K2/Caffeine For Liver Health

[ecstatichamster]

I think it helped me a lot. But how can I really know?

I drink about 3 -5 strong espressos a day and take K2 MK4 most days. I don't get jittery from caffeine and can sleep when I drink coffee at night. I can go between meals without much trouble although I tend to eat pretty consistently during the day.

How would I know my liver is okay without getting an ultrasound and even then...?

 

[Cirion]

I notice this is somewhat of a thread necro, but I wasn't the one who necro'd it so... :p

Yes, because it can interfere with melatonin (just like sunshine should be exposed during the morning/day as part of the body's natural rythmn )

Is this really a problem? My understanding now is that melatonin is actually a hormone of torpor/anti metabolism, and that GABA is what you actually want to have restful sleep. You probably want a little melatonin, but I'd be willing to wager most people make way too much of it and thus never get restful sleep. Yes it helps you to get to sleep, but that sleep isn't restful (trust me I know from experience lol). From Nate's book F*** portion control (and I think RP talks about this too to a degree): the body has two modes of functionality: Activation, and Inhibition. Activation is where you are expending energy. Inhibition is where you are conserving/recharging energy. In a hypothyroid individual, activation is achieved primarily through stress hormones. In the same individual, inhibition is achieved primarily through torpor hormones like melatonin. But, in a healthy individual, activation is achieved through proper thyroid hormones along the kyurenine pathway of energy production, and inhibition is achieved primarily through GABA. From what I have learned, older individuals have declining melatonin production, and because most older individuals have thyroid problems as well, their inhibition is completely dysfunctional. This probably explains why they often don't sleep very long and wake up very early. In fact, continuing this line of discourse, it could also explain eventually why older people die. If your inhibition phase is compromised, your activation phase is going to be fueled using stress hormones. Eventually, the stress builds up (due to lack of inhibition), and kills you, either directly (dying in sleep, happens a lot to old people), or indirectly (degenerative disease).

How would I know my liver is okay without getting an ultrasound and even then...?

Probably by how long you can go without dropping temperature/pulse. If you can go the night, and wake up refreshed and fine without waking up in the middle of the night, you're probably good.

 

[Mauritio]

I notice this is somewhat of a thread necro, but I wasn't the one who necro'd it so... :p







Probably by how long you can go without dropping temperature/pulse. If you can go the night, and wake up refreshed and fine without waking up in the middle of the night, you're probably good.

Also caffeine tolerance seems to be quite a good measure . Think haidut posted a study on this somewhere on the forum...

 

[Amazoniac]

K2, just like caffeine, stimulates the liver to shed its fat.

Zeus, I keep reading posts from various members about this vitamin K property. Was it you who started based on personal experience? How does it work?

 

[haidut]

Zeus, I keep reading posts from various members about this vitamin K property. Was it you who started based on personal experience? How does it work?

The use of vitamin specifically for NAFLD was mentioned by Peat in several emails to people. He cited the studies below showing NAFLD precedes liver cancer and vitamin K preventing the latter. There are also studies on vitamin K preventing NAFLD specifically caused by toxins like "diethylnitrosamine" mentioned in one of the studies below. I think he also mentioned that vitamin K "antagonists" like warfarin are known to cause NAFLD and (naturally) vitamin K opposes this by opposing warfarin.
FEBS Press
https://www.journal-of-hepatology.eu/article/S0168-8278(07)00078-5/abstract

To the best of my memory, most of my own statements on vitamin K concerned its role and current large scale human trials on preventing/treating liver cancer as well as possibly "viral" hepatitis. Both of these are typically seen in the presence of NAFLD and amelioration of either condition typically also benefits the NAFLD too.
Though, I'd concede that caffeine has a much more direct evidence specifically for NAFLD.

 

[Amazoniac]

The use of vitamin specifically for NAFLD was mentioned by Peat in several emails to people. He cited the studies below showing NAFLD precedes liver cancer and vitamin K preventing the latter. There are also studies on vitamin K preventing NAFLD specifically caused by toxins like "diethylnitrosamine" mentioned in one of the studies below. I think he also mentioned that vitamin K "antagonists" like warfarin are known to cause NAFLD and (naturally) vitamin K opposes this by opposing warfarin.
FEBS Press
https://www.journal-of-hepatology.eu/article/S0168-8278(07)00078-5/abstract

To the best of my memory, most of my own statements on vitamin K concerned its role and current large scale human trials on preventing/treating liver cancer as well as possibly "viral" hepatitis. Both of these are typically seen in the presence of NAFLD and amelioration of either condition typically also benefits the NAFLD too.
Though, I'd concede that caffeine has a much more direct evidence specifically for NAFLD.

