Acetyl L- Glutathione, ATP, Baking Soda, Sam-e & Catalase = No PEM after exercise

[MeSci]

What I see lots of in literature is hints of this. For example, this paper:
http://www.fasebj.org/content/early/2001/06/02/fj.00-0652fje.full.pdf
contains lines like "Electrons carried by NADH, in addition to fueling ATP synthesis, also fuel redox signaling pathways to augment blood flow in resting and working tissues."

Another part of that original study I quoted has a more causal statement more in line with what you want: "Depletion of NAD+ following PARP hyperactivation has been shown to deplete intracellular ATP stores." And from the same study "ATP levels significantly (p<0.01) declined in the heart, lung, liver and kidney after 12 months of age. This is in line with increased PARP activation and decline in cellular NAD+ content during the aging process." So they give you the causality in a subjective interpretation of a graph of their study, but they aren't graphing the relationship you want explicitly.

Remember to bear in mind the fact that this is a study on rats. If nothing else, the timescales in humans will be different. Some of the processes may also be different.

So elemental mercury gets into the brain and then it converts to a very toxic inorganic form that is very hard to get rid of. This source on toxicology:
http://labmed.ascpjournals.org/content/33/8/614.full.pdf
says: "In erythrocytes, catalase can oxidize elemental mercury to an inorganic metabolite. If elemental mercury penetrates the blood brain barrier, it is ionized and becomes trapped in the compartment where it is available to exert its neurotoxicity. Elemental mercury has the longest retention in the brain with detectable levels present for years following exposure."

Minor point - I think that 'inorganic' includes elemental.

98% of the articles written on ALA never use the word "chelator". Yet, it's clear that it is in the literature:
http://www.ncbi.nlm.nih.gov/pubmed/17408840

The Examine page on ALA refers to chelation numerous times. It looks interesting.

 

[MeSci]

The other points to consider in asking for a decisive population study:

* Chronic Fatigue is already controversial for allopathic medicine, with many doctors thinking it is not a disease and that the people who complain of symptoms have psychiatric issues.

Important point re terminology - chronic fatigue isn't a disease; it is a symptom which can have a wide range of causes. There is still a major problem with media reporting of our illness as 'chronic fatigue' which can supposedly be cured with a range of quackish 'therapies', so we must make sure to use the right terminology ourselves.

 

[Hip]

He was not just speculating in that study. It was a review of literature with citations for each summary point.

I did include two other links that looked at particular patient populations where fatigue symptoms improved after mercury was removed. I understand it is not the smoking gun you want, but mercury research is today where research on cigarette smoking was in the 1950s, and there just isn't the overwhelming study that puts it all together. There are hundreds of studies that show effects in vitro, various effects in vivo, and small population studies that show relief of fatigue symptoms. It's better than nothing.

He was hypothesizing because he does not provide any refs to empirical evidence. Empirical evidence for mercury exposure being a risk factor for ME/CFS would need to be in the form of a statistical association: for example, out of people with significant industrial or occupational mercury exposure, what percentage went on to develop ME/CFS. Dentists would be a good group to look at, given their daily exposure to elemental mercury vapor from drilling out fillings.

If you do this with pesticides, there are studies which show you are 4 times more likely to develop ME/CFS after significant pesticide exposure. This study was done on farmers in the UK who are occupationally exposed to significant amounts of pesticide, and the prevalence of ME/CFS in this group was 4 times the national average.

A few mercury studies have been conducted for other diseases though, such as Alzheimer's and Parkinson's, with some indications that mercury may play a role in these conditions.

Methyl mercury is easily absorbed through the gut and deposits in many tissues, but does not cross the blood-brain barrier as efficiently as elemental mercury

Nevertheless, methylmercury does cross the blood-brain barrier, and once in the brain it is far more toxic than elemental mercury.

Chelation-knowledgeable people who figured out that ALA in high irregular doses made their symptoms worse complain about this all the time.

It would be interesting to see if there was any association between those who had averse effects from taking alpha lipoic acid, and the amount of mercury in their tissues. In your case, your testing showed high bodily levels; but you would need to do this for many individual cases to see if there was any link.

Mercury explains every single symptom I have, and while it is only a working hypothesis, it is one that is worth putting to rest and testing.

Fair enough. It's a good idea to have a working hypothesis, and to speculatively try out treatment based on it.

Have you looked at fresh coriander (aka cilantro, aka Chinese parsley) as a means to increase the excretion of mercury from the brain and CNS? Dr Yoshiaki Omura worked on this, and his studies are here:

http://www.ncbi.nlm.nih.gov/pubmed/8686573
http://www.ncbi.nlm.nih.gov/pubmed/8914687

I read that it has to be fresh not dried coriander herb. Dried coriander does not work, suggesting the active substance is within the volatile fat-soluble portion of the coriander plant.

