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

[MeSci]

Thanks, that might be the most likely possibility (though wherever they said glucose I mentally ubstituted sucrose). Bread etc never ever bothered me. As they write: things are "depending on the specific bacterial population".

I have been wondering of late whether some of the symptoms I ascribe to candida might really be due to some sucrose-loving bacteria. E.g., if I take 2 iodine tablets as an antimicrobial, I don't get the most noticeable sucrose-candida effects, but do get the acidic urine anyway.

They suggest a strategy:


Sounds like a case for intermittent fasting. Or going back to flooding the intestine with baking soda. Or using potassium bicarbonate - if that is non-laxative.

As this page says:

Regular table sugar is sucrose. It is a double-sugar, or disaccharide. It is composed of one molecule of glucose bonded to one molecule of fructose. Our intestinal cells are unable to absorb sucrose, however. They can absorb glucose and fructose, but not the disaccharide, sucrose. Therefore, our digestive system produces the enzyme, sucrase, which digests sucrose into glucose and fructose.

 

[Sherlock]

As this page says

Regular table sugar is sucrose. It is a double-sugar, or disaccharide. It is composed of one molecule of glucose bonded to one molecule of fructose. Our intestinal cells are unable to absorb sucrose, however. They can absorb glucose and fructose, but not the disaccharide, sucrose. Therefore, our digestive system produces the enzyme, sucrase, which digests sucrose into glucose and fructose.

I'm not seeing the point you're trying to make there, MeSci.

I'm not lacking the ability (e,g., low sucrase) to use sucrose, btw. I get a really good energy repletion from it - which is why I dabble again and again in trying to use it.

 

[MeSci]

I'm not seeing the point you're trying to make there, MeSci.

I'm not lacking the ability (e,g., low sucrase) to use sucrose, btw. I get a really good energy repletion from it - which is why I dabble again and again in trying to use it.

Sorry - I was replying to where you said:

wherever they said glucose I mentally (s)ubstituted sucrose

I was just trying to clarify the differences and relationships.

 

[Sherlock]

Sorry - I was replying to where you said:



I was just trying to clarify the differences and relationships.

Gotcha. Yes it does help to post basic info because not everybody has been plunging into everything since forever

That spares from having every reader needing to go and look up things individually - which is a great advantage of a discussion group.

So I'll give a brief, imperfect summary of the paper you posted: when fuel (glucose) hits the intestine, there might be bacteria there that immediately start using the fuel and they produce organic acids as a byproduct. The cells that line the intestine can take in those acids and use them as fuel. The excess acids might be used as fuel by the kidneys or other organs, and further excess gets converted to fat in the liver via lipogenesis. Still, some acid end up in the urine.

------------------------------------

Btw, my experiment A) : I took potassium gluconate instead of potassium citrate twice. after whey. The alkalizing benefit seemed the same.

Experiment B) was after chinups today, taking whey with no potassium. Felt acidity quickly, within an hour or so. Maybe Steve is right that it is a allergy/sensitivity reaction... yet not a true allergy but an effect made possible when leaky gut lets peptides through the gut barrier into circulation. The leaky gut occurred from sucrose.

 

[Hip]

@swfowkes
Thanks very much for joining this discussion and giving us your insight and chemical expertise.

By the way, I used to be an avid reader of your Cognitive Enhancement Research Institute (CERI) literature, many years ago. Alas, once you get ME/CFS, which I believe is probably driven by an enteroviral brain infection in many cases, you take a huge step backwards as far as cognitive enhancement is concerned: brain fog is the order of the day with this disease. Whereas before nootropics supercharged my brain, now with ME/CFS I need to take piracetam merely in a vain attempt to achieve normal cognition!

First, both the cation and anion of a salt create pH effects. Each has differential affinity for the hydroxide part of water and the proton part of water.

I appreciate that. So each salt will have its own pH when dissolved in water. I found this article which seems to summarize this nicely:

1) A salt of a strong acid and a strong base will produce a solution with pH = 7.
2) A salt of a weak acid and a strong base will produce a solution with pH greater than 7.
3) A salt of a weak base and a strong acid will produce a solution with pH less than 7.
4) A salt of a weak acid and a weak base produces a solution whose pH depends on the strengths of the acid and base which made the salt.

