embarrassing thing was the sudden and uncontrollable need to urinate when I stood in lines (like waiting for the bus at school.) I told my pediatrician about the chest pains and he always told me they were "growing pains" and brushed them off, years later I found out it was my gallbladder. Bright lights would inevitably give me headaches as well.

Though I was not tested till I was in my thirties, I remember having all the symptoms at age six. I had the same breathlessness, dizziness on standing and exercise intolerance. It was a miserable childhood, not knowing why I just could'nt chase after the other kids. All my teachers and doctors told me I was just lazy. There are a few good pediatric POTS specialists. An official diagnosis may help you both cope better and give you the best treatment options.

Handmadebymy- Exercise, particularly vigorous/strenuous exercise, slows down the blood flow to the kidneys and reduces their filtration rate (GFR.) The sudden increase in exertion may have restricted the filtration rate and made you more susceptible to a kidney infection. Sue- the article stated that the renin/aldosterone ratio was improved after exercise, but still was not "normal" like the controls. Also, the catecholamine reaction to standing was reduced. Neither of these improvements were seen in the BB group, so they are saying that exercise was superior to BB.

I just read the fulltext of the article (sent to me by an angel ) and the doc is confusing kidney function with ADRENAL function...close but no cigar. They did not measure (or at least report) kidney function other than urine volumes. Oh well... I'll give it to my nephrologist anyway. Thanks guys!

Thanks Naomi! I was looking for a credible source for his quote and you found it. I'm having a foggy day. I wonder what he's basing that statement on? What data was he using for kidney function? The research part of me wants numbers!!!!

Hi all, I am searching and this may be the fastest way to get what I need. I am looking for the specific quote from Dr. Fu on improved kidney function in POTS patients after completing the Levine exercise protocol. My doc at Vandy says that there is probably no connection between my declining kidney function and POTS, but my nephrologist is not so sure. I'd like to get her the stats and quote from the docs in Dallas so that she can contact them directly. I have the contact emails, but I want to give her the exact quote and numbers if I can get them. Anybody got this? Thanks!

My neurologist wants to send me to an EP for a possible ablation. I have been stalling, but I think I'll simply refuse at this point!

I will have to look into this further as well. I have no measurable vasopressin/ADH and an elevated C peptide, but normal fasting glucose. My endo has never checked it after eating.

"I do have a question as to the kidney failure. Did that come before or after the DDVAP? Do you think the med contributed to it?" The kidney failure came before the dDAVP by six years. The decline in my kidney function stabilized once I started the dDAVP. My nephrologist believes that it does somehow tie in to a lifetime of POTS and that the chronic hypovolemia and hypertension probably caused the damage. Hopefully, by stabilizing my blood volume and controlling the hypertension, we can stop the progression...at least that is the plan.

Debra, I was dxed at Vandy too. Propranolol was best for me since I also went hypertensive on standing. Unfortunately, I also go hypotensive AND bradycardic on lying down, so whatever I took had to wear off by night-time or my HR would drop too low. Unmedicated, it is normally in the low 50's-40 bpm at night. Add the tremor and Propranolol was my only real option. I manage well enough with that, but anything more than a brisk walk will send my HR up. I am happy that Bystolic worked for you, I was eager to try it several years ago and disappointed when it did not work out for me. Like you, POTS has given me "collateral damage," only mine is Chronic Kidney Disease/failure instead of Heart failure.

I am absolutely certain that it was Bystolic (nebivolol 5mg) because I still have the rest of the bottle. It was great for HR, but did nothing for my BP or tremors. I do well with a low dose of Propranolol and a heftier dose of Klonopin and 2xdaily dDAVP. The dDAVP drops my BP to normal levels even better than the BB, but the BB is good for the HR surges. Nothing has dropped my exercising HR, it still climbs to 180+ bpm very quickly, but the BB handles "daily life" rather well.

Debra, I tried Bystolic over a year ago and it did not do much for me, it lowered my HR, but my BP stayed up too high and it did nothing for my tremors. I am glad that it works for you though, your improvement is encouraging!

