beggiatoa
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Posts posted by beggiatoa
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I was going to write a new post but this one is very impressive so I'll add this here. Found some great ANS stimulants. They work via different mechanisms but the final effect is the activation of the autonomic nervous system.
Capsaicin - believe it or not! Works very, very well !
Yohimbe - used a liquid extract and titrated slowly.
Chicken Essence tablets - you read right ; ) I haven't tried this but I'm curious.
CDP choline or alpha GPC - acetylcholine precursors
Green tea
The combined effects of capsaicin, green tea extract and chicken essence tablets on human autonomic nervous system activity.
Source
Laboratory of Applied Physiology, Graduate School of Human and Environmental Studies, Kyoto University, Kyoto 606-8501, Japan.
Abstract
The purpose of this study was to investigate whether combined capsaicin, green tea, and chicken essence tablets (CCGC) enhance human autonomic nervous activities (ANS) associated with thermogenic sympathetic activity without any adverse effect on the cardiac depolarization-repolarization period. Six healthy males (25.2 +/-1.7 y) volunteered for this experiment. Autonomic nervous activities were examined 5-min at rest per 30-min for total 1.5 h after consuming chicken or CCGC or placebo tablets at random on separate days. Using heart rate variability power spectral analysis, we assessed human autonomic nervous activities. In comparison to chicken essence or placebo tablets, it was observed that the consumption of CCGC significantly increased human autonomic nervous activities [Total power representing over-all ANS activity; CCGC trial 160.2 (50.0) vs. placebo 92.8 (53.3)%, p < 0.05; VLF, very low-frequency power associated with thermogenic sympathetic activity: CCGC trial 235.5 (101.7) vs. chicken 130.5 (52.9)%, p < 0.05; LF, low frequency power representing combined sympatho-vagal activity: CCGC trial 199.8 (59.8) vs. placebo 120.6 (49.2)%, p < 0.05] at 60-min and 90-min. There were no significant differences in heart rate corrected cardiac recovery time (RTc) or QT interval (QTc). In conclusion, the consumption of CCGC enhances thermogenic sympathetic activity compared to that of chicken essence or placebo tablets. Therefore, these results suggest that combined capsaicin, green tea, and chicken essence tablets may be a beneficial food ingredient improving human autonomic nervous activities, particularly thermogenic sympathetic activity as a modulator of energy metabolism without any adverse effects on cardiac electrical stability. PMID:17616002
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This might be of interest to some. I'm trying to figure out the dose needed to get on this ASAP.
Effects of melatonin on peripheral nerve regeneration.
Source
Department of Neurosurgery, Adnan Menderes University School of Medicine, Aydin, Turkey. drmturgut@yahoo.com
Abstract
In the available literature, there are thousands of studies on peripheral nerve regeneration using many nerves of several animals at different ages with various types of lesions and different methods of evaluation at certain time of follow-up. Despite many experimental data and clinical observations, there is still no ideal treatment method enhancing peripheral nerve regeneration. In clinical practice, various types of surgical nerve repair techniques do not frequently result in complete recovery due to neuroma formation, lipid peroxidative damage, ischemia and other factors. Recently, a number of neuroscientists demonstrated that pineal neurohormone melatonin (MLT) has an effect on the morphologic features of the nerve tissue, suggesting its neuroprotective, free radical scavenging, antioxidative, and analgesic effects in degenerative diseases of peripheral nerves. At present, it is widely accepted that MLT has a useful effect on axon length and sprouting after traumatic events to peripheral nerves. Our studies using various experimental injury models clearly suggest positive effects of MLT on the number of axons, thickness of myelin sheath by inhibition of collagen accumulation and neuroma formation following traumatic events to peripheral nerves, myelination of developing peripheral nerve after intrauterine ethanol exposure. Nevertheless, further experimental and randomized controlled clinical studies are vital to identify the clinical use of MLT hormone. This is an overview of recent patents and current literature in terms of the effects of MLT on peripheral nerve regeneration based on a critical analysis of electrophysiological, biochemical and light and electron microscopic findings, in addition to functional observations.
