232 replies to this topic

[resveratrol_guy]

I think further experiments with glycine and blood sugar are warranted. For the record, what brand are you using, docmaas?

 

For what it's worth, here is where I got the French data. It's a list of 172 countries and their Alzheimer's rates. Admittedly, it's very dirty data, but I think there are still conclusions that can be drawn. I don't think it's a huge surprise that the charts are topped by Western countries.

[docmaas]

I'm uisng NOW brand 1000mg caps and bulk supplements 1kg bags from Amazon.  Just finished the first kg and will be starting the second later today.  

 

I think that since my normal diet is not pure sugar that I will use 1/2 bagel for the next trial.  I suspect that carbs from bagels stick around long enough that when the glycine is consumed or discarded the blood glucose goes up again.  Not sure if this would happen with sucrose or not.  What do you or anyone else think?  The advantage to sucrose was that it is relatively easy to get equivalent doses between runs.

 

 I notice that when I eat popcorn I can drop the blood glucose quickly with a dose of glycine but the next morning it will be back up again.  Popcorn seldom raises it to dangerous levels though -- usually around 128 which is good since I do like it for a snack.  

 

Mike

[resveratrol_guy]

I'm uisng NOW brand 1000mg caps and bulk supplements 1kg bags from Amazon.  Just finished the first kg and will be starting the second later today.  

 

I think that since my normal diet is not pure sugar that I will use 1/2 bagel for the next trial.  I suspect that carbs from bagels stick around long enough that when the glycine is consumed or discarded the blood glucose goes up again.  Not sure if this would happen with sucrose or not.  What do you or anyone else think?  The advantage to sucrose was that it is relatively easy to get equivalent doses between runs.

 

 I notice that when I eat popcorn I can drop the blood glucose quickly with a dose of glycine but the next morning it will be back up again.  Popcorn seldom raises it to dangerous levels though -- usually around 128 which is good since I do like it for a snack.  

 

Mike

 

A bagel would be a realistic test of glycine vs. SAD diet, indeed. My expectation is that, because it takes some time to convert all that white fluffy industrial goodness into sugar, you would indeed see the dip followed by a resurgence, unless glycine somehow triggers insulin signalling above and beyond what any amino acid would do.

 

So a broader question is... can glycine reduce the amplitude of blood sugar swings over a few weeks of use, like oxaloacetate can reportedly do? If you accumulate enough data, we might get some clue as to the answer. This is entwined with the question of whether glycine actually stimulates a cascade of epigenetic changes like, say, rapamycin or pterostilbene, or whether it's really not more much than another mundane amino acid.

 

BTW you're very brave to be consuming bagels and popcorn in the name of science. So thanks for that, but please don't do too many such experiments in a short period of time, lest you end up in hospital.

[timbur]

I think further experiments with glycine and blood sugar are warranted. For the record, what brand are you using, docmaas?

 

For what it's worth, here is where I got the French data. It's a list of 172 countries and their Alzheimer's rates. Admittedly, it's very dirty data, but I think there are still conclusions that can be drawn. I don't think it's a huge surprise that the charts are topped by Western countries.

 

I found that site too, showing death rate per 100,000 from Alzheimer's.  There, France is #13 here whereas USA is #2.  Based on your comments, I expected to see France higher than #13 in death rate.  On another site, I read that the disease prevalence is most common in Western Europe, with North America being close behind.  But I couldn't find any outright statistics with a few minutes of searching.

 

Anyway, your hypothesis of high protein intake being detrimental is interesting.

[stefan_001]

I think further experiments with glycine and blood sugar are warranted. For the record, what brand are you using, docmaas?

For what it's worth, here is where I got the French data. It's a list of 172 countries and their Alzheimer's rates. Admittedly, it's very dirty data, but I think there are still conclusions that can be drawn. I don't think it's a huge surprise that the charts are topped by Western countries.

I found that site too, showing death rate per 100,000 from Alzheimer's. There, France is #13 here whereas USA is #2. Based on your comments, I expected to see France higher than #13 in death rate. On another site, I read that the disease prevalence is most common in Western Europe, with North America being close behind. But I couldn't find any outright statistics with a few minutes of searching.

Anyway, your hypothesis of high protein intake being detrimental is interesting.

I find it more interesting that Greece is so low on the list. What is different with them that they have so different stats than the rest of Europe?