I wonder if this also applies to us: Intrinsic Aerobic Exercise Capacity Linked to Longevity ScienceDaily (Sep. 30, 2011) — Aerobic exercise capacity has proven to be a good indicator of health. A recent paper in Circulation Research whose authors include researchers from the Norwegian University of Science and Technology's KG Jebsen Center of Exercise in Medicine uses a rat model to show that innate exercise capacity can be linked to longevity. Low aerobic exercise capacity is a strong predictor of premature morbidity and mortality in both healthy adults and people with cardiovascular disease. In the elderly, poor performance on treadmill- or extended walking tests indicates proximity to future health decline. In order to test the association between aerobic exercise capacity and survivability, a rat model was made through artificial selective breeding. Laboratory rats of widely varying genetic backgrounds were bred for low or high intrinsic treadmill running capacity. Rats from multiple generations were followed for survivability and assessed for age-related declines in cardiovascular fitness, such as peak oxygen uptake, myocardial function, endurance performance and change in body mass. We found that the average lifespan of rats with innate low exercise capacity was 28-45% shorter than for rats with an inborn high exercise capacity. Likewise, the peak oxygen uptake measured across adulthood was a reliable predictor of lifespan. As they transitioned to old age, rats with an inborn low capacity for exercise had worse cardiac health by multiple measures (left ventricular myocardial and cardiomyocyte morphology, mean blood pressure, and intracellular calcium handling in both systole and diastole). Moreover, rats with high innate exercise capacities had better sustained physical activity levels, energy expenditures, and lean body mass with age than their low-capacity cohorts. Since the rats came from a wide variety of backgrounds, the results provide strong evidence that innate capacity for exercise can be linked to longevity, thus aerobic exercise capacity can prove useful in future exploration of the mechanisms behind cardiovascular disease. The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by The Norwegian University of Science and Technology (NTNU). Journal Reference: L. G. Koch, O. J. Kemi, N. Qi, S. X. Leng, P. Bijma, L. J. Gilligan, J. E. Wilkinson, H. Wisloff, M. A. Hoydal, N. Rolim, P. M. Abadir, I. Van Grevenhof, G. L. Smith, C. F. Burant, O. Ellingsen, S. L. Britton, U. Wisloff. Intrinsic Aerobic Capacity Sets a Divide for Aging and Longevity. Circulation Research, 2011; DOI: 10.1161/CIRCRESAHA.111.253807

Cardiol J. 2011;18(5):527-31. Clinical presentation and management of patients with hyperadrenergic postural orthostatic tachycardia syndrome. A single center experience. Kanjwal K, Saeed B, Karabin B, Kanjwal Y, Grubb BP. Abstract Background: We present our single center experience of 27 patients of hyperadrenergic postural orthostatic tachycardia syndrome (POTS). Methods: In a retrospective analysis, we reviewed the charts of 300 POTS patients being followed at our autonomic center from 2003 to 2010, and found 27 patients eligible for inclusion in this study. POTS was defined as symptoms of orthostatic intolerance (of greater than six months' duration) accompanied by a heart rate increase of at least 30 bpm (or a rate that exceeds 120 bpm) that occurs in the first 10 min of upright posture or head up tilt test (HUTT) occurring in the absence of other chronic debilitating disorders. Patients were diagnosed as having the hyperadrenergic form based on an increase in their systolic blood pressure of ≥ 10 mm Hg during the HUTT (2) with concomitant tachycardia or their serum catecholamine levels (serum norepinephnrine level ≥ 600 pg/mL) upon standing. Results: Twenty seven patients, aged 39 ± 11 years, 24, (89%) of them female and 22 (82%) Caucasian were included in this study. Most of these patients were refractory to most of the first and second line treatments, and all were on multiple combinations of medications. Conclusions: Hyperadrenergic POTS should be identified and differentiated from neuropathic POTS. These patients are usually difficult to treat and there are no standardized treatment protocols known at this time for patients with hyperadrenergic POTS. (Cardiol J 2011; 18, 5: 527-531). PMID: 21947988

