Acetyl L- Glutathione, ATP, Baking Soda, Sam-e & Catalase = No PEM after exercise
- Thread starter Mya Symons
- Start date
I wouldn't assume that the problem is fixable.
This is a commonly used argument by people who say that changing your macronutrient ratios couldn't possibly have made you sick. It's a fallacy. It doesn't matter what hypothetical healthy humans roaming the savannah could or could not eat. What matters to your situation is only is how fragile your body is, and if you find yourself needing to post on PR, it's unlikely that you are very robust. Sickly people with fatigue who couldn't keep up with the rest would have likely died very quickly anyway. It's only due to the luxuries of modernity that we get to sit here and speculate about what they ate.
It's important to also keep in mind that ancestors weren't eating heavy cream and steak when they were ketogenic. The modern ketogenic diet doesn't make you sick because of what you eat but rather because of what you DON'T eat. Think algae, insects, roots covered with soil, tree bark etc. Most people when they go low carb remove what paltry amount of fibre they were eating before so now you are providing virtually no prebiotic substrate to feed your beneficial bacteria, thus setting yourself up for really big problems. Yes, this can cause a complete metabolic breakdown.
I don't want to drag the thread off-topic so I'll just add a couple of brief comments. With ME/CFS it's really easy to make yourself worse with incorrect assumptions and supplements that stem from those. Based on your comments about having tried to raise NO and believing we are suffering from excess NADH, i.e. reductive stress, I think there is a danger of making yourself sicker because shifting the redox state in an even less favourable direction is the worst thing you could do in this illness since it is the core pathology we're all trying to address. I would recommend familiarising yourself with Paul Cheney's thoughts on the redox issue and the methodology he has used to study this in his patients and what happens when he gives them supplemental oxygen or supplements commonly recommended around here like fish oil, methylcobalamin, 5-MTHF etc. I don't have any handy links since he doesn't publish anything; it's all lectures or transcripts of conversations he's had with his patients. Martin Pall's work on NO/ONOO is also very important.
Sadly, as you've already discovered with low carb and random ALA dosing, people with CFS and those predisposed to develop it are far from robust and sometimes never recover from some seemingly banal experiments/supplements/meds so all I can say is be careful.
Seeing as you have not been sick very long, I would suggest not getting wedded to any particular theory but rather trying to get as much information as possible from clinicians who have dealt with us for decades and have developed an intuitive feel for what works and what doesn't. If you have mercury toxicity, by all means chelate the mercury. No doubt the amalgams and mercury in vaccines are a public health catastrophe which has contributed to the epidemic of chronic illness. But Dr Cutler's protocol has been around for 15 years and if mercury were THE answer, as opposed to an answer for some people some of the time, we would have seen a lot more cures.
Regarding the microbiome, there is an emerging and pretty compelling literature that it is involved in all kinds of chronic disease and I can't possibly summarise it here. Genova and other currently available commercial tests are worthless since the likely problem isn't some huge pathogen in the gut but rather an absence of key anaerobic species that produce butyrate among many other functions. There is a whole subforum here on PR about the gut where you can get a lot of useful information.
This is a commonly used argument by people who say that changing your macronutrient ratios couldn't possibly have made you sick. It's a fallacy. It doesn't matter what hypothetical healthy humans roaming the savannah could or could not eat. What matters to your situation is only is how fragile your body is, and if you find yourself needing to post on PR, it's unlikely that you are very robust. Sickly people with fatigue who couldn't keep up with the rest would have likely died very quickly anyway. It's only due to the luxuries of modernity that we get to sit here and speculate about what they ate.
It's important to also keep in mind that ancestors weren't eating heavy cream and steak when they were ketogenic. The modern ketogenic diet doesn't make you sick because of what you eat but rather because of what you DON'T eat. Think algae, insects, roots covered with soil, tree bark etc. Most people when they go low carb remove what paltry amount of fibre they were eating before so now you are providing virtually no prebiotic substrate to feed your beneficial bacteria, thus setting yourself up for really big problems. Yes, this can cause a complete metabolic breakdown.
I don't want to drag the thread off-topic so I'll just add a couple of brief comments. With ME/CFS it's really easy to make yourself worse with incorrect assumptions and supplements that stem from those. Based on your comments about having tried to raise NO and believing we are suffering from excess NADH, i.e. reductive stress, I think there is a danger of making yourself sicker because shifting the redox state in an even less favourable direction is the worst thing you could do in this illness since it is the core pathology we're all trying to address. I would recommend familiarising yourself with Paul Cheney's thoughts on the redox issue and the methodology he has used to study this in his patients and what happens when he gives them supplemental oxygen or supplements commonly recommended around here like fish oil, methylcobalamin, 5-MTHF etc. I don't have any handy links since he doesn't publish anything; it's all lectures or transcripts of conversations he's had with his patients. Martin Pall's work on NO/ONOO is also very important.