[deeptrance]

I'm surprised there's no discussion of sarcosine in this thread. Sarcosine is a not only a precursor to glycine, it is also a glycine reuptake inhibitor and it has potentially desirable properties of its own. 

 

In preparing to post this comment I searched for comparable research on sarcosine that would mirror the studies on glycine, and cannot find much other than a few studies regarding sarcosine's effect on symptoms of schizophrenia, and one study which found it to be effective in treating depression. Theoretically, it might be useful to supplement this substance if one is practicing MR since it is one of the products of methionine metabolism.

 

Opinions?

[resveratrol_guy]

@ timbur: Dr. Luigi Fontana lamented back in 2007 or so that human caloric restriction failed to lower IGF1. At the time, it was his hypothesis that cutting protein intake to a bare minimum would reduce IGF1, thereby providing a bit more life extension and a bit less by way of inflammation. Sorry, this is just from my memory of his presentation, so I have no link. Personally, on my own caloric restriction regime, I can definitely say that minimizing my protein intake minimizes both bloating (due to drinking too much water?) and brain fog. On the minus side, I have not maintained much musculature. It would be interesting if you could sneak glycine-rich methionine-poor proteins past the IGF1 machinery without it noticing; I rather suspect this is the case, as otherwise the life extension ramifications thereof would be much harder to explain. But don't run out and buy a pound of almonds just yet, because there's this problem.

 

@ stefan_001: Good observation! Cheap and easy access to olive oil, I would presume. Hilly terrain helps too, to the extent that it forces cardiovascular exercise. IMO Alzheimer's usually starts with a breakdown of the blood-brain barrier, which olive oil would protect via increasing HDL production and providing some beneficial polyphenols.

 

@ deeptrance: Sounds like sarcosine deserves its own thread.

 

[Kevnzworld]

I take 5000 mg of BCAA's providing 2500 mg of Leucine, the amino acid responsible for muscle synthesis .
I also take Creatine, 2000 mg and HMB
Both mitigate middle/older age muscle breakdown and sarcopenia.
No methionine.
Both Creatine and BCAA's have been shown to offer modest life extension in rodents. Creatine also blocks the formation of lipofuscin .

[Darryl]

Hashizume O et al. 2015. Epigenetic regulation of the nuclear-coded GCAT and SHMT2 genes confers human age-associated mitochondrial respiration defects. Scientific reports, 5.

Age-associated accumulation of somatic mutations in mitochondrial DNA (mtDNA) has been proposed to be responsible for the age-associated mitochondrial respiration defects found in elderly human subjects. We carried out reprogramming of human fibroblast lines derived from elderly subjects by generating their induced pluripotent stem cells (iPSCs), and examined another possibility, namely that these aging phenotypes are controlled not by mutations but by epigenetic regulation. Here, we show that reprogramming of elderly fibroblasts restores age-associated mitochondrial respiration defects, indicating that these aging phenotypes are reversible and are similar to differentiation phenotypes in that both are controlled by epigenetic regulation, not by mutations in either the nuclear or the mitochondrial genome. Microarray screening revealed that epigenetic downregulation of the nuclear-coded GCAT gene, which is involved in glycine production in mitochondria, is partly responsible for these aging phenotypes. Treatment of elderly fibroblasts with glycine effectively prevented the expression of these aging phenotypes. 

 

 

Because continuous glycine treatment restored respiration defects in elderly human fibroblasts, glycine supplementation may be effective in preventing age-associated respiration defects and thus benefiting the health of elderly human subjects.

 

[Phoenicis]

Waluk, D. P. Et al. (2012). Reversible Lysine Acetylation Regulates Activity of Human Glycine N-Acyltransferase-like 2 (hGLYATL2) IMPLICATIONS FOR PRODUCTION OF GLYCINE-CONJUGATED SIGNALING MOLECULES. Journal of Biological Chemistry, 287(20), 16158-16167.

OGAWA, H. Et al. (1997). Recombinant expression of rat glycine N-methyltransferase and evidence for contribution of N-terminal acetylation to co-operative binding of S-adenosylmethionine. Biochem. J, 327, 407-412.

Edited by Phoenicis, 27 October 2015 - 11:18 PM.