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I just wrote something about thirst and potassium use
By the way, I also used to have MVP and I totally cured it using magnesium supplements for around a year. There some studies on pubmed that talk about that. I imagine magnesium along with potassium will correct the problem faster.
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Something else I've noticed since using potassium; less thirst. Found this study to support my personal observations. Potassium supplentation increased aldosterone production and water retention by the body. An inability to retain water is another problem we face. In the study, they used a dose of 3.9 g in supplements but you should in no way use such a high dose. I suggest anyone interested in using potassium start with the lowest dose possible (99 mg) and let your body ajust slowly. Too much, too soon can be very dangerious with potassium.
Conclusions. Potassium supplementation changed renal tubular function and increased water absorption in the distal part of the nephron. In spite of an increase in aldosterone in plasma, blood pressure remained unchanged after potassium supplementation. -
Metronidazole acts as a thiaminidase so it blocks the action of thiamin. In essence, it causes a type of wernicke encephalopathy. I experienced this once from taking metro. long term. Horrible experience. Finally found relief by using sulbutiamine ( a thiamin derivative that crosses the BBB).
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There could be a logical explanation for this. Garbanzo beans are rich in molybdenum.
http://whfoods.org/genpage.php?dbid=58&tname=foodspice
Molyb. is a cofactor for the enzyme xanthine oxidase which according to one study, "These results suggest that xanthine oxidase accounts for a putative source of oxyradical generation that is associated with an increasing arteriolar microvascular tone in this form of hypertension."
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Some ideas from the study I want to point out.
In addition, subjects with OI showed an inappropri-ate activation of sinus node parasympathetic modulation before the onset of syncope. Another potentially important finding is the significant positive correlation between serum potassium before the race and the maximally achievable sympathetic drive to resistance vessels, as well as the significantly lower serum pot-assium in OI compared with Non-OI before the marathon.We also found significantly lower serum potassium in OI compared with Non-OI before the marathon. None of our sub-jects experienced vomiting or diarrhea prior to the race which could have explained this difference. We do not know whether the lower serum potassium concentrations in OI were caused by differences in potassium intake or intra – extra cellular potassium distribution induced by endogenous catecholamines or other mediators. We were not able to obtain reliable dietary information in these subjects. Thus, we can only speculate whether the lower serum potassium levels in association with a limited sympathetic response were due to differences in potassium intake or to an intra– extracellular potassium distribution effect.
This latter possi-bility is not unlikely since cell membrane potential and electrical discharges are involved in sympathetic responses and both are a matter of intra– extracellular potassium gradient and thus also of extracellular potassium levels. The epinephrine-mediated potass-ium shifts in relation to sympathetic responses should be investi-gated in further studies. A high potassium intake may protect from OI, even in the face of minor, if any, effects on serum potass-ium concentration.
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Came across this study I found interesting. There is a link between exercise intolerance and potassium intake. I have been supplementing with a little potassium along with pantothenic acid and I found this improved exercise capacity, stregth and surprisingly, my OI. I tend to get very lightheaded when I workout, specially with doing squats and this has improved some with the use of potassium. There's also an association between hypothyroidism and weakness, fatigue exercise intolerance and using extra iodine also seems to help.
From another study, it also seems that patients with OI and exercise intolerance have lower levels of potassium in their blood. When they exercise, the serum levels increase rapidly and drop just as rapidly during rest. This could partly explain why we feel so lousy after any kind of exercise. You would think that since potassium is used to lower pressure in the hypertensive, it would have the same effect on us. Well, that hasn't been my experience at least. I'm getting benefits from just using a little extra everyday so there's no need to megadose (that's dangerous). Improving baroreceptor sensitivy also helps OI since they will respond more quickly to drops on BP.
This follows my old post on pantothenic acid.
Full text study I read this from:
http://eurheartj.oxfordjournals.org/content/29/12/1531.full.pdf
This is the original study they cited:
Effect of moderate salt restriction and high potassium intake on pressor hormones, response to noradrenaline and baroreceptor function in man.
Skrabal F, Auböck J, Hörtnagl H, Braunsteiner H.
