firewatcher

Excedrin never worked for me. Frovatriptan works the best in my case, but I have true menstrual migraines. The daily "migraines" that I've had for several years now never responded to typical migraine drugs (triptans) but do respond to Klonopin.

Hmm... I don't really know! Back when I was dancing 20-30 hours a week, I worked really, really hard to develop calluses on my feet so I could dance barefoot. Nowadays, I'd just rub the skin right off, I think. I think that because the back of my heels where my shoes rub just comes off and bleeds.

What do you do about the bandaid problems then? use some sort of gauze wrap I suppose?

I use superglue! The adhesive in bandages and tape causes me to have an allergic reaction, or maybe it just tears off the top layers and it looks that way. I hate bandaids! I had to have stitches and they put a bandage over it that I was not supposed to remove for several days. It ended up looking like orange peel under it, so they had to take it off.

What is the contrast? What is his level of Serum Creatinine/kidney function?

Adrenaline and noradrenaline are "fight or flight" hormones that are stirred up by stress. Noradrenaline is also one of the major hormones that controls "wakefulness." POTS has issues particularly with that hormone (norepinephrine) and excess or heightened response to normal levels. You have probably been "bathing" in it since the accident. With POTS, we just don't calm down like we should, so it is difficult for us to turn it off. Unfortunately, the longer you go, the harder it is to calm down, and so the longer you go...and it is a vicious cycle. If you can do anything to calm and soothe yourself, or try to sleep in for several days, to break the cycle it might help. It took regular doses of propranolol to break it for me.

I have taken multiple antibiotics, many, many times for recurrent sinus infections. The worst problem I get is a yeast infection. I have found that by taking probiotics in between my doses of antibiotic, I can mitigate that now. Don't take the probiotic with your antibiotic or the antibiotic will kill off the good bacteria before it gets to your gut.

There are several people on the forum taking long term antibiotics for Lyme and CFS.

Do any of you with EDS have issues where you DO NOT make calluses?

The bottoms of my feet have always been so soft, even as a teenager going barefoot with karate. I would never be able to grow calluses, the skin was so soft it would rip and tear off my toes. Even now with blisters from burns or wear, they don't callus over, they stay soft and the skin just tears.

I have been told by my PT that I probably do have some sort of connective tissue disorder because of "freakish" flexibility. I don't have stretchy skin or dislocations either, but I am very bendy.

I think you still need the full TB workup, including x-ray, to determine if your TB is latent. When my family was exposed, the doc (who had spent several years in S. America treating active TB) wanted us all to take isoniazid regardless of our skin tests. As for this med and POTS, I have no clue. There are several meds to treat TB, so your doc may want to make you aware of the options and things to watch for.

Just to muddy the waters up on this one, here are two conflicting articles on salt and insulin resistance:

Salt, aldosterone and Insulin Resistance

Salt, aldosterone, and insulin resistance: impact on the cardiovascular system (FULL TEXT in link above)

Guido Lastra, Sonal Dhuper, Megan S. Johnson & James R. Sowers

Nature Reviews Cardiology 7, 577-584 (October 2010) | doi:10.1038/nrcardio.2010.123About the authors

Abstract

Hypertension and type 2 diabetes mellitus (T2DM) are powerful risk factors for cardiovascular disease (CVD) and chronic kidney disease (CKD), both of which are leading causes of morbidity and mortality worldwide. Research into the pathophysiology of CVD and CKD risk factors has identified salt sensitivity and insulin resistance as key elements underlying the relationship between hypertension and T2DM. Excess dietary salt and caloric intake, as commonly found in westernized diets, is linked not only to increased blood pressure, but also to defective insulin sensitivity and impaired glucose homeostasis. In this setting, activation of the sympathetic nervous system and the renin–angiotensin–aldosterone system (RAAS), as well as increased signaling through the mineralocorticoid receptor (MR), result in increased production of reactive oxygen species and oxidative stress, which in turn contribute to insulin resistance and impaired vascular function. In addition, insulin resistance is not limited to classic insulin-sensitive tissues such as skeletal muscle, but it also affects the cardiovascular system, where it participates in the development of CVD and CKD. Current clinical knowledge points towards an impact of salt restriction, RAAS blockade, and MR antagonism on cardiovascular and renal protection, but also on improved insulin sensitivity and glucose homeostasis.

Low-salt diet increases insulin resistance in healthy subjects.

Garg R, Williams GH, Hurwitz S, Brown NJ, Hopkins PN, Adler GK.

Metabolism. 2010 Oct 29. [Epub ahead of print]

Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.