Sadly, as you've already discovered with low carb and random ALA dosing, people with CFS and those predisposed to develop it are far from robust and sometimes never recover from some seemingly banal experiments/supplements/meds so all I can say is be careful.
Seeing as you have not been sick very long, I would suggest not getting wedded to any particular theory but rather trying to get as much information as possible from clinicians who have dealt with us for decades and have developed an intuitive feel for what works and what doesn't. If you have mercury toxicity, by all means chelate the mercury. No doubt the amalgams and mercury in vaccines are a public health catastrophe which has contributed to the epidemic of chronic illness. But Dr Cutler's protocol has been around for 15 years and if mercury were THE answer, as opposed to an answer for some people some of the time, we would have seen a lot more cures.
Regarding the microbiome, there is an emerging and pretty compelling literature that it is involved in all kinds of chronic disease and I can't possibly summarise it here. Genova and other currently available commercial tests are worthless since the likely problem isn't some huge pathogen in the gut but rather an absence of key anaerobic species that produce butyrate among many other functions. There is a whole subforum here on PR about the gut where you can get a lot of useful information.
Hi @pone, no I don't have a link handy. I think it was discussed in a video conference last year, but I am not sure the paper is published yet.
I started to reply earlier but needed to do some research to be sure what I was saying was accurate.
With regard to 2,3 bisphosphoglycerate, there was an interest in this in the late 90s but repeated testing (probably unpublished) could not confirm a deficiency. If this is normal then lactic acidosis is not present. In fact, privately, I was informed that repeat lab testing shows high 2,3bpg, which indicates alkalinity not acidity. However as a marker this is a time average .. it indicates (indirectly) average blood pH . Spot pH will depend on activity, and the activity we use to get a test done may make us acidic. So only in a fully rested state will we get to see alkalinity, and even then not until a while after activity stops.
We will indeed produce lactic acid, but its not that we are stuck in glycolysis but the Krebs cycle cannot ramp up to meet need. Why this is happening is still being debated and investigated. There are lots of theories, and most have some evidence for them. It may also be that several theories are right but its combinations of things or right for different subgroups.
At rest though, in milder patients, we should not see much lactic acid in blood. Now, we might in spinal fluid if our brains are being pushed. In exercise we can expect huge rises in lactic acid.
I first got interested in this line of research in the 90s. Its been looked at for that long. However a decade and a half of testing has failed to find the cause.
All bets are off for the severely disabled with ME. Just surviving might push them in to lactic acid overload. They are the people most at risk.
This table lists many triggers for lactic acidosis:
Hypoxia and carbon monoxide poisoning have both been considered in ME.
http://wp.nyu.edu/biochemistryshowc...14/01/Biochemj-MulQuiney-Kuchel-MCA-23BPG.pdf
(This paper is not very readable, but this comment comes from the intro.)
The shunt is a name for the pathway in which 2,3 BPG is synthesized. It is also known as the Rapoport Leubering Cycle. It is primarily active in red blood cells. I am unsure it makes much of a difference in other tissues. If it disturbs NADH metabolism then it might mean our blood NAD/NADH ratio might not reflect our tissue NAD/NADH ratio. What is more clear is that the NADH/ATP or NAD/ATP ratio in the blood might be disturbed.
What is of interest here is that any form of hypoxia/anoxia might result in these issues, and that includes a bad NAD/NADH ratio as a possible cause out of maybe hundreds of possible causes.
Since there are a great many factors that can cause this, it may be that we are a population with a range of different issues but similar final result. Or it may be that a combination of factors might drive this, and that combination might vary slightly patient by patient.
This last view is the one I favour ... we know of many risk factors, and some like B12 deficiency, EDS and small fiber polyneuropathy may indicate problems with the regulation of peripheral vasculature, resulting in local tissue hypoxia. I am currently of the view that many factors combine to induce final pathophysiology.
I started to reply earlier but needed to do some research to be sure what I was saying was accurate.
With regard to 2,3 bisphosphoglycerate, there was an interest in this in the late 90s but repeated testing (probably unpublished) could not confirm a deficiency. If this is normal then lactic acidosis is not present. In fact, privately, I was informed that repeat lab testing shows high 2,3bpg, which indicates alkalinity not acidity. However as a marker this is a time average .. it indicates (indirectly) average blood pH . Spot pH will depend on activity, and the activity we use to get a test done may make us acidic. So only in a fully rested state will we get to see alkalinity, and even then not until a while after activity stops.
