Glycine, should we be taking it?

Taking 4 grams per day and I haven't grown an extra limb. Beginning to question its effectiveness but 4 grams is nothing substantial anyway. Thanks for the links

Bryan

Came across better evidence of the relative merits of USP glycine vs collagen/gelatin/bone broth with respect to oxalate kidney stones.

Holmes et al, 2007. Origin of urinary oxalate. In Renal Stone Disease (Vol. 900, pp. 176-182).

HepG2 cells possess pathways to metabolize both hydroxyproline and glycine to glycolate and oxalate, but much more is produced from hydroxyproline as the concentration used was 1/200 that of glycine. The daily turnover of glycine in the body, however, may be 200 times that of hydroxyproline. There is a single catabolic pathway for hydroxyproline degradation where one mole of the amino acid results in the formation of one mole of glyoxylate. This glyoxylate can subsequently be converted to glycolate, oxalate and glycine. In contrast, glycine has numerous metabolic fates, including a decarboxylation, a conversion to serine and utilization in protein synthesis as well as oxidation to glyoxylate.

 

A 10-fold differential in the amounts of glycolate and oxalate formed from hydroxyproline and glycine apparently occurs regardless of the subcellular compartmentation of the site of glyoxylate formation (mitochondria for hydroxyproline and peroxisome for glycine).

 

The metabolism of hydroxyproline can potentially make an important contribution to oxalate synthesis as collagen turnover leads to the metabolism of 240 to 420 mg of hydroxyproline each day. Hydroxyproline may be also ingested either as collagen in meats and meat products or as gelatin. We have recently shown that the ingestion of gelatin leads to significant increases in urinary oxalate and glycolate excretion.

Edited by Darryl, 04 October 2016 - 08:35 PM.

 

Came across better evidence of the relative merits of USP glycine vs collagen/gelatin/bone broth with respect to oxalate kidney stones.

 

Holmes et al, 2007. Origin of urinary oxalate. In Renal Stone Disease (Vol. 900, pp. 176-182).

HepG2 cells possess pathways to metabolize both hydroxyproline and glycine to glycolate and oxalate, but much more is produced from hydroxyproline as the concentration used was 1/200 that of glycine. The daily turnover of glycine in the body, however, may be 200 times that of hydroxyproline. There is a single catabolic pathway for hydroxyproline degradation where one mole of the amino acid results in the formation of one mole of glyoxylate. This glyoxylate can subsequently be converted to glycolate, oxalate and glycine. In contrast, glycine has numerous metabolic fates, including a decarboxylation, a conversion to serine and utilization in protein synthesis as well as oxidation to glyoxylate.

 

A 10-fold differential in the amounts of glycolate and oxalate formed from hydroxyproline and glycine apparently occurs regardless of the subcellular compartmentation of the site of glyoxylate formation (mitochondria for hydroxyproline and peroxisome for glycine).

 

The metabolism of hydroxyproline can potentially make an important contribution to oxalate synthesis as collagen turnover leads to the metabolism of 240 to 420 mg of hydroxyproline each day. Hydroxyproline may be also ingested either as collagen in meats and meat products or as gelatin. We have recently shown that the ingestion of gelatin leads to significant increases in urinary oxalate and glycolate excretion.

 

 

Knight et al. 2006. Hydroxyproline ingestion and urinary oxalate and glycolate excretion. Kidney international,70(11), pp.1929-1934.

Responses to the ingestion of 30 g of gelatin or whey protein were compared on controlled oxalate diets. The time course of metabolism of a 10 g gelatin load was determined as well as the response to varying gelatin loads. Urinary glycolate excretion was 5.3-fold higher on the gelatin diet compared to the whey diet and urinary oxalate excretion was 43% higher. Significant changes in plasma hydroxyproline and urinary oxalate and glycolate were observed with 5 and 10 g gelatin loads, but not 1 and 2 g loads. Extrapolation of these results to daily anticipated collagen turnover and hydroxyproline intake suggests that hydroxyproline metabolism contributes 20–50% of glycolate excreted in urine and 5–20% of urinary oxalate derived from endogenous synthesis. 