O+

Gee, any of us could have told them this....and they paid for a study! The inaccuracy of automatic devices taking postural measurements in the emergency department. Dind A, Short A, Ekholm J, Holdgate A. Int J Nurs Pract. 2011 Oct;17(5):525-533. doi: 10.1111/j.1440-172X.2011.01958.x. Source The University of New South Wales, Sydney, New South Wales, Australia Centre for Clinical Governance Research in Health, Australian Institute of Health Innovation, The University of New South Wales, Sydney, and Centre for Health Stewardship, The Australian National University, Canberra, Australian Capital Territory, Australia Centre for Education and Workforce Development, Sydney South West Area Health Service, Eastern Campus, Liverpool Hospital, Liverpool, New South Wales, Australia Emergency Medicine Research Unit, Liverpool Hospital, Sydney, New South Wales, Australia. Abstract Dind A, Short A, Ekholm J, Holdgate A. International Journal of Nursing Practice 2011; 17: 525-533 The inaccuracy of automatic devices taking postural measurements in the emergency department Automatic devices are used to take postural blood pressures in the emergency department despite research proving their inaccuracy in taking single blood pressures. This study assessed the accuracy of an automatic device compared with a manual aneroid reference standard for determining orthostatic hypotension and postural drops at triage. Supine and standing blood pressures were taken with an automatic and a manual device in a sequential and random order, and postural drops were calculated. The manual device indicated 10/150 emergency department patients had orthostatic hypotension (7%) and the automatic device detected this with a sensitivity of 30% and a specificity of 91%. The automatic-manual differences were clinically significant in 13% of systolic drops and 37% of diastolic drops. Findings suggest that automatic devices cannot reliably detect or rule out orthostatic hypotension, indicating that triage nurses need to use manual devices to take accurate postural blood pressures for optimal patient care. © 2011 Blackwell Publishing Asia Pty Ltd. PMID:21939485

My CBCs always come in over the cutoff and get flagged. In January, I was checked for polycythemia and was found to have severe volume deficit without anemia. The hematologist told me to never give blood and do everything I can to keep my volume up.

I was looking for some articles for a friend and found this from 1993. It makes it pretty clear why many of us have had gallbladder issues! Abnormal gallbladder function in patients with irritable bowel syndrome. Am J Gastroenterol. 1993 Sep;88(9):1387-90. Sood GK, Baijal SS, Lahoti D, Broor SL. Source Department of Gastroenterology, G. B. Pant Hospital, New Delhi, India. Abstract Abnormalities of the autonomic nervous system function and cholecystokinin release have been described in patients with irritable bowel syndrome. Because the autonomic nervous system and cholecystokinin have an important role in the normal functioning of the gallbladder, we studied gallbladder contraction in response to a meal, using real time ultrasonography in irritable bowel syndrome patients (n = 20) and healthy controls (n = 15). The following parameters were studied: 1) fasting gallbladder volume, 2) residual volume after maximal contraction and at the end of 2 h, 3) maximum percent of gallbladder emptied, and 4) the time taken for maximal contraction. Fasting gallbladder volume (26.21 +/- 1.81 ml vs 15.21 +/- 1.63 ml, p < 0.001), and residual volume after maximal contraction (14.2 +/- 1.69 ml vs. 5.86 +/- 0.98 ml, p < 0.001) and at the end of 2 h (18.81 +/- 1.73 ml vs. 11.65 +/- 1.45 ml, p < 0.01) were significantly higher in the patient group, compared with controls. The maximum emptying was less (49.55 +/- 2.75% vs. 63.98 +/- 4.55%, p < 0.01) and the time taken for maximal contraction (59.25 +/- 3.8 min vs. 42.33 +/- 2.04 min, p < 0.001) was longer in the patient group than in the controls. Based on these observations, we conclude that patients with irritable bowel syndrome have significant abnormalities of gallbladder motor function. PMID:8362836