(carlos, 2012-19)

You've mentioned an improvement in liver enzymes from it, fast normalization, right? Is it easily lost early in liver issues? Were you previously deficient or is there anything unique in its use before serious liver complications develop that can't be attributed to nourished tissues from adequate nutrition (and so appliable to any missing nutrient)? I'm having trouble understanding how it can make the liver lean through therapeutic means.

https://www.journal-of-hepatology.eu/article/S0168-8278(07)00078-5/abstract

Did you also find it confusing? Not the experiment itself, but how they detail'd it, could've been simpler. Anyway..

"[..]several articles have described the promotion of hepatocarcinogenesis in rats or mice by low-choline diets, especially in the presence of carcinogens such as diethylnitrosamine (DEN) [12–16]."

"In the present study, we examined whether PC acts against hepatocarcinogenesis, as has been reported for MK-4, and whether combined administration of PC and MK-4 could inhibit growth of hepatic cancer cells in vitro and in vivo. Chemical carcinogenesis in the rat liver is a particularly well-studied experimental model of both initiation and promotion phases of cancer growth [17–20]. Accordingly, we initiated hepatocarcinogenesis with DEN enhanced by coadministration with phenobarbital (PB) [21,22] in rats subsequently treated with PC and MK-4."​

Phosphatidylcholine was almost as effective as its combination with mk-4:

Spoiler

Weeks counted from the start.
Experiment end'd after 20 weeks.

Groups..

A: normal diet
B: normal diet + injected carcinogen after 4 weeks + dietary carcinogen potentiator after 6 weeks
C: normal diet + injected carcinogen after 4 weeks + dietary carcinogen potentiator after 6 weeks + PC 16 mg/day/kg
D: normal diet + injected carcinogen after 4 weeks + dietary carcinogen potentiator after 6 weeks + PC 16 mg/day/kg and MK-4 10 mg/day/kg
E: normal diet + injected carcinogen after 4 weeks
F: normal diet + injected carcinogen after 4 weeks + PC 16 mg/day/kg and MK-4 10 mg/day/kg
G: normal diet + PC 16 mg/day/kg and MK-4 10 mg/day/kg
H: normal diet + injected only carcinogen vehicle (unrelated to cars)​

KaytwoN = the product combination of PC and MK-4.

"GST-P-positive foci are considered to be the first discernible evidence of tumor initiation in rat experiments [22,25,28]. Moreover, GST-P-positive foci are recognized to be putative preneoplastic lesions [17,22,33]."

And its dose seemed low (can be equivalent to a serving of your Mitolipid), maybe @ecstatichamster can help us judge. The mk-4 dose was definitely pharma.


Speaking of low-choline, in the 'Amino acids supplementation' thread you've stated something along the lines of not being a problem to exclude methionine from a formula for a while because most people have it accumulated. Do you know how exactly this build-up occurs? Would a theorsaicsalagwcal biopsy reveal?
Proper methylation depends on nutritional and metabolic state, but let's say that someone is fine in terms of regenerating methionine from homocysteine (and therefore not being detectable in blood), is it testable?
Providing ample micronutrition first must be one of the reasons why Gerson recommended avoidance of animal proteins at the beginning of the program, this way the body is finally able to metabolize whatever was impact'd, thereafter its inclusion is no longer problematic.


There's also the frequent comment that mk-4 can substitute coq10 where it's needed (I believe this one originated from Raj). How?

 

[haidut]

(carlos, 2012-19)

You've mentioned an improvement in liver enzymes from it, fast normalization, right? Is it easily lost early in liver issues? Were you previously deficient or is there anything unique in its use before serious liver complications develop that can't be attributed to nourished tissues from adequate nutrition (and so appliable to any missing nutrient)? I'm having trouble understanding how it can make the liver lean through therapeutic means.


Did you also find it confusing? Not the experiment itself, but how they detail'd it, could've been simpler. Anyway..

"[..]several articles have described the promotion of hepatocarcinogenesis in rats or mice by low-choline diets, especially in the presence of carcinogens such as diethylnitrosamine (DEN) [12–16]."