 

I recently came across Hydroxycitrate reserach stating that it can bind to and enable the excretion of calcium oxalate crystals in humans. Maybe gelatin/glycine treatment could be combined with HCA?  

This thread is too long, too complicated, and too confusing for me to digest.

Let me explain a couple of the glycine effects that I comprehend. Of course there is much much more that is beyond me.

"Glycine helps control blood sugar"

1) When glycine is consumed with glucose or any carbohydrate digestible into glucose, the pair stimulates the gut release of GIP (but no GLP-1, the other incretin).

2) The pancreas produces much more insulin in response to incretins than to glucose.

     a) The pancreas produces a big insulin spike when it see GIP, but if and only if the glucose level is elevated above baseline.

     b) The pancreas produces a big insulin spike when it sees the other incretin GLP-1 independent of glucose level.

     c) GIP cannot cause hypoglycemia because the pancreas quits responding to it when glucose returns to baseline.

3) Other amino acids, especially the combination in gelatin, stimulate the gut to release GLP-1. GLP-1 produces a big insulin spike independent of glucose. (To what purpose? Perhaps in preparation for gorging on a kill.)

4) The area under the glucose curve is cut in half when glycine is taken with glucose,  (glycine+glucose) -> GIP,  (GIP+glucose) -> big insulin spike. After glucose drops GIP is ignored and insulin rapidly drops (no hypoglycemia). GIP is a peptide that does not survive when taken orally. It has to be released directly into the portal vein from the gut wall.

 "Glycine is a CR mimetic". 

1) Glycine taken on an empty stomach stimulates the gut to release glucagon. No incretins are released. (Glucagon producing cells in the gut is a recent discovery). Increased serum glucagon after glycine on an empty stomach is well established.

2) The liver chooses between insulin response and glucagon response depending on the insulin/glucagon ratio, independent of absolute values. (Tested with 100:1 variation in absolute values). The normal resting insulin in the liver is high enough that the glucagon released from the gut has no effect on the liver.

In the pancreas the normal resting insulin is very high, inhibiting glucagon production. (In glucagon response mode, the liver releases glucose, first by depleting glycogen stores, then by entering neoglucogenesis). The take away here - there is no glucagon response from the liver following glycine ingestion on an empty stomach.

3) Adipose cells are more sensitive to glucagon than the liver. Ingesting glycine on an empty stomach produces enough glucagon to inhibit lipoprotein lipase (LPL) in adipose tissue (stops adipose tissues from feeding on the triglycerides in VLDL and chylomicrons) and stimulates lipolysis (shifts the balance between the on going lipogenesis and lipolysis) This is the well known adipose tissue response to glucagon. Fat cells start breaking down triglycerides and dumping FFA's. FFA's are transported by albumin.Typically, 20% of FFA's get burned and 80% get relocated.

Daily consumption of glycine on an empty stomach can shrink belly fat and love handles! provided you don't replace it all at meal time.

4) Inhibiting LPL in adipose tissue will keep your triglycerides (VLDL and chylomicrons) in circulation, making your lipid test TRIGS go up, unless you increase your exercise.

Side note: Llipoprotein lipase in muscle tissue is not affected by glucagon. LPL in muscle tissue is usually disabled and only enabled by exercise. ie muscles feed on triglycerides only in response to exercise. Muscle catabolism on the other hand occurs during neoglucogenesis during which the liver requires a supply of amino acids from the muscles.

Edited by RWhigham, 03 November 2016 - 10:31 PM.

Are there any decent sources for Glycine-Alpha-KetoGlutarate?

http://www.ergo-log....supplement.html

I sense this is an important animal study, in particular due to the marked effect on systemic LPS. I'd love to see it replicated in humans.