I understand that you need to use coriander in combination with other chelators (such as selenium, iodine, zinc, silica, chlorella, vitamin C), because coriander may move mercury out of the CNS into the blood and tissues, but then you need something to pick up this mercury and take it out of the body.


My main problem with mercury is that it appears to be one of these things that the general public has fixated on as the cause of all ills. Mercury in vaccines was assumed by the general public to be the cause of autism, and by pressure from the general public it was taken out of many vaccines. This however did not lead to any reduction in the autism rates.

So once you have this fixation, it tends to generate a lot of pseudoscientific articles on the subject, which muddies the waters.

 

[alex3619]

So you can measure blood levels of mercury as low, when in fact the tissues are saturated with it.

I agree this might be a major problem. Mercury binds to existing molecular architecture. Blood, urine etc are new tissue. Its the burden in old tissue that is important. Biobanks and cadaver studies are the obvious solution, and if using those we can ascertain that (for example) a muscle biopsy is accurate, then we have a better test.

 

[nandixon]

I couldn't find Carbicarb for sale, but it's easy to make your own by just mixing sodium bicarbonate (baking soda) and food grade sodium carbonate (washing soda) together in the right proportions.

Food grade sodium carbonate you will find on eBay, and of course the sodium bicarbonate sold in supermarkets is food grade.

What are the right proportions? Well Carbicarb is described here as an "equimolar solution of sodium bicarbonate and sodium carbonate." By equimolar, they mean Carbicarb has one mole of sodium bicarbonate for every one mole of sodium carbonate. But we need to know the proportions of these two chemicals in terms of weight.

Well, sodium bicarbonate has a molecular weight = 84.01, and sodium carbonate a molecular weight = 105.99, so that gives you the ratio by weight, which is: 84.01 / 105.99 = 0.79.

So this means to make to make your own Carbicarb, for every 100 grams of sodium bicarbonate, you mix in 79 grams of sodium carbonate.


I presume Carbicarb is a more potent alkalizer than sodium bicarbonate, so doses of Carbicarb may need to be smaller than those of sodium bicarbonate.

Maybe someone has already mentioned it, but those values are needing to be switched around, i.e., the amount of sodium bicarbonate will be less than the amount of sodium carbonate to make an equimolar solution.

 

[Hip]

Maybe someone has already mentioned it, but those values are needing to be switched around, i.e., the amount of sodium bicarbonate will be less than the amount of sodium carbonate to make an equimolar solution.

Thanks very much @nandixon, you are absolutely right, those values are the wrong way around. I guess brain fog and mathematics don't make good bedfellows.

So the correct formula for Carbicarb is the following:

To make up some Carbicarb, you measure out 100 grams of sodium carbonate, and then mix in 79 grams of sodium bicarbonate.

I have also now edited my original post to correct this error.

 

[Gondwanaland]

Which specific foods, and why?

Celery, beets, lettuce, herbal teas. I feel like I am suffocating if I overdo with them (especially around the thymus and the glottis). I eat them regularly, but small amounts at a time

Now I know why I can better tolerate high nitrate foods when I put lots of salt on them.

 

[wastwater]

My genetic disorder mentions cyclic Amp and I saw that it relates to krebs cycle. I will get round to trying baking soda eventually

 

[Hip]

I have just noticed that lactate is available as a supplement: it can be bought in the form of calcium lactate.

If lactate released from the muscles during exercise is playing a role in creating PEM (as the efficacy of sodium bicarbonate in mitigating PEM might suggest), then taking calcium lactate as a supplement should also bring on the symptoms of PEM.

So you could use this calcium lactate supplement as a way to test whether lactate released from muscles is causing PEM.

I wonder if any ME/CFS patient has tried calcium lactate?

 

[Sidereal]

I have just noticed that lactate is available as a supplement: it can be bought in the form of calcium lactate.

If lactate released from the muscles during exercise is playing a role in creating PEM (as the efficacy of sodium bicarbonate in mitigating PEM might suggest), then taking calcium lactate as a supplement should also bring on the symptoms of PEM.

So you could use this calcium lactate supplement as a way to test whether lactate released from muscles is causing PEM.

I wonder if any ME/CFS patient has tried calcium lactate?

Great question. I think I recall @Gestalt supplementing lactate.

 

[Sherlock]

If lactate released from the muscles during exercise is playing a role in creating PEM (as the efficacy of sodium bicarbonate in mitigating PEM might suggest),

I think it's been pretty well established all around that other acids are responsible for the effects that have long been ascribed to lactic acid - at least in normals. IIRC, Alan Light also said that's true in CFS.

 

[Hip]

I think it's been pretty well established all around that other acids are responsible for the effects that have long been ascribed to lactic acid - at least in normals. IIRC, Alan Light also said that's true in CFS.