"In the present study, we examined whether PC acts against hepatocarcinogenesis, as has been reported for MK-4, and whether combined administration of PC and MK-4 could inhibit growth of hepatic cancer cells in vitro and in vivo. Chemical carcinogenesis in the rat liver is a particularly well-studied experimental model of both initiation and promotion phases of cancer growth [17–20]. Accordingly, we initiated hepatocarcinogenesis with DEN enhanced by coadministration with phenobarbital (PB) [21,22] in rats subsequently treated with PC and MK-4."​

Phosphatidylcholine was almost as effective as its combination with mk-4:

Spoiler

Weeks counted from the start.
Experiment end'd after 20 weeks.

Groups..

A: normal diet
B: normal diet + injected carcinogen after 4 weeks + dietary carcinogen potentiator after 6 weeks
C: normal diet + injected carcinogen after 4 weeks + dietary carcinogen potentiator after 6 weeks + PC 16 mg/day/kg
D: normal diet + injected carcinogen after 4 weeks + dietary carcinogen potentiator after 6 weeks + PC 16 mg/day/kg and MK-4 10 mg/day/kg
E: normal diet + injected carcinogen after 4 weeks
F: normal diet + injected carcinogen after 4 weeks + PC 16 mg/day/kg and MK-4 10 mg/day/kg
G: normal diet + PC 16 mg/day/kg and MK-4 10 mg/day/kg
H: normal diet + injected only carcinogen vehicle (unrelated to cars)​

View attachment 13675

View attachment 13676

KaytwoN = the product combination of PC and MK-4.

"GST-P-positive foci are considered to be the first discernible evidence of tumor initiation in rat experiments [22,25,28]. Moreover, GST-P-positive foci are recognized to be putative preneoplastic lesions [17,22,33]."

And its dose seemed low (can be equivalent to a serving of your Mitolipid), maybe @ecstatichamster can help us judge. The mk-4 dose was definitely pharma.


Speaking of low-choline, in the 'Amino acids supplementation' thread you've stated something along the lines of not being a problem to exclude methionine from a formula for a while because most people have it accumulated. Do you know how exactly this build-up occurs? Would a theorsaicsalagwcal biopsy reveal?
Proper methylation depends on nutritional and metabolic state, but let's say that someone is fine in terms of regenerating methionine from homocysteine (and therefore not being detectable in blood), is it testable?
Providing ample micronutrition first must be one of the reasons why Gerson recommended avoidance of animal proteins at the beginning of the program, this way the body is finally able to metabolize whatever was impact'd, thereafter its inclusion is no longer problematic.


There's also the frequent comment that mk-4 can substitute coq10 where it's needed (I believe this one originated from Raj). How?

I don't know of a hypo methionine-status test but since there is one for HYPER, then there is probably a slight variation of that test for HYPO.
Newborn screening information for hypermethioninemia | Baby's First Test | Newborn Screening | Baby Health

As far as vitamin K - I had elevated AST and ALT, and slightly elevated GGT back in 2014/2015 timeframe and 30mg MK-4 brought them back to normal within 3-4 days. I know because I was freaked out by the high values and has my doctor retest (against his wishes) only 4 days later. A 15mg dose was able to do the same in a week.
Vitamin K is known to be able to fill in for CoQ10.
Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency. - PubMed - NCBI
"...Human UBIAD1 localizes to mitochondria and converts vitamin K(1) to vitamin K(2). Vitamin K(2) is best known as a cofactor in blood coagulation, but in bacteria it is a membrane-bound electron carrier. Whether vitamin K(2) exerts a similar carrier function in eukaryotic cells is unknown. We identified Drosophila UBIAD1/Heix as a modifier of pink1, a gene mutated in Parkinson's disease that affects mitochondrial function. We found that vitamin K(2) was necessary and sufficient to transfer electrons in Drosophila mitochondria. Heix mutants showed severe mitochondrial defects that were rescued by vitamin K(2), and, similar to ubiquinone, vitamin K(2) transferred electrons in Drosophila mitochondria, resulting in more efficient adenosine triphosphate (ATP) production. Thus, mitochondrial dysfunction was rescued by vitamin K(2) that serves as a mitochondrial electron carrier, helping to maintain normal ATP production."