One question I would like to ask: when it comes to acids, bases and aqueous solutions of salts, is there anything analogous to the conservation of energy law of physics? For example, if I have 100 ml of solution at pH 6, and 100 ml of another solution at pH 8, when I mix these together, will they always come out at the same resultant pH, no matter what the solutions are?

Second, the terms acid, acidifying and alkaline, alkalinizing have a non-chemical meaning in the context of biological systems and metabolism.

If I understand you correctly here, you are hinting that since the body contains thousands of dynamic systems, and numerous different buffers that are dynamically acting to tightly control pH values in various compartments of the body, the effects of foods or supplements on body pH values cannot be modeled or calculated as if the body were just a collections of chemicals in a glass flask. Each food or supplement can affect many of these dynamic bodily systems, and thereby alter body pH values in a complex fashion.

Furthermore, the body is not a closed system with respect to acids and bases: as you know, the body can get rid of acidity by increasing the amount of carbon dioxide breathed out by the lungs, thereby reducing carbonic acid in the blood; plus acids or bases can be eliminated by the kidneys to help control body pH.

So I guess the fact that the body has thousands of dynamic processes, and is not a closed system with respect to acids and bases, makes it complex to try to model the biochemical effects that ingested foods or supplements have on body pH.


As an aside, I also wonder whether the health effects derived from alkalizing foods or supplements may only in part be due to changes in body pH. pH levels are tightly controlled in the body (eg, the blood is kept between 7.35 and 7.45 under normal circumstances), and if you go out of the normal pH ranges, then bad things start happening, like enzymes will fail to work; so any changes in pH made by an alkalizing regimen are very small.

Thus might it be the case that the effects of alkalizing are not just due to changes in pH, but also due to changes in the functioning of the dynamic systems (the pH buffer systems) of the body that maintain body pH values at precise levels?

For example, if you apply an "alkalizing force" to the body by taking ½ a teaspoon of sodium bicarbonate each day, that means in order for the blood pH buffer system (the bicarbonate/carbonic acid buffer) to maintain blood pH with precise limits, this blood buffer system will have to adjust your breathing such that less carbon dioxide is expelled with every breath, so that more carbonic acid-forming carbon dioxide is kept in the blood, to counteract the alkalizing effect of bicarbonate and maintain blood pH within its normal limits.

So alkalizing not only changes pH slightly, but also alters carbon dioxide metabolism, and no doubt other aspects of metabolism.

Experientially, there is no connection between the acidic or alkaline taste of a food or substance and its acid or alkaline metabolic effect. Lemon juice is very acidic (tart) on the tongue, but is substantially alkaline-anabolic-anaerobic in its metabolic effect.

Any idea of what it is within a lemon that makes it alkalizing in its metabolic effect? I find it hard to imagine that with all that citric acid in lemons, a lemon would have an alkalizing effect metabolically. It's easy to see how an alkaline substance such as sodium bicarbonate in solution could alkalize the body, but surely not citric acid?

Since I am new to this forum, I'd like any clarification from members as to whether this discussion is best kept as part of this thread or should be handled in a different manner.

Usually if a major subtopic emerges in a thread, and it goes on for several pages, the moderators may move that subtopic to its own thread. But for the moment, I should think it will be fine to continue with this alkalizing topic in this thread. We can always move these posts later.

It is scientific. (1) It is defined: the residue left over after combustion. (2) It is measurable: pH effects in urine, blood, tissue, cells and organelles (the latter two are exceedingly difficult). (3) It has been measured and found to be consistent. In other words, its predictions have been tested. (4) It has been systematized, and resulting predictions tested. (5) It has been applied practically, and clinically, with considerable success.

I can appreciate that the alkalizing or acidifying effects of foods or supplements may be measured, so it's scientific in this empirical sense. But I just have not seen any scientific explanation as to the mechanism by which various foods and supplements achieve their alkalizing or acidifying effects.