Abstract

Low-salt (LS) diet activates the renin-angiotensin-aldosterone and sympathetic nervous systems, both of which can increase insulin resistance (IR). We investigated the hypothesis that LS diet is associated with an increase in IR in healthy subjects. Healthy individuals were studied after 7 days of LS diet (urine sodium <20 mmol/d) and 7 days of high-salt (HS) diet (urine sodium >150 mmol/d) in a random order. Insulin resistance was measured after each diet and compared statistically, unadjusted and adjusted for important covariates. One hundred fifty-two healthy men and women, aged 39.1 ± 12.5 years (range, 18-65) and with body mass index of 25.3 ± 4.0 kg/m(2), were included in this study. Mean (SD) homeostasis model assessment index was significantly higher on LS compared with HS diet (2.8 ± 1.6 vs 2.4 ± 1.7, P < .01). Serum aldosterone (21.0 ± 14.3 vs 3.4 ± 1.5 ng/dL, P < .001), 24-hour urine aldosterone (63.0 ± 34.0 vs 9.5 ± 6.5 μg/d, P < .001), and 24-hour urine norepinephrine excretion (78.0 ± 36.7 vs 67.9 ± 39.8 μg/d, P < .05) were higher on LS diet compared with HS diet. Low-salt diet was significantly associated with higher homeostasis model assessment index independent of age, sex, blood pressure, body mass index, serum sodium and potassium, serum angiotensin II, plasma renin activity, serum and urine aldosterone, and urine epinephrine and norepinephrine. Low-salt diet is associated with an increase in IR. The impact of our findings on the pathogenesis of diabetes and cardiovascular disease needs further investigation.

Copyright © 2010 Elsevier Inc. All rights reserved.

PMID: 21036373

I would guess that our sodium intake and reactions are based on our genetic predisposition towards sodium handling. Some of us should salt load and others of us shouldn't. Or perhaps we should salt load to a point and then reduce our salt as time goes by. I'm attempting to find that balance point with salt myself.

Julie, that IS good news! I too am interested in how much sodium you were consuming. My doc has just told me to double my sodium intake.

I was about to suggest exactly the same thing.

I did not gain weight with propranolol. Actually, I dropped two dress sizes since I was able to exercise without my heart beating out of my chest!

This has been one of the best drugs for me; I've taken it for the last three years. I am only on 20 mg, once a day though. There was a recent Vanderbilt article on "Less is more" stating that the lower dose is more effective for POTS HR issues. If I am supine, my BP is usually 90/50, but it increases greatly with standing. I would probably start with 10 mg and work up from there. It may not take much to bring your HR down, and a smaller dose is easier to counteract if you needed to.

Body's Clock May Lead to Increased Risk for Fainting During the Nighttime

from ScienceDaily.com reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Brigham and Women's Hospital, via EurekAlert!, a service of AAAS.

Journal Reference:

1. K. Hu, F. A. J. L. Scheer, M. Laker, C. Smales, S. A. Shea. Endogenous Circadian Rhythm in Vasovagal Response to Head-Up Tilt. Circulation, 2011; DOI: 10.1161/CIRCULATIONAHA.110.943019

ScienceDaily (Mar. 7, 2011) — Fainting, or syncope, is quite common. About 50% of people will experience fainting at some point during their lifetime. The most common type of fainting is vasovagal syncope (VVS) that is caused by a sudden drop in blood pressure resulting in reduced blood flow to the brain. VVS can occur in healthy people due to inappropriate cardiovascular responses to certain behavioral or emotional triggers such as fear, needle prick or even standing up. VVS has a daily pattern with more occurrences during the morning.

This daily pattern is possibly due to the daily distribution of behavioral and emotional stimuli or perhaps due to influences from the internal circadian system, or 'body clock'. In a new study, researchers at Brigham and Women's Hospital (BWH) provide strong evidence that the circadian system may contribute to the daily pattern of VVS via its influences on physiological responses to changes in body posture. These findings are published on March 8, 2011 in the journal Circulation.

Lead study author Kun Hu, PhD, of the Division of Sleep Medicine at BWH said that "the susceptibility to VVS is probably present in all healthy humans. Fainting can cause an individual to fall which can result in severe trauma, including skull and limb bone fractures. Recurrent VVS can also affect quality of life due to reduced activities and social adjustment. Understanding the causes of VVS is important for diagnosis, prevention and treatment of people with a history of recurrent VVS."

In this study, repeated tilt-table tests were used to determine the susceptibility to VVS across the day and night in twelve healthy participants who stayed in a controlled laboratory environment for almost 2 weeks. To measure the influence of the internal body clock on VVS while controlling for other factors including the sleep/wake cycle, meals and the environment, the researchers scheduled all behaviors of participants while they lived on a recurring 20-hour "day" (with 6.7 hours scheduled for sleep and 13.3 hours for wake).

The study was performed in dim light so that the internal body clock still oscillated with an approximate 24-hour period. Core body temperature was measured throughout to indicate the times of the internal body clock. To stop the participants from actually fainting, signs of imminent VVS (presyncope) were closely monitored and tilt-table tests were immediately aborted whenever there were notable symptoms of nausea, dry mouth, dizziness, or low blood pressure or rapidly falling blood pressure.

The researchers found that the vulnerability to presyncope has a strong connection to the internal body clock, with susceptibility nine times higher at the circadian times between 10:30 PM and 10:30 AM compared to between 10:30 AM through 10:30 PM. The highest risk for presyncope occurred at the circadian time corresponding to 4:30 AM. "This vulnerable period may have relevance to individuals who remain awake or wake up frequently during the night, such as shift workers, parents feeding their infants and elderly people with increased nocturia or insomnia. These people may be at higher risk for syncope due to their postural changes during the night" said one of the investigators, Dr. Steven Shea of the Division of Sleep Medicine at BWH.