[IWS]

I read that taurine promotes some way the nitric oxide production and that taurine and glycine seem similar (for example acting on same receptors) so my question is does glycine promote or inhibit endogenous nitric oxide production ? I know that the glycine propionyl L-carnitine compound increases the NO but i'm interested to know about the glycine alone, I cannot find a clear answer, I have to take NO donors by medical prescription and before taking a large amount of glycine for inflammation (which worked fine for me in the past) would like to be sure that it wouldnt interfere, thanks for your help.

[Kevnzworld]

I take 5000 mg of BCAA's providing 2500 mg of Leucine, the amino acid responsible for muscle synthesis .
I also take Creatine, 2000 mg and HMB
Both mitigate middle/older age muscle breakdown and sarcopenia.
No methionine.
Both Creatine and BCAA's have been shown to offer modest life extension in rodents. Creatine also blocks the formation of lipofuscin .

Here are some references...
Re; Branch Chained Amino Acids/ Leucine :
http://www.sciencedi...550413110003049
Branched-Chain Amino Acid Supplementation Promotes Survival and Supports Cardiac and Skeletal Muscle Mitochondrial Biogenesis in Middle-Aged Mice
http://jn.nutrition....130/2/139.short
http://journals.lww....ation_of.6.aspx

BCAAem supplementation increases the average life span of male mice
BCAAem activates mTOR and eNOS signaling pathways
BCAAem increases mitochondrial biogenesis and ROS defense system in middle-aged mice
BCAAem supplementation improves age-related muscle deficits
http://www.cell.com/...t/S1550-4131(10)00304-9

Re : HMB
http://www.super-sup...ntervention.pdf

Re : Creatine
http://search.proque...igsite=gscholar
The effects of age on skeletal muscle and the phosphocreatine energy system: can creatine supplementation help older adults
http://www.dynamic-m...m/content/8/1/6
http://www.lifeexten...f-aging/page-01

[LaViidaLocaa]

 

I take 5000 mg of BCAA's providing 2500 mg of Leucine, the amino acid responsible for muscle synthesis .
I also take Creatine, 2000 mg and HMB
Both mitigate middle/older age muscle breakdown and sarcopenia.
No methionine.
Both Creatine and BCAA's have been shown to offer modest life extension in rodents. Creatine also blocks the formation of lipofuscin .

Here are some references...
Re; Branch Chained Amino Acids/ Leucine :
http://www.sciencedi...550413110003049
Branched-Chain Amino Acid Supplementation Promotes Survival and Supports Cardiac and Skeletal Muscle Mitochondrial Biogenesis in Middle-Aged Mice
http://jn.nutrition....130/2/139.short
http://journals.lww....ation_of.6.aspx

BCAAem supplementation increases the average life span of male mice
BCAAem activates mTOR and eNOS signaling pathways
BCAAem increases mitochondrial biogenesis and ROS defense system in middle-aged mice
BCAAem supplementation improves age-related muscle deficits
http://www.cell.com/...t/S1550-4131(10)00304-9

Re : HMB
http://www.super-sup...ntervention.pdf

Re : Creatine
http://search.proque...igsite=gscholar
The effects of age on skeletal muscle and the phosphocreatine energy system: can creatine supplementation help older adults
http://www.dynamic-m...m/content/8/1/6
http://www.lifeexten...f-aging/page-01

 

 

It's pretty much accepted that these substances stimulate muscle building (or, in the case of HMB, work anti-catabolic), but without sufficient protein intake, you will still be disadvantaged. 

 

On Topic: interesting reads about Glycine, will be incorporating it soon myself!

[Phoenicis]

New open access paper on SAMe, GNMT, glycine and sarcosine.

Btw I'm getting really interested in sarcosine. Just me, or does glycine look poised to become a central pillar of current longevity enhancement?

SAMe + glycine > Gnmt > sarcosine + SAH
Sarcosine > sarcosine oxidase > glycine + Co2

Obata, F., & Miura, M. (2015). Enhancing S-adenosyl-methionine catabolism extends Drosophila lifespan. Nature communications, 6:

"Methionine restriction extends the lifespan of various model organisms. Limiting S-adenosyl-methionine (SAM) synthesis, the first metabolic reaction of dietary methionine, extends longevity in Caenorhabditis elegans but accelerates pathology in mammals. Here, we show that, as an alternative to inhibiting SAM synthesis, enhancement of SAM catabolism by glycine N-methyltransferase (Gnmt) extends the lifespan in Drosophila. Gnmt strongly buffers systemic SAM levels by producing sarcosine in either high-methionine or low-sams conditions. During ageing, systemic SAM levels in flies are increased. Gnmt is transcriptionally induced in a dFoxO-dependent manner; however, this is insufficient to suppress SAM elevation completely in old flies. Overexpression of gnmt suppresses this age-dependent SAM increase and extends longevity. Pro-longevity regimens, such as dietary restriction or reduced insulin signalling, attenuate the age-dependent SAM increase, and rely at least partially on Gnmt function to exert their lifespan-extending effect in Drosophila. Our study suggests that regulation of SAM levels by Gnmt is a key component of lifespan extension."

http://www.nature.co...ncomms9332.html

Edited by Phoenicis, 30 October 2015 - 12:26 AM.

[Dracula]

Today I have seen the dragon.

[Phoenicis]

Interesting new study on the gut microbiome's role in glutathione sythesis and its dependance on glycine:

 

• Mardinoglu, A. et al. (2015). The gut microbiota modulates host amino acid and glutathione metabolism in mice. Molecular systems biology, 11(10), 834.
• http://www.scienceda...51106062708.htm

 

 

 

[motorcitykid]

New open access paper on SAMe, GNMT, glycine and sarcosine.

Btw I'm getting really interested in sarcosine. Just me, or does glycine look poised to become a central pillar of current longevity enhancement?

SAMe + glycine > Gnmt > sarcosine + SAH
Sarcosine > sarcosine oxidase > glycine + Co2

Obata, F., & Miura, M. (2015). Enhancing S-adenosyl-methionine catabolism extends Drosophila lifespan. Nature communications, 6:

"Methionine restriction extends the lifespan of various model organisms. Limiting S-adenosyl-methionine (SAM) synthesis, the first metabolic reaction of dietary methionine, extends longevity in Caenorhabditis elegans but accelerates pathology in mammals. Here, we show that, as an alternative to inhibiting SAM synthesis, enhancement of SAM catabolism by glycine N-methyltransferase (Gnmt) extends the lifespan in Drosophila. Gnmt strongly buffers systemic SAM levels by producing sarcosine in either high-methionine or low-sams conditions. During ageing, systemic SAM levels in flies are increased. Gnmt is transcriptionally induced in a dFoxO-dependent manner; however, this is insufficient to suppress SAM elevation completely in old flies. Overexpression of gnmt suppresses this age-dependent SAM increase and extends longevity. Pro-longevity regimens, such as dietary restriction or reduced insulin signalling, attenuate the age-dependent SAM increase, and rely at least partially on Gnmt function to exert their lifespan-extending effect in Drosophila. Our study suggests that regulation of SAM levels by Gnmt is a key component of lifespan extension."

http://www.nature.co...ncomms9332.html

 

 

Does anyone care to guess what the implications might be for someone(me) taking 400mg of SAMe on a daily basis? I"m worried that I might be helping to catapult myself toward the golden years.

 

I drop my SAMe in the morning and I sprint in the evening. Taking SAMe offers significant pain relief for my knees. I'd hate to have to give SAMe the boot from my supplement regimen.

 

I don't know if it would make much sense to take glycine along with SAMe, as they might just cancel each other out.

 

Any thoughts on this appreciated.

 

Edited by motorcitykid, 09 November 2015 - 06:41 AM.

[motorcitykid]

 

New open access paper on SAMe, GNMT, glycine and sarcosine.

Btw I'm getting really interested in sarcosine. Just me, or does glycine look poised to become a central pillar of current longevity enhancement?

SAMe + glycine > Gnmt > sarcosine + SAH
Sarcosine > sarcosine oxidase > glycine + Co2

Obata, F., & Miura, M. (2015). Enhancing S-adenosyl-methionine catabolism extends Drosophila lifespan. Nature communications, 6:

"Methionine restriction extends the lifespan of various model organisms. Limiting S-adenosyl-methionine (SAM) synthesis, the first metabolic reaction of dietary methionine, extends longevity in Caenorhabditis elegans but accelerates pathology in mammals. Here, we show that, as an alternative to inhibiting SAM synthesis, enhancement of SAM catabolism by glycine N-methyltransferase (Gnmt) extends the lifespan in Drosophila. Gnmt strongly buffers systemic SAM levels by producing sarcosine in either high-methionine or low-sams conditions. During ageing, systemic SAM levels in flies are increased. Gnmt is transcriptionally induced in a dFoxO-dependent manner; however, this is insufficient to suppress SAM elevation completely in old flies. Overexpression of gnmt suppresses this age-dependent SAM increase and extends longevity. Pro-longevity regimens, such as dietary restriction or reduced insulin signalling, attenuate the age-dependent SAM increase, and rely at least partially on Gnmt function to exert their lifespan-extending effect in Drosophila. Our study suggests that regulation of SAM levels by Gnmt is a key component of lifespan extension."