Vitamin K2 Prevents Lymphoma in Drosophila
"...We evaluated the inhibitory effect of VK2 on the progression and recurrence of lymphoma in Drosophila. When VK2 feeding was stopped, most lymphoma phenotypes recurred. We found that VK2 prevents lymphoma by acting as a mitochondrial electron carrier, which is necessary for establishing mitochondrial membrane potential and facilitating ATP production."

My suspicion is that several quinones can fulfill that function, including vitamin K, MB, and possibly "named" 1,4-benzoquinone, 1,2-benzoquinone, 1,2 and 1-4 naphthoquinones, etc.
Alternative Mitochondrial Electron Transfer for the Treatment of Neurodegenerative Diseases and Cancers: Methylene Blue Connects the Dots
Bypassing the compromised mitochondrial electron transport with methylene blue alleviates efavirenz/isoniazid-induced oxidant stress and mitochondria-mediated cell death in mouse hepatocytes
Alternative Mitochondrial Electron Transfer as a Novel Strategy for Neuroprotection

 

[Amazoniac]

I don't know of a hypo methionine-status test but since there is one for HYPER, then there is probably a slight variation of that test for HYPO.
Newborn screening information for hypermethioninemia | Baby's First Test | Newborn Screening | Baby Health

Cool, I didn't know it exist! I had in mind a functional deficiency with elevation of methionid. Why this isn't tested along with homocysteine more often (given that some people consume enough methionine and still benefit from SAMe supplements)? Do you use this test in your clinical practice? <calling lawyer>

--
Regarding the doses used in the ptdcholine and mk-4 experiment that you posted, should we extralotape based on requirements or body proportions?
By the way, isn't it curious that the choline was sourced from soy and still protected the animals?

 

[haidut]

Cool, I didn't know it exist! I had in mind a functional deficiency with elevation of methionid. Why this isn't tested along with homocysteine more often (given that some people consume enough methionine and still benefit from SAMe supplements)? Do you use this test in your clinical practice? <calling lawyer>

--
Regarding the doses used in the ptdcholine and mk-4 experiment that you posted, should we extralotape based on requirements or body proportions?
By the way, isn't it curious that the choline was sourced from soy and still protected the animals?

I think this test actually measures total "methylation status".
https://www.dhalab.com/shop/sam-esah-methylation-profile-plasma/

In general, even testing SAM-E would probably be good enough as if SAM-E is low then methionine stores are also probably low, even though it could also mean low metabolism as SAM-E depends also on ATP.
Sometimes they hydrogenate the PC extracted from soy so it has much longer shelf life. So, if it does not say anything in the actual study I would not assume it was PUFA PC.

 

[Amazoniac]

I think this test actually measures total "methylation status".
https://www.dhalab.com/shop/sam-esah-methylation-profile-plasma/

In general, even testing SAM-E would probably be good enough as if SAM-E is low then methionine stores are also probably low, even though it could also mean low metabolism as SAM-E depends also on ATP.
Sometimes they hydrogenate the PC extracted from soy so it has much longer shelf life. So, if it does not say anything in the actual study I would not assume it was PUFA PC.

When you commented about people having an excess of methionine, what did you have in mind? Isn't the excess supposed to be degraded? No sarcasm.

--
They didn't specify which one was used in the living, it seemed to be the one from soy. The following is all that was available and either was effective in glass. But I don't know if it was supplied hydrogenated.

"All PC (obtained at 96.5% purity from soybeans), MK-4, and KaytwoN, which contains 5 mg MK-4/ml and 8 mg PC/ml, were kindly supplied by Eisai Pharmaceutical (Tokyo, Japan)."

"Additionally, we performed MTT assays using PC (approximate purity 99%) extracted from egg yolk (Sigma–Aldrich) rather than soybeans to confirm that observed growth inhibition was caused by PC and not soybean-derived impurities."

"Similar to PC from soybeans, PC from egg yolk showed dose-dependent growth inhibition in Hep-3B and Hep-G2 cultures (data not shown). Thus, PC showed growth-inhibitory effects on human hepatic cancer cell lines."​

 

[Amazoniac]