We will indeed produce lactic acid, but its not that we are stuck in glycolysis but the Krebs cycle cannot ramp up to meet need. Why this is happening is still being debated and investigated. There are lots of theories, and most have some evidence for them. It may also be that several theories are right but its combinations of things or right for different subgroups.
At rest though, in milder patients, we should not see much lactic acid in blood. Now, we might in spinal fluid if our brains are being pushed. In exercise we can expect huge rises in lactic acid.
I first got interested in this line of research in the 90s. Its been looked at for that long. However a decade and a half of testing has failed to find the cause.
All bets are off for the severely disabled with ME. Just surviving might push them in to lactic acid overload. They are the people most at risk.
This table lists many triggers for lactic acidosis:
Hypoxia and carbon monoxide poisoning have both been considered in ME.
http://wp.nyu.edu/biochemistryshowc...14/01/Biochemj-MulQuiney-Kuchel-MCA-23BPG.pdf
(This paper is not very readable, but this comment comes from the intro.)
The shunt is a name for the pathway in which 2,3 BPG is synthesized. It is also known as the Rapoport Leubering Cycle. It is primarily active in red blood cells. I am unsure it makes much of a difference in other tissues. If it disturbs NADH metabolism then it might mean our blood NAD/NADH ratio might not reflect our tissue NAD/NADH ratio. What is more clear is that the NADH/ATP or NAD/ATP ratio in the blood might be disturbed.
What is of interest here is that any form of hypoxia/anoxia might result in these issues, and that includes a bad NAD/NADH ratio as a possible cause out of maybe hundreds of possible causes.
Since there are a great many factors that can cause this, it may be that we are a population with a range of different issues but similar final result. Or it may be that a combination of factors might drive this, and that combination might vary slightly patient by patient.
This last view is the one I favour ... we know of many risk factors, and some like B12 deficiency, EDS and small fiber polyneuropathy may indicate problems with the regulation of peripheral vasculature, resulting in local tissue hypoxia. I am currently of the view that many factors combine to induce final pathophysiology.
Do you have a reference for prostaglandins acidifying the blood/body? I can't find anything that says this; in fact this page says
With regard to 2,3 bisphosphoglycerate, there was an interest in this in the late 90s but repeated testing (probably unpublished) could not confirm a deficiency. If this is normal then lactic acidosis is not present. In fact, privately, I was informed that repeat lab testing shows high 2,3bpg, which indicates alkalinity not acidity. However as a marker this is a time average .. it indicates (indirectly) average blood pH . Spot pH will depend on activity, and the activity we use to get a test done may make us acidic. So only in a fully rested state will we get to see alkalinity, and even then not until a while after activity stops.
We will indeed produce lactic acid, but its not that we are stuck in glycolysis but the Krebs cycle cannot ramp up to meet need. Why this is happening is still being debated and investigated. There are lots of theories, and most have some evidence for them. It may also be that several theories are right but its combinations of things or right for different subgroups.
At rest though, in milder patients, we should not see much lactic acid in blood. Now, we might in spinal fluid if our brains are being pushed. In exercise we can expect huge rises in lactic acid.
I first got interested in this line of research in the 90s. Its been looked at for that long. However a decade and a half of testing has failed to find the cause.
All bets are off for the severely disabled with ME. Just surviving might push them in to lactic acid overload. They are the people most at risk.
This table lists many triggers for lactic acidosis:
Hypoxia and carbon monoxide poisoning have both been considered in ME.
http://wp.nyu.edu/biochemistryshowc...14/01/Biochemj-MulQuiney-Kuchel-MCA-23BPG.pdf
(This paper is not very readable, but this comment comes from the intro.)
The shunt is a name for the pathway in which 2,3 BPG is synthesized. It is also known as the Rapoport Leubering Cycle. It is primarily active in red blood cells. I am unsure it makes much of a difference in other tissues. If it disturbs NADH metabolism then it might mean our blood NAD/NADH ratio might not reflect our tissue NAD/NADH ratio. What is more clear is that the NADH/ATP or NAD/ATP ratio in the blood might be disturbed.
What is of interest here is that any form of hypoxia/anoxia might result in these issues, and that includes a bad NAD/NADH ratio as a possible cause out of maybe hundreds of possible causes.
Since there are a great many factors that can cause this, it may be that we are a population with a range of different issues but similar final result. Or it may be that a combination of factors might drive this, and that combination might vary slightly patient by patient.