As you mentioned, the terms alkalizing or acidifying when applied to the effect of foods and supplements on the body don't have their normal chemical meaning. Nevertheless, there must be some underlying biological mechanism(s) that can explain why a given food or supplement is alkalizing or acidifying to the body, even if we don't yet know what this mechanism is.

I don't understand this definition of "ash" being the residue left over after combustion. If by combustion you mean oxidation, well, there's not a lot of that going on in the body as far as I am aware. The liver employs oxidation to breakdown some dietary components, but oxidation is not the universal fate of dietary components.

It is true that "ash" is not widely used by scientists in this field (biologists, physiologists, biophysicists) nor taught to physicians in medical school or in continuing medical education courses. But to the extent that I have discussed the issue with many scientists and alternative medical practitioners, the vast majority do readily understand the concept even if they do not have an intuitive or practical appreciation of it.

I have no problem in trying out a treatment such as an alkalizing diet to see what health benefits it might provide, especially if there are reports of good effects. It's not necessary know the biochemical mechanisms to obtain benefit.

I would actually like to follow an alkalizing regimen for 6 to 12 months; however, every time I try this, I get horribly lightheaded. I have speculated in an earlier post that this lightheadedness side effect arises because of the brain's mechanism which dilates the cerebral blood vessels when the blood is acidic, and constricts the blood vessels when the blood is alkaline. This mechanism is keyed on the concentration of hydrogen ions in the blood.

So I think what happens is when the blood is made more alkaline, the brain constricts its blood vessels and the blood supply to the brain is chronically reduced, leading to a feeling of lightheadedness. Cerebral vasoconstriction is a known cause of lightheadedness. Do you think hypothesis might be correct?

I wish I could find a workaround for this lightheadedness, because I would like to try out an alkalizing regimen.

 

[Hip]

Hip, you feel better when taking a known cerebral vasodilator. Your hands are cold all the time. You start to feel neurological symptoms when you eat foods that are known to lower bloodflow. It all paints a very consistent picture doesn't it? Your body is sending a really clear message.

I think you are exactly the guy for whom restoring nitric oxide *might* have a dramatic good result.

I think you may be right, but this is easier said than done. I few years ago I did a lot of reading about nitric oxide metabolism, and one of its features is that it is very tightly controlled. So it you try to change NO levels, systems will kick into operation that bring the levels back to what they were.

I read a lot of stuff written by nitric oxide expert Dave Whitlock. He thinks ME/CFS is due to low basal levels of NO.

I did try raising NO by administering 10 to 20 mg of sodium nitrite (NaNO2) transdermally each day. But don't try this at home, kids, because you can very easily and very quickly kill yourself with sodium nitrite. As little as 1000 mg of sodium nitrite, oral or transdermal, can be fatal. It kills you by methemoglobinemia. Needless to say, I quadruple checked my dose calculations before applying transdermal sodium nitrite (but even then I was worried that with the ME/CFS brain fog, I would make a fatal mistake in my dose calculations).

I speculate in this post that NO might be low because one enzyme that makes it, eNOS, might be down-regulated due to the epigenetic mechanism of histone acetylation.

What are your primary exhaustion symptoms and what brings those on? What other symptoms make you think this is CFS? To me the hallmark of true CFS is the PEM. PEM on exertion is to me all about the mitochondria shouting for help. The body is in glycolysis. The electron transport chain is highly inefficient. The acidity in muscle tissue builds up and paralyzes muscle. The acidity becomes systemic and causes neurologic symptoms.

I get PEM mostly from mental exertion, rather than physical exertion. The ME/CFS defining criteria recognize that both mental and physical exertion PEM exist. Plus I have a large range of classic ME/CFS symptoms, right across the board.

I wouldn't trust small vendors selling a chemical like this and calling it "food grade". Some of that stuff will be from China, loaded with heavy metals, and I don't believe for a second that the manufacturer really tested the product widely. One manufacturer might source from 10 different vendors and not test every one of those.

You can always ask the vendor for a certificate of anaylsis. Also, note that major companies often sell on eBay, so there's not just small vendors there.