Zhou et al, 2016. Glycine protects against high sucrose and high fat-induced non-alcoholic steatohepatitis in rats. Oncotarget.

 

We set out to explore the hypothesis that glycine attenuates non-alcoholic steatohepatitis (NASH) in rats and the possible mechanism by which is it does. Male Sprague-Dawley (SD) rats were fed a diet containing high fat and high sucrose (HSHF) for 24 weeks to induce NASH... Compared with control animals, the content of alanine transaminase (ALT), triglycerides (TGs), and free fatty acids (FFAs) in plasma and the TG and FFA content in the liver was increased from week 4 to 24. The level of TNFα and MCP-1 in plasma, the content of TNFα in the liver, the insulin resistance index, inflammatory cell infiltration, hepatocyte apoptosis, reactive oxygen species (ROS) generation, and endoplasmic stress-associated protein expression ... were significantly elevated in HSHF fed rats at 12 weeks. At the same time, the level of endotoxin progressively increased from 0.08 ± 0.02 endotoxin EU/ml at week 4 to 0.7 ± 0.19 EU/ml at week 24. Moreover, these rats had elevated blood endotoxin levels, which were positively associated with their NASH indexes. Liver histology progressively worsened over the course of the study. However, we found that with concomitant treatment with glycine, the level of endotoxin decreased, while NASH indexes significantly decreased and liver status markedly improved.

 

The C group received regular diet and tap water; the H group (high sucrose and high fat group, n = 24) received high sucrose and high fat diet (HSHF; 52% of calories from carbohydrates, 25% from fat, and 10% from protein); the H+G group (high sucrose and high fat + glycine) received the HSHF diet and 3.5 g/kg of glycine per day, while the G group received 3.5 g/kg of glycine per day and a regular diet

 

 

I sense this is an important animal study, in particular due to the marked effect on systemic LPS. I'd love to see it replicated in humans.

No human study, but this author discusses LPS inhibiting mechanisms of spirulina, glycine, folate, metformin, and berberine.  http://catalyticlong...s-to-endotoxin/ "Sepsis is a leading cause of death in hospitalized patients who have developed infections with gram negative bacteria. A cell wall component in these bacteria, known as lipopolysaccharide (LPS) or endotoxin, triggers this syndrome by strongly activating immune cells known as macrophages, which subsequently secrete a wide range of pro-inflammatory, pro-coagulant and vasodilatory compounds that can collaborate to induce circulatory shock and damage to vital organs." He goes on to recommend a stack for sepsis (to be taken with antibiotic)

http://www.functiona...ective-glycine/  -  glycine LPS-inhibition.

[From my notes]

LPS is bad news, but inhibiting it may prevent your immune system from attacking gram-negative bacteria.

When LPS is absorbed from the gut without any functional bacteria (the usual source), then inhibition is highly desirable.

Probably should stop occasionally, letting your immune system clean out gram-negative bacteria.

LPS inhibitors include - glycine, garlicin, spirulina, metformin, lipoic acid, high-folate, and berberine.

However, as little as 500 mcg/d of folate taken long term has sometimes caused CNS damage.

Berberine may cause DNA damage, and it lowered my blood glucose from 55 (ok) to 45 (felt poorly) mg/dl when fasting.

I discontinued lipoic acid years ago for some forgotten reason.

Metformin lowered my TSH causing the doctor to cut my thyroxine. I discontinued metformin until after my next TSH test.

Glycine (10-15g/d), garlicin (4 tabs/d), and Nutrex spirulina (2 tbsp/d) are in my stack 5 days/wk.

as little as 500 mcg/d of folate taken long term has sometimes caused CNS damage.

Can you provide some references for this conclusion?

 

Can you provide some references for this conclusion?

"During three decades of neurological practice I have witnessed a remarkable change in attitudes to the benefits and risks of folic acid therapy in nervous system disorders. In the 1960s all that was known and taught was that folic acid was harmful to the nervous system." 

