Exercise combined with a high salt diet

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For one thing, muscular contraction releases interleukin-6, which plays a role in some of the vasopressinergic effects of physical exercise, and this should also help to rein in the excessive acetylcholine levels found in some autists due to some of the anticholinergic effects of interleukin-6. For another, sodium chloride should reverse some of the effects of elevated interleukin-2 levels found in autists, and it would also affect an increased production and release of vasopressin via its effects on nitric oxide synthase (NOS).

An l-arginine blocker might produce similar effects, but this could lead to an elevated risk of Alzheimer's Disease and other forms of old age dementia. I wouldn't recommend it.

Whether this would have any chance of helping in autists lacking the NOS gene remains to be known.

First of all, what behavioral/cognitive/perceptual effects do high acetylcholine or interleukin-2 levels, or increased vasopressin cause? Why would it be beneficial to alter the body's chemistry in this particular manner?

Second, I'm pretty sure that high salt intake + exercise cause thirst and possible dehydration pretty quickly, so I can't see anyone sticking with such a plan very long.

Interleukin-2 inhibits the flow of sodium to muscle cells, which can impede development. It also impedes the production of progesterone and promotes endogenous opioid activity, both of which are problems common in autism (as seen in our oddball reactions to gluten and casein, which break down into opioid peptides). Acetylcholine is valuable for the formation of memories, but, unfortunately, excessive cholinergic activity has been found to impede certain forms of memory in healthy test subjects; it's probable that moderate acetylcholine levels are ideal for healthy memory formation. Vasopression is an important social hormone, and autists have often been found to be lacking in it.

Incorrect. Salt improves water retention, and sodium is essential for certain bodily functions. People have been taking salt pills to prevent dehydration for years. Its negative reputation is completely undeserved except in the case of highly sedentary lifestyles, and I'm suggesting the opposite. Sodium is a very undervalued nutrient. Chloride is also necessary for a number of functions, including the production of vasopressin. Excessive IL-2 production undermines GABA-induced Cl- currents, which is another reason that it would be beneficial to pursue a diet and lifestyle that would counter this.

Salt can cause thirst which doesn't cause dehydration. Sometimes your thirst signals can shut off and you dehydrate unwittingly. MOre likely we tend to ignore thirst or mistake it for hunger and eat solids instead.
So, yeah, salt causes water retention and contains minerals and elements that your body loses when you are sweating profusely or otherwise dehydrated. My dad worked in construction in the summer and they were given salt pills during the day.

And l-canavanine, which is abundant in many commonly consumed legumes, is a highly selective inhibitor of l-arginine, which is a likely culprit in both our low vasopressin production AND our high acetylcholine levels! It also has the effect of increasing Natural Killer T Cell activity, in which autists have a natural deficiency. It all ties together. Excessive L-arginine production would explain a number of the most common symptoms of autism, and they can be countered through physical exercise, standard defenses against dehydration, and vegan-friendly sources of both protein and vitamin B6 (which is popular and well-supported as a treatment for autism in megavitamin therapy). I certainly don't propose that diet and exercise alone are sufficient for highly affected individuals, but the data I'm looking at strongly suggests that the alterations that I have suggested could be highly effective in relieving some of the symptoms affecting sufferers of HFA.

A high sodium diet isn't safe for anyone. Exercise is healthy for all people, unless they have specific restrictions.

I haven't had time to trace out the merits of this theory, and am leaving for the weekend. So I will just put some preliminary thoughts.

I am skeptical of whether I want more IL-6 in my body. I have several conditions associated with high IL-6. I am also skeptical of whether exercise increases IL-6; it appears that occasional exercise or overtraining may do so (via oxidative burst), but a healthy exercise training program decreases IL-6 and other inflammatory cytokines.

Salt is essential, but at what dose? Migraines and other related conditions (which I also have) seem to be aggravated by extra sodium and/or chloride, while they benefit from magnesium. And there are some studies that suggest that magnesium (often with vitamin B-6) may help with Autism spectrum disorders ... and there is also evidence that magnesium/B-6 can also help with migraine.

I think your reasoning on arginine and vasopressin is hard to follow. There are two forms of vasopressin (arginine-V and lysine-V). But where is the link between arginine levels in the diet/blood and vasopressin production?

Both vasopressins are nonapeptides (chains of 9 amino acids), and arginine (or lysine) occurs only once. Taking arginine lowers blood pressure, while vasopressin increases it. And given the complexities of how the body regulates and produces vasopressin, I am not at all convinced that blocking or reducing arginine will reduce vasopressin.

There may be something to your ideas. But the theory appears somewhat over-reaching to me and is not laid out clearly.

Actually, I've had several doctors tell me to eat lots of salt because of my low blood pressure.

I totally crave salt, too, and when I'm criticized for it I can say "doctor's orders!"

Wow Griff you have some knowledge there! Are you a medical doctor or pharmacist? I do feel a bit better after salt because I have low blood pressure, the only thing I am not keen on is fluid retention in the leg area! High salt diets are also useful for people with adrenal insufficiency/addisons.

My sodium levels are usually good. What I tend to have trouble with is potassium. A time it has been at dangerous levels especially if I get ill. If I have vomited I know it is usually to late and have to start replacing the potassium as soon as possible. Once when was in hospital I had a reading of 1.6. I think that is not very good, they gave me an ECG as I had before. It has never damaged my heart yet, but I do get severe cramping that I buckle over in pain. I think the combination of hyperventilating and the low potassium will do that. A drip electrolite for 24 hours is the usual treatment.