I am not sure if I follow what you are saying here.

 

[Sidereal]

I am not sure if I follow what you are saying here.

Lactic acid is not the acid responsible for muscle pain/fatigue symptoms following exercise in normal individuals. This is a myth. Other acids produce these symptoms.

 

[Hip]

Lactic acid is not the acid responsible for muscle pain/fatigue symptoms following exercise in normal individuals. This is a myth. Other acids produce these symptoms.

Oh OK, got it.

Though whether muscle fatigue in athletics, which I believe is about the loss of performance as a result of intense muscle usage, has any bearing on or relation to the PEM found in ME/CFS, that's another question.


The interesting thing about lactate, and what I think makes it a possible candidate for explaining PEM, at least in part, is the fact that in rat models, lactate induces IL-1β, IL-6 and TNF-α release from rat microglia, as well as IL-6 and TNF-α release from rat astrocytes. These are all the inflammation cytokines associated with sickness behavior and mental fatigue. And lactate can cross the blood-brain barrier quite easily.

So if ME/CFS patients already have high levels of these sickness behavior cytokines in their brains, due to chronic infection, and then the brain is also hit by lactate from physical exercise, this might greatly increase sickness behavior, which the ME/CFS patient may feel as PEM.

http://www.ncbi.nlm.nih.gov/pubmed/15934951

 

[MeSci]

Lactic acid is not the acid responsible for muscle pain/fatigue symptoms following exercise in normal individuals. This is a myth. Other acids produce these symptoms.

Do you have a link for this? I would be interested to know what the acids are, as I am sure others would.

 

[Sidereal]

Do you have a link for this? I would be interested to know what the acids are, as I am sure others would.

A couple of plain language articles on the topic of lactic acid not being responsible for delayed onset muscle soreness (DOMS):

http://www.scientificamerican.com/article/why-does-lactic-acid-buil/

http://www.nytimes.com/2006/05/16/health/nutrition/16run.html?_r=0

Note that this is referring to mechanism of muscle pain and fatigue in normal individuals who exercise. PEM is NOT the same thing as DOMS so it is of course possible that excess lactic acid accumulates in ME/CFS muscle and contributes to symptoms.

 

[MeSci]

A couple of plain language articles on the topic of lactic acid not being responsible for delayed onset muscle soreness (DOMS):

http://www.scientificamerican.com/article/why-does-lactic-acid-buil/

http://www.nytimes.com/2006/05/16/health/nutrition/16run.html?_r=0

Note that this is referring to mechanism of muscle pain and fatigue in normal individuals who exercise. PEM is NOT the same thing as DOMS so it is of course possible that excess lactic acid accumulates in ME/CFS muscle and contributes to symptoms.

That's not new info, and it doesn't specify specific acids as far as I can see from a quick look.

And muscle soreness in healthy people is very different from PEM.

I think that prostaglandins are a possible culprit downstream of lactic acid.

But lactic acidosis is a very real phenomenon, and so are other types of acidosis, as a result of anaerobic exertion or a gut disorder.

I and others have probably given links to scientific papers in this thread, so I won't repeat them here.

 

[Sidereal]

That's not new info, and it doesn't specify specific acids as far as I can see from a quick look.

And muscle soreness in healthy people is very different from PEM.

I think that prostaglandins are a possible culprit downstream of lactic acid.

But lactic acidosis is a very real phenomenon, and so are other types of acidosis, as a result of anaerobic exertion or a gut disorder.

I and others have probably given links to scientific papers in this thread, so I won't repeat them here.

I didn't say it was new information; I was merely responding to Hip who asked for clarification in relation to lactic acid not causing symptoms in normals. I also specifically stated that muscle soreness in normals is not the same as PEM.

Lactic acidosis is a real phenomenon but there is no evidence that people with ME/CFS suffer from it.

 

[MeSci]

I didn't say it was new information; I was merely responding to Hip who asked for clarification in relation to lactic acid not causing symptoms in normals. I also specifically stated that muscle soreness in normals is not the same as PEM.

Lactic acidosis is a real phenomenon but there is no evidence that people with ME/CFS suffer from it.

Have you looked for it?

There are threads about it here.

And there are plenty of threads, including Phoenix Rising articles, on muscle acidosis in ME, and our apparent difficulty in clearing lactate.

There is a paper here reporting d-lactic acidosis in ME.

 

[Sidereal]

Have you looked for it?

There are threads about it here.

And there are plenty of threads, including Phoenix Rising articles, on muscle acidosis in ME, and our apparent difficulty in clearing lactate.

There is a paper here reporting d-lactic acidosis in ME.

I'm well aware of the papers you are referring to and I am not disputing that there is a problem with excess lactate in muscle and gut in ME but that's not the same as having actual lactic acidosis which is very serious and can be fatal.