Abstract
1. Twenty-one normotensive subjects were studied to assess any possible benefits of moderate salt restriction and of high potassium intake in the prevention of hypertension in man. 2. The effects of salt reduction from 200 to 50 mmol/day and/or of an increase of potassium intake from 80 to 200 mmol/day over a 2 week period, on blood pressure, plasma noradrenaline, adrenaline, vasopressin, renin and aldosterone, were measured both at rest and after mental stress. The effects of graded infusion of noradrenaline on blood pressure and heart rate were also studied. 3. Salt restriction lessened the increase of blood pressure during noradrenaline infusion; the combination with high potassium intake also reduced the pressure rise after mental stress. There were no major changes in plasma levels of vasopressin and adrenaline. Plasma noradrenaline increased during the low sodium diet. 4. High potassium intake improved baroreceptor function as revealed by the greater decrease in heart rate for a given rise in pressure after noradrenaline infusion. 5. The results of this study are compatible with a protective effect of a practicable low sodium/high potassium diet on the development of human hypertension.
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Magnesium also increases noradrenaline. Higher doses seem to work better.
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Not to go off topic Dizzy, but have you considered using triphala for your celiacs related complication ? It's great stuff !
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B5 is found in most foods, has anyone tested deficient in it? Could be our bodies aren't absorbing it and vitamins supplements wouldn't help. Natural sources are usually the best way. Even if our bodies have enough maybe they aren't using it correctly, maybe something is blocking the natural use of it..?
As far as the why, I have no idea but my body seems to be functioning better with extra B5. I read a lot of studies on pubmed. One study I came across referring to nutritional deficiencies said that there could be some kind of genetic mutation that predisposes the patient to require more of a certain nutrient. This is all speculation though. I've had low muscle tone for a long time. I remember people touching me and telling me how I had "soft muscles". The problem got worse in my 30's where it started affecting my respiratory muscles and I started having shortness of breath. 2010 was a bad year for me but the shortness of breath is finally gone and I think these nutritional interventions have helped.
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Here's another interesting tid bit. It seems that increasing co A also increases aldosterone. I got curious after taking 1 gram of B5 today and noticed how I wasn't thirsty at all. In fact, I had to remind myself to drink water. I can normally drink gallons everyday without feeling quenced. There was no abstract but the title made it clear enough.
Acetyl coenzyme A requirement for the stimulation of sodium transport by aldosterone.
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The cause of your SOB could be muscular in origin. Since acetylcholine plays such an important role in POTS and seem to be in the low end for the most part. This could be preventing your respiratory muscles from contracting efficiently enough to fully expand your lungs. Is that what it feel like ? Like you can't expand your lungs fully. I have this same problem and after a thorough evalution by the pneumologist, he suggested the problem could be muscular in origin. He found nothing wrong with my lungs and could be seen or measured. Does using mestinon help with sob ?
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There is another vitamin that I find equally as interesting as B5. That is vitamin C. I was going to write another post for it but might as well keep it all here. It was mentioned before in this post by ramakentesh and waterbaby mentioned how helpful it was for her in another one of his posts. She is right. Sue1234 also theorized that Vitamin C may be involved in Dysautonomia because of all the related connective tissue problems that are seen in this post.
Vitamin C has a interesting action in potentiating the effect of norepineprhine in the body. It binds to NE and helps it attach to its receptor more strongly. But, vitamin C wont make you feel better by itself ! If you already have low levels of NE it wont do much. It'll probably work better when you combine with other vitamins that increase norepinephrine like thiamine, pantothenic acid and B12. You also need about 2 grams of vitamin c per dose to fully saturate the body.
Antioxidant-independent ascorbate enhancement of catecholamine-induced contractions of vascular smooth muscle.
Dillon PF, Root-Bernstein RS, Lieder CM.