This last view is the one I favour ... we know of many risk factors, and some like B12 deficiency, EDS and small fiber polyneuropathy may indicate problems with the regulation of peripheral vasculature, resulting in local tissue hypoxia. I am currently of the view that many factors combine to induce final pathophysiology.
We will indeed produce lactic acid, but its not that we are stuck in glycolysis but the Krebs cycle cannot ramp up to meet need. Why this is happening is still being debated and investigated. There are lots of theories, and most have some evidence for them. It may also be that several theories are right but its combinations of things or right for different subgroups.
At rest though, in milder patients, we should not see much lactic acid in blood. Now, we might in spinal fluid if our brains are being pushed. In exercise we can expect huge rises in lactic acid.
I first got interested in this line of research in the 90s. Its been looked at for that long. However a decade and a half of testing has failed to find the cause.
All bets are off for the severely disabled with ME. Just surviving might push them in to lactic acid overload. They are the people most at risk.
This table lists many triggers for lactic acidosis:
Hypoxia and carbon monoxide poisoning have both been considered in ME.
http://wp.nyu.edu/biochemistryshowc...14/01/Biochemj-MulQuiney-Kuchel-MCA-23BPG.pdf
(This paper is not very readable, but this comment comes from the intro.)
The shunt is a name for the pathway in which 2,3 BPG is synthesized. It is also known as the Rapoport Leubering Cycle. It is primarily active in red blood cells. I am unsure it makes much of a difference in other tissues. If it disturbs NADH metabolism then it might mean our blood NAD/NADH ratio might not reflect our tissue NAD/NADH ratio. What is more clear is that the NADH/ATP or NAD/ATP ratio in the blood might be disturbed.
What is of interest here is that any form of hypoxia/anoxia might result in these issues, and that includes a bad NAD/NADH ratio as a possible cause out of maybe hundreds of possible causes.
Since there are a great many factors that can cause this, it may be that we are a population with a range of different issues but similar final result. Or it may be that a combination of factors might drive this, and that combination might vary slightly patient by patient.
This last view is the one I favour ... we know of many risk factors, and some like B12 deficiency, EDS and small fiber polyneuropathy may indicate problems with the regulation of peripheral vasculature, resulting in local tissue hypoxia. I am currently of the view that many factors combine to induce final pathophysiology.
I have for some years suspected uncoupling, but was unclear as to the mechanism that might cause it. The reason I suspected it is that when I exert myself, the exhaustion is accompanied by feeling extremely hot, which could indicate uncoupling - instead of producing ATP, the body produces heat, as in the non-shivering thermogenesis used by hibernating animals.
I wonder whether I could deduce anything from taking my temperature before and after exertion. I'd need to have the thermometer ready, as when I get exhausted and hot I have to sit down! Would an oral temperature reading pick up any temperature change?
Sorry everyone for the cross-talk and for going a little off-topic (it's all related after all...
)
I never got sustained benefit from probx. I feel that both prebx and probx are immunostimulants and harmful to me right now (trigger inflammation).
)I never got sustained benefit from probx. I feel that both prebx and probx are immunostimulants and harmful to me right now (trigger inflammation).
Prostaglandins are the full range of vasodilator, inflammatory, antiinflammatory and more. WHICH prostaglandins are produced and in what amounts are the key. They are critical for healing. They are also critical for inflammation. Its a broad family of hormones, and I do not fully understand them - not even close. The research on this is broad, deep, and confused, or was the last time I looked. I suspect prostaglandins are not even fully understood by "experts".
Think of them this way. They are one of several classes of hormones that a cell uses to communicate with itself and with nearby cells. Whatever its triggering can then become a chain reaction throughout a tissue. Half-lives are typically only seconds. Some breakdown products tend to be more stable though, and often these are what we measure and then infer the presence of the prostaglandin.
Prostaglandins fit within a larger family of hormones called eicosanoids.
If someone finds a really good text on them, online, free, please post a link.
PS If COX is the key, then all the eicosanoids may be affected, not just prostaglandins.
Think of them this way. They are one of several classes of hormones that a cell uses to communicate with itself and with nearby cells. Whatever its triggering can then become a chain reaction throughout a tissue. Half-lives are typically only seconds. Some breakdown products tend to be more stable though, and often these are what we measure and then infer the presence of the prostaglandin.
Prostaglandins fit within a larger family of hormones called eicosanoids.
If someone finds a really good text on them, online, free, please post a link.
PS If COX is the key, then all the eicosanoids may be affected, not just prostaglandins.
Maybe, in a large controlled study. As an individual, how do you tell what is due simply to activity? Exercise produces heat anyway. To use temperature as a measure would, I think, require many samples and statistical analysis.