"Savage and Lindenbaum³¹ reviewed reports of 38 patients with vitamin B12 deficiency treated with 1 mg or less of folic acid, 30% of whom showed a significant haematological response. Of 25 patients treated for seven to 19 days, none developed nervous system disorder, whereas of 12 treated for 90 to 930 days six did so. Isolated examples of a reticulocyte response and neurological deterioration were seen with doses of folic acid as low as 0.3 to 0.5 mg daily. As in the case of the benefits of folic acid, and for the same reasons, the duration of folic acid therapy may be as important as the dose of the vitamin." 

"Such is the new enthusiasm for the preventive potential of folic acid for neural tube defects and possibly for vascular disease that the United States FDA has authorised fortification of grains with folic acid since 1 January 1998,⁸ and similar suggestions are being made in the United Kingdom.⁹ Some of the advocates of these policies have cast doubt on or even dismissed the risks of folic acid to the nervous system".

http://jnnp.bmj.com/...t/72/5/567.full

So while essential to have enough folate, "high-folate dosing" may be contraindicated (except short-term, such as in a  stack to reduce LPS while fighting gram negative bacteremia.)

The substitution of "folic acid" for folate as if they are equivalent is unfortunate. Folic acid in supplements instead of true folate (eg methylfolate) is an anachronism from the past. Folic acid =! folate. Folic acid has to be converted to folate in vivo. The required MTHFR gene is frequently mutated and defective leaving people folate deficient. 

https://www.ncbi.nlm...les/PMC1123448/

A lot of illness may be caused by unrecognized folate deficiency, including mental illness.

https://www.ncbi.nlm...les/PMC1123448/

Folic acid may saturate the transport system into the CNS, and interfere with actual folate getting into the CNS. https://www.ncbi.nlm...pubmed/10213373

Edited by RWhigham, 18 November 2016 - 09:02 PM.

Thanks for the info!

Folate was interchangeably used with folic acid while we all know it it is not the same then , incorrectly IMO, compared in vitro with in vivo results and while both substances were used and appeared to cause similar reactions.

I will dismiss this (methyl)folate "concern" at 500 mcg/d as insufficiently corroborated, especially in light of MTHFR gene mutation which I am carrier of. 

Chances are that it is most probably net positive,even taken long-term, given its beneficial effect on so many etiologies .

This glyine angle is potentially huge. I ironically ended up supplementing with collagen/gelatin through a very different logic, not emphasizing the role of glycine. Yet, I always intuited that there is something special about glycine. As the smallest amino acid, it should logically be in the highest demand as a building block. Then this thread provided the connection to the gut biota. Anything big for health should have that connection. And glycine does. It is also soothing for us all having downed 30-50 gelatin capsule vitamin and mineral pills for ages...that eating all those pills was at least to some benefit After all, they are all coated in gelatin capsules being high on glycine. I even wonder if some placebo effects could, to some degree, be explained by gelatin pills.

Anyhow, want to provide a few additional angles:

1) the enzyme producing glycine needs vit B6 to work. In its active P5P form. Yet many of us have genetic issues with phosphorylation, so probably best to supplement as pyridoxine. But the point being that this vitamin is easily rate limiting for many things in the body, including glycine production.

2) TMG is short for trimethylglycine. I have always had a strong response to that compound. Note that TMG (betaine) is about 2/3 glycine by molecular weight, rest of its weight are the 3 CH3 or methyl group moities. Now what a super molecule this should be. The three methyl groups provide methyl groups to the methylation cycle, yet the glycine moiety will convert some methionine out of the methylation cycle. Wow !!! So the methylation cycle revs faster and better, yet also excess methionine is sucked out of it lessening the methylation demands. Can it get any better? Yes. Buy it as betaine HCL The HCL moiety then helps wih digestion and increases the acidicity in the digestive system, which helps with good bacteria and, who knows, might knock down some of the bad bacteria draining your glycine pool. WIN - WIN - WIN.