http://www.nature.co...ncomms9332.html

 

 

Does anyone care to guess what the implications might be for someone(me) taking 400mg of SAMe on a daily basis? I"m worried that I might be helping to catapult myself toward the golden years.

 

I drop my SAMe in the morning and I sprint in the evening. Taking SAMe offers significant pain relief for my knees. I'd hate to have to give SAMe the boot from my supplement regimen.

 

I don't know if it would make much sense to take glycine along with SAMe, as they might just cancel each other out.

 

Any thoughts on this appreciated.

 

 

I took Life Extension's SAMe(400mg) this morning (as I do every morning) along with B-Complex and 500mg of sublingual B-12. As an experiment, I added 2.5 grams of glycine. 

 

I usually get a noticeable mind buzz accompanied with a good mood spike when I take the above-mentioned SAMe stack (without glycine). The mind buzz usually kicks in about 15 minutes after taking it and peaks at about 25 minutes.

 

With the 2.5 grams of glycine thrown into the mix, there was no mind buzz, no uplifting mood. Nada.

 

 

[aribadabar]

Glycine has anxiolytic effect so your reaction is understandable.

[motorcitykid]

Glycine has anxiolytic effect so your reaction is understandable.

 

Appologies for not being clear in my last post.

 

I'm aware of glycine's anxiolytic effect but I was wondering if what I experienced has more to do with glycine "buffering" SAMe(as stated in the paper Phoenics posted).

 

If glycine is in fact buffering the exogenous SAMe that I"m taking, then I wont be getting any of the pain relief benefits(knee pain) from taking SAMe along with glycine. 

 

You see, I want to keep my knee pain at bay by popping me SAMe's, but I'm concerned about  SAMe shortening my life.

 

It's hard to come to terms with the idea that SAMe is liver protective, joint protective, and exerts a positive effect on mood yet the very same supplement might be contributing to a shorter lifespan. 

 

 Wishful Speculation: maybe it's the active metabolism of methionine into SAMe that contributes to a shorter lifespan, and SAMe is just the smoking gun. If that were the case, I could continue taking SAMe without worry.

Edited by motorcitykid, 11 November 2015 - 02:07 AM.

[Logic]

You see, I want to keep my knee pain at bay by popping me SAMe's, but I'm concerned about  SAMe shortening my life.

 

It's hard to come to terms with the idea that SAMe is liver protective, joint protective, and exerts a positive effect on mood yet the very same supplement might be contributing to a shorter lifespan. 

 

 Wishful Speculation: maybe it's the active metabolism of methionine into SAMe that contributes to a shorter lifespan, and SAMe is just the smoking gun. If that were the case, I could continue taking SAMe without worry.

 

 

http://www.longecity...ndpost&p=750272

[deeptrance]

Interesting new study on the gut microbiome's role in glutathione sythesis and its dependance on glycine:

• Mardinoglu, A. et al. (2015). The gut microbiota modulates host amino acid and glutathione metabolism in mice. Molecular systems biology, 11(10), 834.
• http://www.sciencedaily.com/releases/2015/11/151106062708.htm

 

I don't recommend the first article to anyone who isn't willing to temporarily memorize dozens of obscure acronyms and pore over the arcane presentation of the complex research. Instead, you'll find the glycine-related takeaway below, excerpted from the Science Daily press release:

 

"Some bacteria in our gut consume glycine, which is required for the synthesis of the glutathione, and imbalances in the composition of the bacteria may lead to the progression of the chronic diseases," says Chalmers researcher Adil Mardinoglu, first author of the paper.

In previous independent studies, imbalances in the plasma level of glycine as well as other amino acids have been shown to exist in obesity, type 2 diabetes and non-alcoholic fatty liver disease.