I believe you can get a simple portable prick test much like sugar level test for your essential minerals. Well they appeared to have such a thing in the ambulance, though I didn't see where the reading came out of.

Okay, before I say anything further on this, I need more information on CHaT activity, as observed in autists vs. controls. I think that I misunderstood something important here, and I may have to throw the whole hypothesis into the recycle bin. Rather than having high acetylcholine receptor populations, autists seem to have specific deficiencies here. However, this does not necessarily suggest anything about their CHaT levels. If their CHaT levels are normal, then there is definitely something fishy here.

Actually, autists having low ACh receptor populations in some areas might actually make some amount of sense. If I'm not mistaken, aren't most types of ACh receptor anti-excitory? Another important thing is that high cholinergic activity usually stimulates the release of vasopressin, which is one of the reasons I was so excited by the prospect of something that results in both lower vasopressinergic activity and higher acetylcholinergic activity.

It should be recognized that many anticholinergic (particularly antimuscarinic) drugs are associated with disturbing hallucinations/delusions. In addition to these effects, however, a common side-effect of such drugs is dry mouth, which allows for speculation upon the relationship between endocannabinoids and the ACh receptors.

You guys, I'm really stumped here. For a little while, I thought I might have been on to something, but I've run into a brick wall here. The ideas presented above might be useful in treating something, but I'll have to do more reading before I can say much else on its possibilities insofar as helping autists.

The interesting thing is that both high functioning and low functioning autists, including Aspies, have generally exhibited little inclination toward smoking behavior. This suggests either that they already produce sufficient acetylcholine or just don't have the receptors to accept it. I'll figure this stuff out eventually. This is all just very confusing.

No, but I can assure you that most medical doctors and pharmacists are just as daft on this subject matter as I am.

Interestingly, there actually does seem to be a link between low blood pressure and dyslexia. More on this later.

Anecdotally, I've always suspected a thyroid-asperger's link. And hypothyroidism/low blood pressure do go together.

Let me know when you've figured all this out for me, would you? Thanks!

However, I've never really heard of any correlation between AS and blood pressure. This is why any heightening in salt intake would HAVE to be accompanied by an increase in physical exercise. Otherwise, health could be negatively affected.

Incorrect. A diet too low in sodium, for that matter, can be lethal to someone affected by low blood pressure.

But would probably be an excellent method to induce a heart attack

When you get to it, I'd appreciate any thoughts on what this combination might be good for if possible. If you can, would you also try to find out what might cause excessive respiratory mucosal secretion? This is a severe problem in me that has caused me all sorts of trouble.

So am I. To tell you the truth, it can do some pretty nasty things if you're making too much of it. However, some studies suggest that it could have anti-convulsive properties.

Funny. This is really more associated with treatment-responsive schizophrenia than with autism. That you're producing it in high quantities, however, might suggest high dopamine levels, which is also a common symptom in both schizophrenia and autism. In autism, however, it's more likely that high dopaminergic activity is a result of elevated interleukin-2 secretion, which seems to express an affinity for certain opioid receptors, particularly the kappa-opioids. Kappa-opioid activation...oh, dear. Umm, it appears to inhibit the release of acetylcholine, which, come to think of it, I recall reading somewhere, a while back. Here's the crazy thing, though: interleukin-6 appears to regulate kappa-opioid gene expression. Now my above hypothesis seems to make a little more sense, although a few of its contingent variables will have to be subjected to reanalysis. It does, however, seem that I may have been correct in suggesting that physical exercise could improve NK cell production. The increase there in IL-2 receptors is peculiar, though, because endurance training increases acetylcholine receptor quantity, at least at neuro-muscular junctions.. Could IL-2 be stimulating kappa-opioid receptors somehow when there is an IL-2R deficit? High interleukin-2 levels in autists doesn't make sense when they also exhibit tendencies toward NK cell deficits! The only context in which this would make sense is that NK cells also somehow down-regulate IL-2 production.

Oh, and interleukin-2 decreased serum magnesium and ionized magnesium levels, which is noteworthy.

These inflammatory cytokines are necessary for proper immune function, though, which is very peculiar. I wouldn't think that you'd make less of them when engaged in activities that supposedly improve immune function unless physical exercise actually improves the action of these cytokines thereby down-regulating their production.

I don't know. These propellor-tops won't put numbers in the abstracts. It makes me want to punch them.

Funny. Caffeine, which raises norepinephrine levels, is useful for treating migraine headaches. Kappa-opioid receptor activation inhibits the release of both norepinephrine and acetylcholine. Interesting.

I was referring specifically to nitro-l-arginine, actually. I should have specified this. It seems to down-regulate vasopressin.

Blood pressure.. Vasopressin. This is very interesting subject matter. It gets more fascinating every time I look at it.

I'm saying the opposite, though. I'm saying that blocking it would increase vasopressin production. I've done more reading, though, and this aspect of the hypothesis is looking weaker. Apparently, there's a connection between diabetes mellitus and autism, and I'm reading studies here showing that l-arginine promotes insulin secretion. I am going to have to reassess my reasoning.

It's not laid out clearly because I am voicing my thoughts on this as I think about it. Everything that I write is a direct feed from my frontal lobe. My speech is similar.