"For us with HyperPOTS wouldn't this be a good thing, to have higher hydrogen levels? That may explain why my body's renin is so very low - it's trying to lower my bp - since my bp stays in the high range." Since this is a study on children with POTS, I am presuming that they are more likely to be the genetic variant, instead of post-viral. I could be completely wrong. BUT...I had POTS as a child and always had incredibly LOW blood pressure whenever it was taken. Who knows what happens to the body after a lifetime of crazy autonomic stuff?! I know that my BP swings higher now than it ever has. I also don't know if this is the "chicken" or the "egg." Having high H2S could be the cause or the result. Pure oxygen also seems to help break down H2S in the system, could that be why my Hb and Hct are so high...a compensatory mechanism? But then our H2S may be high due to chronic hypoxia in the brain.... this all goes in circles.

for Naomi.

I could only wish that it was a "suburban, white lady disease," and that no others were afflicted. Unfortunately, it is more probable that the demographic that you speak of is simply more persistent about getting a diagnosis. There are too many studies from other places like Taiwan, China, Japan and Russia with decent sized patient groups for this to be racially isolated. I know that most of the people on the forum do fit the demographic, but unfortunately again, we have a genetic sampling of just about everyone here as well (from African, Asian and other ancestry...and don't forget the men!) Honestly, it would be better if this condition only attacked a certain demographic, because it could be limited and easier to study, but unfortunately I don't think any ethnicity is immune.

This might explain why NO levels are low in hyper-POTS as well. Unfortunately, there is not enough known about gasotransmitters and disease to determine any effective treatments that manipulate them. We also have no idea whether this is a chicken or egg scenario: H2S is elevated in hypoxic conditions, so is it high in POTS patients due to postural hypoxia or is it contributing to/causing POTS because it is elevated? Hydrogen sulfide inhibits nitric oxide production and nuclear factor-kappaB via heme oxygenase-1 expression in RAW264.7 macrophages stimulated with lipopolysaccharide. Oh GS, Pae HO, Lee BS, Kim BN, Kim JM, Kim HR, Jeon SB, Jeon WK, Chae HJ, Chung HT. Free Radic Biol Med. 2006 Jul 1;41(1):106-19. Epub 2006 Apr 25. Source Department of Microbiology and Immunology and Medicinal Resources Research Institute, Wonkwang University School of Medicine, Iksan, Chonbuk 570-749, Republic of Korea. Abstract Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or cystathionine beta-synthase (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored. Here, we show that at noncytotoxic concentrations, H(2)S was able to inhibit NO production and inducible NO synthase (iNOS) expression via heme oxygenase (HO-1) expression in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS). Both H(2)S solution prepared by bubbling pure H(2)S gas and NaSH, a H(2)S donor, dose dependently induced HO-1 expression through the activation of the extracellular signal-regulated kinase (ERK). Pretreatment with H(2)S or NaHS significantly inhibited LPS-induced iNOS expression and NO production. Moreover, NO production in LPS-stimulated macrophages that are expressing CSE mRNA was significantly reduced by the addition of L-Cys, a substrate for H(2)S, but enhanced by the selective CSE inhibitor beta-cyano-L-alanine but not by the CBS inhibitor aminooxyacetic acid. While either blockage of HO activity by the HO inhibitor, tin protoporphyrin IX, or down-regulation of HO-1 expression by HO-1 small interfering RNA (siRNA) reversed the inhibitory effects of H(2)S on iNOS expression and NO production, HO-1 overexpression produced the same inhibitory effects of H(2)S. In addition, LPS-induced nuclear factor (NF)-kappaB activation was diminished in RAW264.7 macrophages preincubated with H(2)S. Interestingly, the inhibitory effect of H(2)S on NF-kappaB activation was reversed by the transient transfection with HO-1 siRNA, but was mimicked by either HO-1 gene transfection or treatment with carbon monoxide (CO), an end product of HO-1. CO treatment also inhibited LPS-induced NO production and iNOS expression via its inactivation of NF-kappaB. Collectively, our results suggest that H(2)S can inhibit NO production and NF-kappaB activation in LPS-stimulated macrophages through a mechanism that involves the action of HO-1/CO. PMID:16781459