"Strikingly, the plasma levels of glycine are decreased in all subjects with the above-mentioned diseases compared to the healthy subjects," says Professor Jens Nielsen at Chalmers. "In this context, it may be of interest to study the microbial amino acids in the human gut in relation to their potential role in the development of such metabolism-related disorders.

"The discovery that the bacteria in our small intestine consume glycine and regulate glutathione metabolism may led to the development of food products that can deliver beneficial bacteria (probiotics) to the gut. The results of the study can help us understand how bacteria play a role in the metabolic processes involved in the development of obesity, type 2 diabetes, non-alcoholic fatty liver disease and malnutrition."

 

 

What are the implications for supplementation with glycine? It certainly suggests the necessity of adequate amounts of dietary glycine but says little about taking glycine to higher levels than would be obtained from a healthy diet. Still, it adds one more potential benefit to the growing list of reasons why it might be useful to supplement glycine.

[motorcitykid]

 

You see, I want to keep my knee pain at bay by popping me SAMe's, but I'm concerned about  SAMe shortening my life.

 

It's hard to come to terms with the idea that SAMe is liver protective, joint protective, and exerts a positive effect on mood yet the very same supplement might be contributing to a shorter lifespan. 

 

 Wishful Speculation: maybe it's the active metabolism of methionine into SAMe that contributes to a shorter lifespan, and SAMe is just the smoking gun. If that were the case, I could continue taking SAMe without worry.

 

 

http://www.longecity...ndpost&p=750272

 

 

Thanks!

 

[motorcitykid]

I'd also like to add that when I took approx 4grams of glycine along with my B-complex, I was quite surprised to not have experienced the accompanying niacin flush. I always experience a niacin flush when I take Jarrow's B-complex.

 

Maybe glycine blocks the absorption of niacin.

 

Edited by motorcitykid, 11 November 2015 - 06:45 PM.

[Dracula]

I find it cool that glycine has the lowest atomic weight of all amino acids :D

[Kalliste]

Added 20-30g of gelatine powder 5 days a week to my regimen. Tastes alright and cheap enough. Have not felt any clear effects.

[motorcitykid]

I wonder if an extreme, long term methionine restricted diet might not be a good thing.

 

According to this info http://www.ncbi.nlm....pubmed/18331185  methionine deficiency has been shown to cause to fatty liver disease.

[docmaas]

I wonder if an extreme, long term methionine restricted diet might not be a good thing.

 

According to this info http://www.ncbi.nlm....pubmed/18331185  methionine deficiency has been shown to cause to fatty liver disease.

 

But there is also this:

 

http://www.fasebj.or...Abstracts/528.2

 

I already posted this earlier in the thread and wrote to the author for more info but never received a response so I have no further info.

 

Mike

[niner]

I wonder if an extreme, long term methionine restricted diet might not be a good thing.

 

According to this info http://www.ncbi.nlm....pubmed/18331185  methionine deficiency has been shown to cause to fatty liver disease.

 

Well, it wasn't just methionine deficiency, but rather a deficiency in all labile methyl groups (choline, methionine, betaine, folate).  Thus the problem here isn't lack of Met, but lack of methyl groups.  Further, they're talking about an actual deficiency, while what we're doing with glycine is more like met restriction-- in other words, the idea is to have enough Met, but not too much.  So our situation is different from this paper in two ways, both quantitative and qualitative.

[motorcitykid]

 

I wonder if an extreme, long term methionine restricted diet might not be a good thing.
 
According to this info http://www.ncbi.nlm....pubmed/18331185  methionine deficiency has been shown to cause to fatty liver disease.

 
Well, it wasn't just methionine deficiency, but rather a deficiency in all labile methyl groups (choline, methionine, betaine, folate).  Thus the problem here isn't lack of Met, but lack of methyl groups.  Further, they're talking about an actual deficiency, while what we're doing with glycine is more like met restriction--
in other words, the idea is to have enough Met, but not too much.

 
This is the thought that floated through my mind while estimating what an optimal daily dose of glycine might be as it relates to MR.   It seems some people are taking upwards of 10grams, that sounded a bit high to me and then I came across the above cited paper. Understood that the paper does not directly apply to what we're doing w/ MR, but still had me thinking because methionine was one of the methyl groups mentioned.

This paper shows glycine alleviates liver injury induced by defeciency in methionine:
 
http://www.ncbi.nlm....pubmed/22913202

EDIT: Fixed attributions.

Edited by niner, 16 November 2015 - 09:56 PM.