 

[pemone]

IME reversing excess acidity with oral magnesium oxide and sodium bicarbonate baths helped me to erradicate my polyuria. In addition, Saccharomyces boulardii helped in reducing histamine and vitamin A helped in solubilizing calcium.
My urine pH was 4.5 in the evening when I took my 1st bicarb bath. If I only knew it was that simple!

How does sodium bicarbonate baths address polyuria?

 

[Gondwanaland]

How does sodium bicarbonate baths address polyuria?

In my case polyuria was from high acidity.

 

[Gondwanaland]

But am I noticing the increased acidity because the AAs that I drink are going directly to the bladder?

Isn't it increasing your uric acid?

 

[pemone]

Some recent work by Julia Newton's group in Newcastle has suggested problems with acid buildup in and/or disposal from the muscle in ME/CFS. Work that has been done over the last decade by Snell's group has suggested pathologically low anaerobic threshold in ME/CFS, especially on repeated cardiopulmonary exercise test taking place 24 hours after the initial test. This presentation by Prof Van Ness may be of interest. He argues that lactic acid is not the acid responsible for these symptoms:

No, he is not saying that the acid in CFS is not lactic acid. The section in this video you are referring to is pointing out that a "normal" person with intact aerobic metabolism would produce CO2, as a byproduct of aerobic metabolism. CO2 is easy to get rid of. We just breath it out. It quickly converts in body to carbonic acid and the lungs are very efficient at disposing of it.

What CFS sufferers do instead is get stuck in glycolysis, which does produce lactic acid. CFS means you produce a lot of lactic acid instead of producing the more efficiently disposed CO2.

 

[pemone]

Actually, that is one of my suspicions. I would love to see some blood work looking for this in patients. Its not a sure thing though.

Lactic acidosis takes time to develop. Julia Newton's work suggests we are highly acidic during and after exercise, but excessively alkaline at rest (one of our adaptations?). Lactic acidosis increases oxygen dumping in the short term as acidic conditions increase oxygen release from red blood cells.

Do you have a link to her claim that CFS patients are alkaline at rest?

I'm very confident that CFS patients with PEM get stuck in glycolysis and produce lactic acid. And what is frustrating is that it is fairly easy to diagnose this. It's just that the medical community isn't treating the disease as a metabolic disorder, and in fact there are no metabolic specialists for adult patients in most major medical centers.

Take an RBC lactate and pyruvate reading and I have a formula to convert that to NAD+/NADH. That ratio is well known for healthy adults and I'm sure most CFS patients will exhibit low ratios. They are in a reduced state, unable to generate NAD+ needed to power many metabolic processes. Krebs cycle slows down because of excess NADH. That result by itself suggests that the electron transport chain is not working efficiently because it is the ETC that converts NADH to NAD+, in complex I.

In addition. there are sensors used in research for measuring ATP production. If those would be made available to CFS patients, you could also test ATP production. A combination of low NAD+/NADH and low ATP would decisively point to a failure of the electron transport chain.

The pyruvate/lactate test is not expensive, and the main problem is finding a vendor who can provide it from RBC. I am tracking that down now.

The beauty of having that test is that you can then measure efficacy of different therapies by spot checking the effect on NAD+/NADH.

I'm anxious to start trying oxidative therapies like ozone because they result in a massive NADH to NAD+ conversion. I'm also starting to wonder if the reason that eating nitrate foods is making me feel better is as much from their oxidative effects as from their ability to create nitric oxide that dilates blood vessels.

 

[pemone]

Not to be argumentative, but I'd guess that only the opposite is true: if one finds cardiac calcium then one probably has intracranial calcium, too - which I think was your main point. But OTOH if one has zero calcium, then that likely means only that the exaggerated inflammatory response which produces calcification is missing. (AFAIK, calcification is a step beyond fibrosis, and fibroblasts can turn into osteoblasts in severe inflammation. That can also occur in lymph nodes, though it's rare there.)

But even if you accept your idea, and allow that there is a constant inflammatory process that attracts LDL and is not calcified, are those types of soft tissue LDL patches in the artery really dangerous? What does the literature say about that? I thought it was the breaking off of the hard calcifications that carried the greatest risk, because the calcification cannot be absorbed or bypassed rapidly.