A vegan diet probably provides a lot of resistant starch but there are many different types of prebiotics which feed different bacteria and thus produce vastly different effects. Diet is generally not enough to steer things in the gut in a better direction. A lot of people with ME/CFS eat really great clean diets and are still sick.
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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.
And I doubt the healthiest ones would live more than 30 years. With my SNPs and lifestyle, my real problems only started at 42.
And I doubt the healthiest ones would live more than 30 years. With my SNPs and lifestyle, my real problems only started at 42.
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In my defense, several months ago I bought a rebounder and could only use it for about 3-4 times for no longer than 30-40 seconds.
-by microscope
-a fast SED
you can look for gums bleeding, or easy bruising
[edit: the chances of a problem are probably very small, unless you have some special risk]
hypercoaguable blood would be a risk in Coronary Artery Disease (plaques, e.g) or Cerebral Vascular Accident (stroke) -- then also DVT, claudication (leg pain from blocked arteries), etc
I'd guess you'd want PT PTT INR or whatever, That's beyond me.
Thick blood might be from dehydration, then you'd see that in creatinine, BUN ratio (I think)
-a fast SED
you can look for gums bleeding, or easy bruising
[edit: the chances of a problem are probably very small, unless you have some special risk]
hypercoaguable blood would be a risk in Coronary Artery Disease (plaques, e.g) or Cerebral Vascular Accident (stroke) -- then also DVT, claudication (leg pain from blocked arteries), etc
I'd guess you'd want PT PTT INR or whatever, That's beyond me.
Thick blood might be from dehydration, then you'd see that in creatinine, BUN ratio (I think)
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There are the POTS people and others who would get more syncope from more NO mediated vasodilation --> lowered BP.
I have just realised that I have a genetic polymorphism (SNP) in the eNOS gene. The SNP is
G894T, which according to some sources leads to less nitric oxide, so less smooth muscle relaxation, and reduced platelet activity. Other names and details re the SNP:
The recommendation I have been given for this SNP is to take more omega-3, and I am now, but am also on a beta blocker for seriously-high blood pressure. I have long wondered why I suddenly developed high BP after it being normal for decades, and about ten years after getting ME. Something must have affected/amplified the way the SNP affects me, or maybe removed/inhibited something that was countering it. I did become briefly borderline obese about five years before the hypertension was spotted, and was overweight for maybe a decade.
But I always suspected that the immediate cause of my high bp was excessive vasoconstriction. Shame some/most doctors appear to have no interest in the cause of things and just throw drugs at them in a random way.
Looks like I could do with something that boosts nitric oxide.
G894T, which according to some sources leads to less nitric oxide, so less smooth muscle relaxation, and reduced platelet activity. Other names and details re the SNP:
- eNOS aka NOS3
- Ex8-63G>T
- rs1799983
- amino acid change Glu298Asp
The recommendation I have been given for this SNP is to take more omega-3, and I am now, but am also on a beta blocker for seriously-high blood pressure. I have long wondered why I suddenly developed high BP after it being normal for decades, and about ten years after getting ME. Something must have affected/amplified the way the SNP affects me, or maybe removed/inhibited something that was countering it. I did become briefly borderline obese about five years before the hypertension was spotted, and was overweight for maybe a decade.
But I always suspected that the immediate cause of my high bp was excessive vasoconstriction. Shame some/most doctors appear to have no interest in the cause of things and just throw drugs at them in a random way.
Looks like I could do with something that boosts nitric oxide.
How about a book from a Nobel Prize winning co-discoverer of NO, Louis Ignarro?
http://www.amazon.com/More-Heart-Disease-Prevent--Even-Reverse--Heart/dp/0312335822
Arginine, Citrulline, maybe also Mg. Probably won't work, though. I see he also has a newer book now.
http://www.amazon.com/More-Heart-Disease-Prevent--Even-Reverse--Heart/dp/0312335822
Arginine, Citrulline, maybe also Mg. Probably won't work, though. I see he also has a newer book now.
I don't have the time or energy to read books, I'm afraid. I have lots I haven't got round to reading! But I may try Mg sometime.
What are the other details about your NOS3 SNP? The letters, amino acids, etc. (I can't get into that site as I'm not registered.)
This is probably way off topic but I was researching sodium bicarbonate in a round about kind of way. I was trying to find a natural ACE inhibitor and stumbled upon SB. It's very interesting that it could be used for PEM as well. I don't have PEM anymore, but I have NO issues which I think may be related to ammonia, or histamines. It seems to all fit together somehow.