Source
Dept. of Physiology, Michigan State University, East Lansing, MI 48824, USA. Dillon@msu.edu
Abstract
Ascorbate reduces the oxidation rate of catecholamines and, by an independent mechanism, enhances rabbit aortic ring contractions initiated by catecholamines. The largest significantly different fractional increases in force produced by ascorbate enhancement of norepinephrine (NE), epinephrine, phenylpropanolamine (PPA), and ephedrine (Eph) are 5.5, 1.8, 1.6, and 1.3 times, respectively. In physiological salt solutions bubbled with 95% O(2) at 37 degrees C, NE, PPA, and Eph have oxidation rate constants of 1.24, 247, and 643 h, respectively. Ascorbate significantly enhances 100 nM NE contractions by at least twofold at all ascorbate concentrations >15 microM, including the entire physiological range of 40-100 microM. Ascorbate preloading and washout followed by NE exposure produces significantly greater contractions than NE without ascorbate preloading but significantly lower than NE simultaneously with ascorbate. Ascorbate does not enhance K(+)- or angiotensin II-induced contractions. Ascorbate enhancement of catecholamine contractions occurs in addition to the reduction in oxidation rate, because the increases in force occur faster than oxidation can occur, the increases occur with compounds that have negligible oxidation rates, and the increases occur when ascorbate and NE are not physically present together. These results are consistent with ascorbate acting on the adrenergic receptor. Ascorbate may play a role in shock and asthma treatments and potentiate the cardiovascular health consequences of PPA and Eph (Ephedra).
The full study is available if anyone wants to read it. Ascorbate works so well that it makes ephedrine toxic when combined. Ephedrine potently increases norepinephrine levels.
Waterbaby did a really good job in covering the effect of B1 in this post. B1 works together with pantothenic acid in increasing acetylcholine. Acetylcholine will then stimulate the release of norepinephrine. But again, B1 wont work alone. I think the combination thiamin, pantothenic acid, vitamin C and b12 is more effective !
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Here's that study on Obesity I was talking about.
http://en.wikipedia....ic_acid#Obesity
In a report published in 1997 by Lit-Hung Leung,[34][unreliable source?] it was hypothesized that pantothenic acid also has an effect on weight management. Leung proposed that those who were deficient in pantothenic acid would feel the effects of hunger and weakness more strongly. To access fat storages in the body in times of fasting or dieting requires CoA. Diets high in pantothenic acid produce more CoA.[citation needed] In a study done on 100 Chinese individuals from age range 15–55 it was observed that on a diet of 1000 calories a day and 10 g pantothenic acid, the dieters could lose on average 1.2 kg/week with lessened effects from hunger or weakness.[citation needed] Ketone bodies in urine indicated that some dieters required more than 10 g of pantothenic acid a day. The possibilities of pantothenic acid in weight management have not been fully explored, but remain an area of research.Pantothenic acid as a weight-reducing agent: fasting without hunger, weakness and ketosis.
Source
Department of General Surgery, Hong Kong Central Hospital.
Abstract
With the conventional method of fasting or aggressive dieting to reduce excess body fat, hunger, weakness, ketogenesis and ketosis are the sequential events that follow. It is not fully understood why, under conditions of negative calorie balance where complete energy release from storage fat is critical, ketosis should arise with a concomitant wastage of energy. Here, I wish to propose a theory that relates the formation of ketone bodies under such conditions to a deficiency in dietary pantothenic acid. Supplementation of this vitamin would facilitate complete catabolism of fatty acids and thus the formation of ketone bodies could be circumvented. As a result, a sufficient amount of energy would be released from storage fat to relieve dieters of the sensation of hunger and weakness which otherwise would be difficult to endure. Hence, using this method for weight reduction together with a careful observation of calorie intake, I have great success in treating overweight-to-obese patients to lose weight. PMID:8583972 [PubMed - indexed for MEDLINE]
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The B5 will increase acetylcholine levels which will have an effect on muscle tone. My experience was similar. I had some muscle tension at first but overall my muscle tone has improved. With this, I went to the gym and my strength was up in most of my lifts. I normally go 3 times per week. Better muscle contration = better strength.