3) Creatine. Is formed in part of glycine. Interestingly creatine production uses a massive amount of methyl groups. So, stack creatine with TMG for synergy? As actually many sports suppements already do. Not sure how big of a drain cretatine production is on your glycine levels. But could be huge, as it surely is for methyl groups. So, supplement with preformed creatine to reduce both the metabolic stress on your methyl group and glycine levels.

4) Phosphatidylcholine. This is the other big drain on your methylation system, in addition to creatine production that is. Choline is closely related to TMG (betaine). Actually converted to it. And then further converted to glycine. Betaine, glycine and choline deficiencies all have very similar impact e.g. on liver. So, hike up choline consumption also through something like lecithin.

So, a stack like glycine + collagen/gelatin + lecithin (choline) + creatine + TMG (betaine) should be very good for most of us. And, incidentally, more or less my classic stack, save for the separate glycine part. But I have been eating a ton of magnesium glycinate and TMG for years.

It all makes sense, from yet another angle. In particular, I find it fascinating that bacteria, also of the pathogenic human gut biota type, basically convert choline to TMG type compounds for osmolytic purposes. That can use up a lot of glycine in your gut. So drown them in glycine and TMG ... and thereby make sure that you, the primary organism in your body, have enough of them to go around.

Finally, I started supplementing with free form L-threonine some years ago, once I realized that it was the moiety doing the magic of the magnesium threonate compound. Think of it as magnesium being the carrier of threonate through the blood brain barrier. This was actually also just recently also confirmed through a scientific study, but was pretty obvious even before. To digress, it could be the glycine doing most of the magic in the magnesium glycinate compund that many people so like. Anyhow, threonine gets converted to glycine through the enzyme coded by the GCAT gene. That is the one using B6. So, maybe add free form threonine to your regime, like I did some years ago. Again, ironically, for entirely different reasons.

Edited by Ukko, 20 November 2016 - 07:38 AM.

One addition. Also SHMT2 is involved together with GCAT in the production of glycine within our cells. Both were involved as key findings in that Japanese study involing glycine and mitochondrial aging. Interestingly, both SHMT2 and GCAT depend on vitamin B6 to work. Cannot work without B6. So, make sure you get enough B6.

http://ajcn.nutritio...138594.abstract

Results: Supplementation with increasing amounts of gelatin increased circulating glycine, proline, hydroxyproline, and hydroxylysine, peaking 1 h after the supplement was given. Engineered ligaments treated for 6 d with serum from samples collected before or 1 h after subjects consumed a placebo or 5 or 15 g gelatin showed increased collagen content and improved mechanics. Subjects who took 15 g gelatin 1 h before exercise showed double the amino-terminal propeptide of collagen I in their blood, indicating increased collagen synthesis.

Finally, I started supplementing with free form L-threonine some years ago, once I realized that it was the moiety doing the magic of the magnesium threonate compound. Think of it as magnesium being the carrier of threonate through the blood brain barrier. This was actually also just recently also confirmed through a scientific study, but was pretty obvious even before. To digress, it could be the glycine doing most of the magic in the magnesium glycinate compund that many people so like. Anyhow, threonine gets converted to glycine through the enzyme coded by the GCAT gene. That is the one using B6. So, maybe add free form threonine to your regime, like I did some years ago. Again, ironically, for entirely different reasons.

Are you sure you're taking the right stuff?  Magnesium threonate is a salt of trihydroxy butanoic acid, also known as threonic acid.  L-threonine, on the other hand, is a small amino acid.  It probably won't hurt you, but it's unlikely to act the same way that magnesium threonate would act.