Choline has much to do with the oxidation of fats. That it prevents the conversion of amino acids and of sugars to fats under the influence of cholesterol, it seems there is sufficient evidence when the rest of the oxidation mechanism is normal. It does not aid the burning of aceto-acetic acid, but where the rest of the oxidation mechanism is sound, its presence favors the burning of fats or their precursors by another route. It is, therefore, an important link in the oxidation mechanism, but of course where the oxidation process is otherwise impaired we must assume that it not only fails to function and therefore accumulates or is formed in greater quantity for compensation than normally occurs; and worst of all it is not burned itself and produces its toxic effects. Thus one might well assume that it is a factor in coronary disease, much like cholesterol is in other vascular degeneration that are so well known. In fact they both accumulate where the normal catalysis of oxidation is broken, and therefore both coronary disease and atheromatous degeneration and arterial sclerosis depend upon one basic deficiency, a crippled oxidation catalysis." "Vascular normalcy is important to tissue function and obliterative vascular disease so often the cause of tissue degeneration that one might say that all disease shows its marks on the vascular system early or late. The infectious granulomata all start out with an obliterative endarteritis. Cancer does also, and cancer should be classified with the granulomata. They are all based upon toxic activity that destroys oxidation catalysis. They are all curable by restoration of the oxidation catalysis to normal or to better than normal.

 

[haidut]

When you commented about people having an excess of methionine, what did you have in mind? Isn't the excess supposed to be degraded? No sarcasm.

Humans likely do not need more than 2mg/kg methionine daily. Anything more than that is excess. I don't think all excess is degraded but even if the extra is simply converted to more SAM-E and cysteine that's probably not desirable. Most people consume WAY more than 2mg/kg methionine daily.
The Impact of Dietary Methionine Restriction on Biomarkers of Metabolic Health
"...Calorie restriction without malnutrition, commonly referred to as dietary restriction (DR), results in a well-documented extension of life span. DR also produces significant, long-lasting improvements in biomarkers of metabolic health that begin to accrue soon after its introduction. The improvements are attributable in part to the effects of DR on energy balance, which limit fat accumulation through reduction in energy intake. Accumulation of excess body fat occurs when energy intake chronically exceeds the energy costs for growth and maintenance of existing tissue. The resulting obesity promotes the development of insulin resistance, disordered lipid metabolism, and increased expression of inflammatory markers in peripheral tissues. The link between the life-extending effects of DR and adiposity is the subject of an ongoing debate, but it is clear that decreased fat accumulation improves insulin sensitivity and produces beneficial effects on overall metabolic health. Over the last 20 years, dietary methionine restriction (MR) has emerged as a promising DR mimetic because it produces a comparable extension in life span, but surprisingly, does not require food restriction. Dietary MR also reduces adiposity but does so through a paradoxical increase in both energy intake and expenditure. The increase in energy expenditure fully compensates for increased energy intake and effectively limits fat deposition. Perhaps more importantly, the diet increases metabolic flexibility and overall insulin sensitivity and improves lipid metabolism while decreasing systemic inflammation. In this chapter, we describe recent advances in our understanding of the mechanisms and effects of dietary MR and discuss the remaining obstacles to implementing MR as a treatment for metabolic disease."
Methionine-Restriction Diet (MRD) in Obese Adults With Metabolic Syndrome - Full Text View - ClinicalTrials.gov

 

[PurpleHeart]

I actually think that k2 is extremely important i actually made the connection recently.

Long story short i had an accident that left me with some fractures and the doctors gave me warfarin injections.
I was at a bad place at the time so i didn't even question it.
I was injecting that rat poison on my belly every day and my health started going downhill from there.
Only recently i made the connection that the depleted vitamin k levels from the warfarin is what causes my health to worsen.

 

[berk]

I've spent some time trying to find the threads where this is talked about, and there were several, so it got confusing. I wanted a thread for those who have done the protocol, are doing it, or thinking about it.

Some background: I was told I have mildly fatty liver a few years ago. I've never had weight issues, other than occasional gains that seem like insulin resistance (being on ssri's, being sedentary and eating too much over the winter, etc.) but mostly normal weight.

I gained the most weight of my life after eating this Peat way (25 pounds, most of it came on from last Jan - June), I figure the fattiness in my liver probably got worse. I suspect cortisol problems (probably had them my whole life), plus I have other issues like PCOS, and this weight gain might have happened to me even if I wasn't eating the Peat foods. however, though I've gained weight before, it was never this hard to lose before.

I did manage to get the weight gain to stop at least, by last July, but losing anything has been impossible, even with weights, walking, calorie restrictions, changing up macros, eliminating certain foods, taking supplements, and so on.