Dizzysillyak,
You are very good at listening to your body. It most probably is the B5. The was a study showing that B5 favors the burning of stored fats over producing ketone bodies. They tested this on some chinese volunteers and gave them 1000 calorie diets plus a lot of B5. They all stated no feelings of hunger at all despite losing weight. I've noticed the same also. For the last couple of days, I've had my first meal of the day around 5 pm or so. I'm also trying to lose weight at the moment so I'm happy this is helping.
By the way, it wasn't the B5 that was interfering with my sleep, it was something else I'm taking.
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1 gram a day seems like it's too much. I'm getting some muscle tension and it's interfering with sleep. Going to decrease the dose to 500 mg per day.
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I'm using d-calcium pantothenate. Started off with a gram and will increase the dose to tolerance. I'm using it to increase acetylcholine production which I think it's working well. Haven't measured my BP yet but I have noticed that I can go longer without food without feeling hungry like some studies proposed.
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I was looking over some of the posts here and some of the same problems keep coming up:
-Burning hands and feet of tingling in the legs and arms
-Emotional lability (crying for no reason)
-intolerance to cold temperature
-GI problems
-memory problems
These were all listed as symptoms of B5 deficiency in the monograph I posted above. What's even more interesting is that B5 is contraindicated with the use of mestinon because it can raise the levels of acetylcholine too high when combined. If they both do the same thing, I'd rather use the vitamin and not the expensive medication that comes with side effects !
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If anything, I would think it would help with the POTS. By the way, I came across this research while seeing how B5 helps hair. How wwas the shampoo ? lol
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There is one study I found that can lead evidence. It's a little hard to read but essentially, they used SART-stressed mice as a model of dysautonomia and then tested the effects of of a pantothenic acid derivate called hopantenate. They found this drug effective in treating the mice.
http://www.ncbi.nlm.nih.gov/pubmed?term=dysautonomia%20pantothenic
"SART stressed animals have been reported to exhibit a decreased acetylcholine content" These chronically stressed animals with dysautonomia also implies some sort of adrenal dysfunction, which Vitamin B5 can also treat.
"Hopantenate has been shown to exert its improvable effect on scopolamine-induced impairment in the passive avoidance task, and it is suggested that the effect may be due to activating the cholinergic system via the GABAergic system"
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I was reading a monograph of vitamin B5 or pantothenic acid. You can read it here. Among the many symptoms caused by a mild deficiency, orthostatic hypotention was one of them. B5 is needed to make acetyl coa. Acetyl coa together with choline make acetylcholine (Ach). This is the main neurotransmitter in the autonomic nervous system. Low Ach levels lead to hypotonia, hypotension, weakness, etc. Mestinon works by increasing levels of Ach so you get the idea.
B5 is found is most b complex supplements but in small doses but higher, therapeutic doses may work in this case. Other symptoms of low B5 can include dry eyes, hair falling out, weakness, adrenal fatigue, exercise intolerance, low muscle tone, etc.
I used 1 gram this morning and I can feel an increase in muscle tone and concentration. I usually have problems with both. Anyone else try this ?
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Ever had an electromyography done? This will tell you exactly where the problem is..
I knew I had dysautonomia but that test helped me figure out what type of nerve damage it was exactly. There's a long list of different types of peripheral and polyneuropathy and all can have an autonomic component but the causes are different. After that test, I learned that I have a distal axonopathy with a sensory, motor and autonomic component. I'm working with a neurologist to find the cause. Most likely, it's viral in origin.
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Butcher's broom is an amazing herb. Aside from being an alpha-agonist and causing moderate vasoconstriction, it also inhibits Elastase. Increased levels of elastase is implicated in inflammation, cancer and it causes axonal neuropathy, a type of peripheal neuropathy.
I'm using 1 pill 3 times a day. If I use more than 1 pill at once I feel anxiety. Up to now, I haven't come across any tolerance issue. The elastase inhibiting action is important for me because I have a lot of saggy skin and the butcher's broom is doing a fantastic job of tighetening everything up.
As far as improving the OH, not so well, but I see some small veins around my feet appear less noticeable with time.
The Complete Guide To Pots Therapies
in Dysautonomia Discussion
Posted
Ginkgo and folic acid. From 1989!