I also wonder won't some percentage of LDL collection in the artery always become calcified, assuming there is a persistent lesion?

Also, it's been known e.g. that carotid atheroma is not a surefire proxy for cardiac atheroma, so the underlying process/environment is somewhat different in different locations anyway.

So really your point is do both: carotid ultrasound to detect other sources of narrowing, and maybe EBT Scan to find calcified areas. That's what my Osteopath does by the way, and now I understand why

pone, have you had an LDL-P or APO-B done?

My LDL-P was bad in Nov 2013, which is how I started this whole journey. I went low carb and tried to change diet. Within a month of all of those experiments I lost all energy and started to encounter the bad neurological symptoms I have been dealing with (i.e., auditory sound of tuning fork 24x7, brain fog, sense of burning sensation in brain).

What I have discovered since then was the whipping cream I was eating from a Paleo diet sent my cholesterol and LDL-P skyrocketing. LDL-P started out around 2300. I removed all dairy from diet, went for coconut milk, and those numbers have been coming down. Every LDL-P test was lower than the last, and my last one in August 2014 was around at 1600.

One of the things I have learned through much dietary experiment is that not all saturated fatty acids are the same. "Saturated Fat" can be any combination of four fatty acids: Lauric, Myristic, Palmitic, and Stearic. Coconut oil is mostly Lauric. Chocolate is mostly Stearic. Dairy fats are mostly Palmitic. I don't know if I was having a reaction to dairy proteins that somehow made me process the fats differently, or if it was the Palmitic acid. Whatever it was, the dairy fat sent my lipids into orbit, and removing dairy has resulted in their slowly coming down.

I'm testing this now by using Indian Ghee on my meals, which is organic butter with all of the dairy proteins burned away. If my LDL-P goes back up, I'll know the problem was in the Palmitic acids and I'll have to get rid of ghee from diet. If the LDL-P continues down, then I'll know the problem was dairy protein.

My only APO marker that is bad is APO-B at around 106. The others are in range. The cardiac CRP is low. Thankfully, my APO-E is 3/3, where I understand that 4 would mean you have brain issues to worry about and APO-E=2 would mean you have cardiac issues. I'm in the middle where risks are balanced.

If I were not dealing with CFS, my main risks are glucose metabolism and LDL. I am starting to believe that the glucose and LDL may have been brought on by mercury over time, and that the CFS was just a different manifestation of the same thing.

Hey this is fun - I get to brush up on cardiac diagnostics

Yeah, if this disease doesn't kill me I'm going to end up being ridiculously healthy from all of the knowledge I am having to pick up to save myself.

 

[Sidereal]

Take an RBC lactate and pyruvate reading and I have a formula to convert that to NAD+/NADH. That ratio is well known for healthy adults and I'm sure most CFS patients will exhibit low ratios. They are in a reduced state, unable to generate NAD+ needed to power many metabolic processes. Krebs cycle slows down because of excess NADH. That result by itself suggests that the electron transport chain is not working efficiently because it is the ETC that converts NADH to NAD+, in complex I.

In addition. there are sensors used in research for measuring ATP production. If those would be made available to CFS patients, you could also test ATP production. A combination of low NAD+/NADH and low ATP would decisively point to a failure of the electron transport chain.

My LDL-P was bad in Nov 2013, which is how I started this whole journey. I went low carb and tried to change diet. Within a month of all of those experiments I lost all energy and started to encounter the bad neurological symptoms I have been dealing with (i.e., auditory sound of tuning fork 24x7, brain fog, sense of burning sensation in brain).

If the first statement were true about excess NADH being the problem, then how come a ketogenic diet made you (and many others with ME/CFS) dramatically sicker? By removing glucose and eating a high fat diet you sharply decreased NADH input to complex I and instead relied on FADH2 and complex II to get your energy which sounds like it went down to about zero using this approach.

 

[Sherlock]

uric acid

AFAIK, whey has no purines. As far as excess protein overloading the kidneys? Is that what you are referring to? As far as I know, that has been abandoned as a valid concern, unless a person has malfunctioning kidneys (I don't). Plus, I don't get a huge amount of protein, maybe 130g per day.