 

Finally, I started supplementing with free form L-threonine some years ago, once I realized that it was the moiety doing the magic of the magnesium threonate compound. Think of it as magnesium being the carrier of threonate through the blood brain barrier. This was actually also just recently also confirmed through a scientific study, but was pretty obvious even before. To digress, it could be the glycine doing most of the magic in the magnesium glycinate compund that many people so like. Anyhow, threonine gets converted to glycine through the enzyme coded by the GCAT gene. That is the one using B6. So, maybe add free form threonine to your regime, like I did some years ago. Again, ironically, for entirely different reasons.

 

Are you sure you're taking the right stuff?  Magnesium threonate is a salt of trihydroxy butanoic acid, also known as threonic acid.  L-threonine, on the other hand, is a small amino acid.  It probably won't hurt you, but it's unlikely to act the same way that magnesium threonate would act.

 

You are correct. I did make the mistake of mixing Threonic Acid with L-Threonine. But the irony is that Threonine has been useful in its own right. Both for the digestive tract and then also as a subtance to create glycine.

Just in case you have not seen the last blog by Josh Mitteldorf on mitochondrial health which includes glycine:

http://joshmitteldor...d-mitochondria/

"Glycine

The theory in the Japanese paper is that glycine treats the downstream symptom of epigenetic reprogramming in the mitochondria.  In other words, glycine does not stop the detrimental epigenetic changes in mitochondria that come with age, however one of the most important of these changes results in a glycine shortage in the mitochondria.  Hence, glycine supplementation effectively attacks the problem at an intermediate stage.

Could a molecule as simple (non-specific) as glycine be an anti-aging compound?  Glycine comes to us with a sketchy but promising history.  In one rat study, a hefty dose of glycine increased lifespan by 27% longer than controls.  “Hefty” is the human equivalent of ~3 ounces per day.  I’m tentatively filing this study in the “too good to be true” drawer, because it appeared only as a conference abstract 5 years ago and has never been fleshed out with a peer-reviewed full text.

A shortage of protein has a powerful anti-aging effect across many species.  And a shortage of one critical amino acid–methionine–is sufficient to trigger this response.  This may be because methionine is the “start codon”; every gene begins with a methionine, and a severe shortage of methionine can slow down all protein synthesis.  

Directly engineering a shortage of methionine in the human body is just too difficult to manage, because too many protein foods have methionine, and we’re too fond of protein.  (Animal proteins are consistently loaded with methionine, whereas some vegetable sources have less.)  In studies of lab animals, a methionine shortage is engineered by using fully artificial protein sources, constituted from individual amino acids.  People would never want to live this way on synthetic food, even if we could afford it; but using glycine to create a methionine shortage sounds more palatable.  Glycine plays a role in breaking down methionine in the liver, and if the glycine level is jacked up super-high, it is (theoretically) possible to force this reaction so far as to create a methionine shortage.

For some of us, methionine restriction holds up the tantalizing prospect of gaining benefits of dietary restriction while allowing us to eat to satiety.  But the idea remains untested in humans.  Protein deficiency can lead to loss of strength and endurance and the ability to concentrate–even as it increases life expectancy.  Depression is another risk.  Rats that have tried methionine restriction are not recommending it for humans; in fact, they quickly come to crave methionine; they recognize methionine-deficient foods and shun them.

On the other hand, there are other diverse benefits documented for glycine supplementation, beginning with better sleep, insulin sensitivity and cancer resistance.  A minimum of 3 or 4 grams is required to have any effect.  You can buy it in powder form by the pound.  From Finland, here’s Valdu Heiskanen’s comprehensive page on glycine."

Edited by albedo, 06 February 2017 - 05:43 PM.

Note that SENS Question of the month had a feature on Glycine and that famous Japanese study.

I started supplementing Glycine because of this thread, but my experience wasn't good:
 
https://www.reddit.c...ee_times_and_i/
 
Plus, the research scares me: 

Glycine-induced CA1 excitotoxicity in the rat hippocampal slice

The electrophysiological pattern of glycine injury was similar to the excitotoxic damage produced by 8 min exposure to sodium glutamate 9 mM.

http://www.sciencedi...006899395004653
 
 
Glycine-induced neurotoxicity in organotypic hippocampal slice cultures.
https://www.ncbi.nlm...pubmed/15490133
 

Contribution of endogenous glycine site NMDA agonists to excitotoxic retinal damage in vivo. 