With the estrogen dominance and other issues, I figure it's not necessarily the "Peat" foods I'm eating causing huge issues (though eating too much or too little calories contributes no doubt), but my body is in a mildy hypo state and can't do the things with the food that it should for maximum health. There's something else going on under the surface preventing the weight loss. For example, I tried eating high protein (at least 80 g.) for a long time, but it didn't help my liver like it was supposed to. I feel the liver could be the source of many problems, and until I get it's main problems taken care of it feels like I'm putting a bandaid on. Another example, I love how progest e helps with estrogen dominance symptoms, but even months of taking high doses did not correct things (get my body to produce more progesterone). So there's something getting in the way of things. I've been doing this peat stuff for going on 2 years, and there should be more improvement, imo. BTW, I don't take thyroid and don't want to go that route if I can work on things another way.

This is getting too long, so let me say that what I I"M hoping if I can get my liver in shape, that would surely help a number of problems right at the source.

The supplements are K2 and Caffeine. Optional are Taurine and Glycine.

I know K2 amount is 15 mg. What is the caffeine amount? I saw 400 mg. (divided dose of course) mentioned.

I have had plenty of caffeine daily for a long, long time (most of my life), and that hasn't seemed to help my problem. So perhaps caffeine alone isn't enough for me to clear up my liver of the estrogens and other toxins.

I started yesterday with 15 mg. K2, divided. So, 5 mg. am, afternoon, before bed. I didn't get the caffeine nearly high enough since I've been feeling high cortisol and caffeine bothers me, but today I feel better, and so I plan to increase caffeine.

I know there were some success stories on the forum already with this. Would love to hear from anyone on this topic of fatty liver, clearing it up, dosages, etc.

you started this topic in 2015, now its 2020.
What are your results?

 

[maillol]

As far as vitamin K - I had elevated AST and ALT, and slightly elevated GGT back in 2014/2015 timeframe and 30mg MK-4 brought them back to normal within 3-4 days. I know because I was freaked out by the high values and has my doctor retest (against his wishes) only 4 days later. A 15mg dose was able to do the same in a week.

After you lowered your liver values with 4 days of 30mg, your liver values became elevated again at some point leading you to do the week of 15mg?

 

[Mauritio]

Bump

 

[Dr. B]

Charlie, didn't your teeth get bad from K2? Could it be a vitamin D deficiency? Maybe K2 requires high D?

whats going on with K2 and teeth, are the teeth getting crooked or what kind of effects

 

[ddjd]

Humans likely do not need more than 2mg/kg methionine daily. Anything more than that is excess. I don't think all excess is degraded but even if the extra is simply converted to more SAM-E and cysteine that's probably not desirable. Most people consume WAY more than 2mg/kg methionine daily.
The Impact of Dietary Methionine Restriction on Biomarkers of Metabolic Health
"...Calorie restriction without malnutrition, commonly referred to as dietary restriction (DR), results in a well-documented extension of life span. DR also produces significant, long-lasting improvements in biomarkers of metabolic health that begin to accrue soon after its introduction. The improvements are attributable in part to the effects of DR on energy balance, which limit fat accumulation through reduction in energy intake. Accumulation of excess body fat occurs when energy intake chronically exceeds the energy costs for growth and maintenance of existing tissue. The resulting obesity promotes the development of insulin resistance, disordered lipid metabolism, and increased expression of inflammatory markers in peripheral tissues. The link between the life-extending effects of DR and adiposity is the subject of an ongoing debate, but it is clear that decreased fat accumulation improves insulin sensitivity and produces beneficial effects on overall metabolic health. Over the last 20 years, dietary methionine restriction (MR) has emerged as a promising DR mimetic because it produces a comparable extension in life span, but surprisingly, does not require food restriction. Dietary MR also reduces adiposity but does so through a paradoxical increase in both energy intake and expenditure. The increase in energy expenditure fully compensates for increased energy intake and effectively limits fat deposition. Perhaps more importantly, the diet increases metabolic flexibility and overall insulin sensitivity and improves lipid metabolism while decreasing systemic inflammation. In this chapter, we describe recent advances in our understanding of the mechanisms and effects of dietary MR and discuss the remaining obstacles to implementing MR as a treatment for metabolic disease."
Methionine-Restriction Diet (MRD) in Obese Adults With Metabolic Syndrome - Full Text View - ClinicalTrials.gov

Haidut if you had to choose between methionine and cysteine as being the most negative for health which would it be?

 

[Dr. B]

Haidut if you had to choose between methionine and cysteine as being the most negative for health which would it be?

What about histidine, tryptophan and others