Anything else I should be aware of?

 

[Gondwanaland]

@Sherlock I don't know, just brainstorming
I stumbled upon a site alerting gout sufferers to stay awy from whey, but I don't think it is a valid concern.

 

[Sherlock]

But even if you accept your idea, and allow that there is a constant inflammatory process that attracts LDL and is not calcified, are those types of soft tissue LDL patches in the artery really dangerous? What does the literature say about that? I thought it was the breaking off of the hard calcifications that carried the greatest risk, because the calcification cannot be absorbed or bypassed rapidly.

A plaque is covered with a fibrous matrix cap. What's accepted is that most AMI occurs when inflammatory Matrix MettaloProteinases break down the cap enough so that it either ruptures or erodes. That exposes material to circulation that sets off the coagulation cascade, just like forming a scab on a skin cut. If this clot (thrombosis) blocks offf the entire artery flow, then that's an infarction. (Though most cell death actually occurs during reperfusion, when blood flow is eventually restored and large amounts of damage occur from free radicals. So taking antioxidants when in danger of thrombosis is probably a good idea. They actually tie off rat brain arteries, then after a few minutes untie and measure resulting damage in the antioxidant versus control groups. )

Keeping the clot from getting big enough to completely block off an artery is a good idea That's why aspirin, clopidigrel and other antiplatelet drugs work to prevent death. A small clot that blocks off only partially would be an episode of unstable angina.

Burt a piece of an atheroma breaking off and blocking a smaller diameter section downstream is probably also unstable angina, and a harbinger of worse to come.

Stable angina, OTOH, occurs during exercise when a heart artery is severely but partially blocked and can't allow enough blood to pass during need for increased blood flow to heart muscle. Eventually, the blockage can become 100% and cause an AMI / heart attack, but those are only ~15% of total heart attacks. Also since they take a lot of time to develop, there was also time to develop corollary arteries to supply blood flow around the blockage.

I also wonder won't some percentage of LDL collection in the artery always become calcified, assuming there is a persistent lesion?

I don't know -- presumably that takes fiercer inflammation and more years. But it's the cap that gets calcified AFAIK, not the foam cells or other matter inside the plaque.

Yeah, if this disease doesn't kill me I'm going to end up being ridiculously healthy from all of the knowledge I am having to pick up to save myself.

Touche' But hey, maybe CFS can save one's life by making a person health-aware. After all, the first sign of heart disease in most people is sudden cardiac death, so they were quite unaware.

P.S. If you were the one that got Steve Fowkes here, then bravo and thanks go to you.

P.P.S. You sound as if you might be an atypical responder to diet. So yes, your experimentation is the best way to go, IMO. One example: the Pritikin group has study wherein some hi-carb lo-fatters don't get smaller LDL - so they are opposite of typical.

Also IMO Paleo had a lot of cool hype and a lot of false preaching, but only some truths underneath.

 

[Sherlock]

@Sherlock I don't know, just brainstorming
I stumbled upon a site alerting gout sufferers to stay awy from whey, but I don't think it is a valid concern.

Thanks, brainstorming is appreciated. I just took a look myself and find contradictory advice. So I will not have any whey every 3-4 days, just in case. I wouldn't take any supplement every day, month after month, because that might be dangerous.

 

[Gondwanaland]

@Sherlock don't you have pH strips at home?

 

[Sherlock]

@Sherlock don't you have pH strips at home?

Yes, which is how I went to pH school so to speak It was really impressive to me how I could turn the strip to blue by taking enough bicarb. When alkaline, there also was no burning sensation - which was really a very valuable learning experience. So now I go by the presence or lack or burning.

I also happe to be partly color blind, so I have to use a camera and my computer to know what color the strip turns to.

 

[Sherlock]

I'm also starting to wonder if the reason that eating nitrate foods is making me feel better is as much from their oxidative effects as from their ability to create nitric oxide that dilates blood vessels.

Have you ever tried a nitroglycerin tablet just to see what happens? I got hold of one years ago, it was quite an experience but now I wonder if my experience was typical.