These results suggest that the severity of excitotoxic retinal damage in vivo depends on the levels of both glycine and D-serine.

https://www.ncbi.nlm...pubmed/16934894
 

Progression of ischaemic stroke and excitotoxic aminoacids.

43 (33.6%) patients had progressing ischaemic stroke. Concentrations of glutamate and glycine in plasma and CSF were higher in patients with progressing stroke than in those with stable cerebral infarcts (p < 0.0001).

https://www.ncbi.nlm.../pubmed/8996418


Glycine antagonist and NO synthase inhibitor protect the developing mouse brain against neonatal excitotoxic lesions.
https://www.ncbi.nlm...pubmed/10088651
 
 
The role of D-serine and glycine as co-agonists of NMDA receptors in motor neuron degeneration and amyotrophic lateral sclerosis (ALS)

Previous studies in our laboratory examining levels of common amino acids in CSF in ALS showed significant increases in four amino acids (L-threonine, glycine, L-valine and L-phenylalanine) compared to controls, the greatest change being an increase of 57% in glycine

https://www.ncbi.nlm...les/PMC3997022/

Another bad experience with Glycine in this forum:

http://www.longecity...ion-to-glycine/

Edited by William Sterog, 08 February 2017 - 11:04 AM.

Interesting results, would the result for the supplement-part of the papers you linked be different if they used whole Gelatine instead of isolated glycine?

Is it also possible that it has some downsides but generally improve lifespan? (Hormesis)

Interesting results, would the result for the supplement-part of the papers you linked be different if they used whole Gelatine instead of isolated glycine?

 

Is it also possible that it has some downsides but generally improve lifespan? (Hormesis)

I was wondering the same thing. Also, I think that Proline, also present in gelatin, plays a role in the cognitive enhancements seen with glycine peptides.

http://www.longecity...as-a-nootropic/

 

Interesting results, would the result for the supplement-part of the papers you linked be different if they used whole Gelatine instead of isolated glycine?

 

Is it also possible that it has some downsides but generally improve lifespan? (Hormesis)

 

I was wondering the same thing. Also, I think that Proline, also present in gelatin, plays a role in the cognitive enhancements seen with glycine peptides.

 

http://www.longecity...as-a-nootropic/

 

Any risk of BSE with beef gelatins?  That would be a drag to supplement the stuff for your brain health only to fall victim to prions.  I was thinking about picking up "Marine Collagen Peptides" although I'm also curious if these might easily be contaminated with PCBs / dioxin-like compounds as such.  It's a drag the ocean is getting so dirty.

Edited by brosci, 09 February 2017 - 10:49 PM.

Resident member Logic posted some good info on source a while back, I cant find it now. Chicken gelatine was supposed to be good.

Resident member Logic posted some good info on source a while back, I cant find it now. Chicken gelatine was supposed to be good.

I think you refer to earlier posts in this thread. Around post #150 there is an interesting discussion about glycine vs gelatine.

But this other thread mentions pros and cons and recommendations:

http://www.longecity...cine-for-sleep/

Examin.com does not have any reservations about glycine:

https://examine.com/...ements/Glycine/

And here is a very recent overview of all benefits:

https://www.hindawi....l/2017/1716701/

This looks bad.

Cutting out certain amino acids -- the building blocks of proteins -- from the diet of mice slows tumor growth and prolongs survival, according to new research published in Nature.

https://www.scienced...70419130352.htm

This looks bad.

Cutting out certain amino acids -- the building blocks of proteins -- from the diet of mice slows tumor growth and prolongs survival, according to new research published in Nature.