In addition, this study highlights the importance of performing tilt-table tests at similar circadian times when comparing responses of different individuals or the same person before and after treatments for syncope. The results also suggest that a higher sensitivity may be achieved by performing tilt-table testing during early morning hours or the night.

The research was funded by grants from the National Institutes of Health and the Harvard Catalyst.

This is what hubby got for me:

Reuasable hand warmers from REI

You just boil them for seven minutes and they return to their gel state to be used again. Eventually, they won't work anymore, but it took dozens of times for that to happen. Just google reusable hand warmers and you can find others.

Amazon.com has this BIG one in stock! Looks great to slide under a coat over your tummy!

Big heat pad

You can get "rechargeable" heating packets from an outdoors/hunting store. My husband bought mine from Wal-Mart and REI. You click this metal disc inside the bag and it sets off a chemical reaction that creates heat for at least an hour. You could get several and put them in your pockets and socks. They are too hot to just hold, so they need to be wrapped in a cloth or put in a pocket. They are really good to put in the abdominal pockets of zipped-up sweatshirts...keeps the core warm.

The urine test is supposed to be a pretty good indicator of your daily sodium intake. The serum sodium is a spot check of your "working" electrolytes and for us, volume status.

My serum Na was 133, it has been anywhere from 132-148 depending on the time of day and hydration. I've upped my Thermotabs and tried to up my salt intake, but I get super thirsty and nauseated. I'm taking my estrogen again and the daily weight swings are not as large as they were and I am up 8 pounds from where I was 2 weeks ago (all water.) I'm supposed to get better control of my serum sodium levels, but unless I get a blood draw several times a day over several days and collect every drop of urine, I'm not sure how I'm going to do this!

How do your docs monitor your sodium intake? My serum sodium ranges low to high depending on the time of day and fluid intake (low on dDAVP and high when it quits in the afternoon and early morning.) I have seen several studies that mention a 24 hour urine sodium of at least 170 mEq/24hr/mg/dl as a target for POTS patients. My 24 hr. urine sodium was 66.8. The last doc I saw wanted me to up my sodium so that I don't have the low serum levels on the dDAVP and try to get my plasma volume up, but I know those levels are going to swing high twice a day.

Any experience or words of wisdom on how to gauge this? I've never tried florinef and my other docs are hesitant due to kidney issues.

I came across this during my weekly web search:

Neighborly love in Medfield

I am orthostatically HYPERtensive. All my ANS testing came back with hypertensive responses (148/98, 145/117, 150/99.) Last summer my BP was really high (186/168) and my HR was incredibly low (40-50s.) I noticed that I was dehydrated when I'd get these hypertensive/bradycardic episodes and that they would improve with fluid ingestion. Vandy labeled me as having hyperadrenergic responses.

I have not seen the full text, but I am betting that they picked POTS patients with KNOWN low blood volume for the study. It also does not say if that increase was sustained. A control may have a HR surge, but then drop back down, a POTS patient would have a higher surge and settle at a sustained higher HR (which is why we aren't "normal.")

I use it with the mucinex to clear out my nose. I have not had any issues with it systemically.

The three day warning is for rebound congestion. If you use it for longer than 3 days, you may get stuffy once you quit using it for the cold. I typically use it to open up my nose enough to use the neti pot if I get that clogged.

What is it I should be aware of and watch firewatcher?

There are recent strains of TB that are unaffected by the usual treatments. You can go through the treatments and not kill it off. If you EVER show signs of active TB, you should bring it up to your doc.

Most of my cautions were for the medicines though. While good at treating TB, there can be side effects. You absolutely have to treat it, just tell your doc if any weirder things happen than POTS.

(I am overly cautious because of my kidneys...I'm not even supposed to take tylenol or aspirin. Every body is different and those "just you" reactions can be signs that you need to watch for. I'm not trying to scare anyone, just make them cautious and aware...like we always are with meds. )

I was exposed to ACTIVE TB 11 years ago. For me, it took at least three tests for the docs to rule it a negative; I was red, but had no wheal. My 3 month old son, however, had to undergo six months of Isoniazide treatments since he was too young to test (a very scary time for a new Mommy!) He turned out to be negative. My doc told me that most healthcare workers will test positive, but that their bodies have developed immunity and "walled off" the virus. You probably need a chest x-ray to see if that has occurred.

The strange thing about TB is that it doesn't always settle in the lungs. It can hit the kidneys, brain or other organs. I have wondered if I really had a negative, or if it just landed someplace else (like my kidneys!)

Watch it closely and report any medications side effects to your doc.

Be well!

I am on Allegra (Fexofenadine), which supposedly has the fewest central nervous system side effects. It is only available by prescription.

I came back negative for the JAK2 mutation! The hematologist says that it can only be a plasma volume issue without anemia. I am supposed to find a weight where my BP is "normal" and stay there if I can. He also told me to never allow a doc to "take a pint" out of me...that would be bad! duh.