Researchers at the Cancer Research UK Beatson Institute and the University of Glasgow found that removing two non-essential amino acids -- serine and glycine -- from the diet of mice slowed the development of lymphoma and intestinal cancer.

https://www.scienced...70419130352.htm

Thanks for sharing VP, I have also stopped taking glycine, at least until additional proof comes in....

Edited by Harkijn, 26 April 2017 - 05:41 PM.

I added it to my stack for anxiety, I take 3 grams a day because that is what it says to take on the bottle. My stack seems to be working. Glycine is an inhibitory neurotransmitter.

Edited by Jiminy Glick, 28 April 2017 - 12:38 PM.

 

This looks bad.

Cutting out certain amino acids -- the building blocks of proteins -- from the diet of mice slows tumor growth and prolongs survival, according to new research published in Nature.

Researchers at the Cancer Research UK Beatson Institute and the University of Glasgow found that removing two non-essential amino acids -- serine and glycine -- from the diet of mice slowed the development of lymphoma and intestinal cancer.

https://www.scienced...70419130352.htm

Thanks for sharing VP, I have also stopped taking glycine, at least until additional proof comes in....

 

On the other hand, after reading this study:

Serine, but Not Glycine, Supports One-Carbon Metabolism and Proliferation of Cancer Cells”.
cell.com/cell-reports/abstract/S2211-1247(14)00347-7

and after coming across this very recent description:

https://www.hindawi....l/2017/1716701/

I am considering to take glycine again.

Edited by Harkijn, 02 May 2017 - 08:12 AM.

Reading about Glycine here brought me to this from Examine.com:

"D-Serine is another molecule that acts on the same receptor classes that glycine can, but appears to be practically more potent since it is cleared from the receptors at a lower rate"

Here D-Serine is discussed.

"D-Serine shares many mechanisms similar to Glycine, in the sense that it can bind to the glycine-dependent binding site on NMDA receptors (the subtype of NR1,[63][64] as NR2 binds glutamate[65]and any one NMDA receptor is a tetramer made of usually two of each) which then potentiates signalling through these NMDA receptors initially caused by glutamate or other agonists.[63][6][66]Unlike glycine, D-Serine appears to be more effective and is active at a concentration as low as 1µM (Glycine requiring 10µM)[6] which may not be related to their acting on the receptor itself (the two are quite comparable[3][4][5]) but may be due to less glial cell reuptake of serine than there is with glycine."

The effect matrix nearly duplicates Glycine (lacking sleep aid effect), but continues with interesting things like "Subjective Wellbeing" and "Working Memory" and "Attention".

D-Serine is not the naturally occurring L-Serine.

Wikipedia:

"D-Serine, synthesized in the brain by serine racemase from L-serine (its enantiomer), serves as a neuromodulator by coactivating NMDA receptors, making them able to open if they then also bind glutamate. D-serine is a potent agonist at the glycine site (NR1) of the NMDA-type glutamate receptor (NMDAR). For the receptor to open, glutamate and either glycine or D-serine must bind to it; in addition a pore blocker must not be bound (e.g. Mg2+ or Pb2+).^[11] In fact, D-serine is a more potent agonist at the glycine site on the NMDAR than glycine itself.

D-serine was thought to exist only in bacteria until relatively recently; it was the second D amino acid discovered to naturally exist in humans, present as a signalling molecule in the brain, soon after the discovery of D-aspartate. Had D amino acids been discovered in humans sooner, the glycine site on the NMDA receptor might instead be named the D-serine site.^[12] Apart from central nervous system, D-serine plays a signaling role in peripheral tissues and organs such as cartilage,^[13] kidney^[14] and corpus cavernosum.^[15]"

Has anyone tried supplementing with D-Serine? It fairly cheap, such as this.

Joseph Cohen wrote an article about why methionine is good and why restriction might be bad: https://selfhacked.c...ne-restriction/

What do you guys think of this? I know we do need methionine to make SAMe to methylate DNA.