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Glycine

Overview

Glycine is a nonessential amino acid in food protein, including collagen and gelatin from cartilage, skin, and slow-cooked bone-in meats. The body can also make it. This page keeps that food constituent separate from glycine taken alone as a powder, tablet, or solution.

Glycine taken alone has its clearest nervous-system results in psychiatric illness, after weeks of high oral doses, and small high-bias trials reported better sleep after 3 g before bed [1]. A single much larger dose worsened sensorimotor gating and cognitive performance [1]. Glycine is also the amino acid added in the second step of glutathione assembly [2]. In older adults, glycine given with a cysteine precursor raised red-cell glutathione synthesis. That trial does not isolate glycine, and it did not measure the brain [3].

Dietary Origin

Foods supply glycine inside protein. Collagen and gelatin are rich in it, which is why cartilage, skin, and broths from bone-in cuts are grouped here as dietary sources. The human trials gave glycine by itself. In the psychiatric studies that was about 0.2–0.8 g per kilogram of body weight per day for 6–12 weeks. In the healthy sleep studies it was 3 g, taken 30–60 minutes before bed, for two to four days [1]. The glutathione result used glycine together with a cysteine precursor, not a serving of collagen-rich food [3].

Research Spotlights & Evidence Checks

🔎 Evidence Check · isolated-substance

Does glycine improve sleep in healthy adults?

Three small trials reported better sleep quality, alertness, and cognition, and less fatigue and sleepiness, after 3 g of glycine before bed for two to four days. The review rates that evidence as high risk of bias [1].

Read the evidence

The trials were in healthy adults, or in women dissatisfied with their sleep, and used flavoured glycine rather than food [1]. Sample sizes were about 10–19 people. The reviewers treat the healthy-adult sleep, fatigue, and alertness findings cautiously because of those sizes and the high risk of bias [1]. A separate four-week study in overactive bladder reported shorter sleep latency at 3 g twice a day. That is a different population and dose from the healthy bedtime trials [1].

A single oral dose of about 0.8 g per kilogram, or an intravenous dose of 200 mg per kilogram, worsened sensorimotor gating and cognitive performance in healthy adults [1]. The bedtime finding and that large single dose are different exposures.

🔎 Evidence Check · isolated-substance

Do the psychiatric findings apply to ordinary food?

The clearer symptom changes were in people with psychiatric illness, using high oral doses for 6–12 weeks. The review found limited evidence that glycine prevents nervous-system decline in healthy adults [1].

Read the evidence

Fifteen of 18 studies in illness reported a positive nervous-system change, most clearly for psychiatric symptoms in schizophrenia and related conditions, and in some of those studies for cognition or extrapyramidal symptoms [1]. The oral doses were about 0.2–0.8 g per kilogram of body weight per day, continued for 6–12 weeks. The reviewers suggest these effects may involve the NMDA receptor, and they say that explanation still needs testing [1]. The same review found limited evidence for a preventative effect in healthy people, and it calls for larger trials before glycine is used to prevent age-related decline [1].

Recipes

No recipes are linked through verified direct-content food relationships. Upstream dietary pathways are shown separately.

Foods

No verified food-composition relationship is currently recorded; this does not determine scientific admission.

Biological Regulatory Systems

Biological Regulatory System	Evidence-qualified relationship	Evidence
Methylation & One-Carbon Metabolism (BRS2)	Glycine is the amino acid added by glutathione synthetase in glutathione assembly. In older adults, glycine given with a cysteine precursor raised red-cell synthesis. A formula that removed methionine and cysteine slowed synthesis while glycine intake was increased, so that slowdown is not a glycine shortage.	[2,3,4]
Inflammation & Oxidative Stress (BRS3)	Glutathione precursor sufficiency treats glycine as able to co-limit glutathione synthesis with cysteine when synthesis is already low in older adults. The evidence is that same combined supplement.	[3]

References

[1] Soh et al. (2024). The effect of glycine administration on the characteristics of physiological systems in human adults: A systematic review. Review of glycine given by itself to adults. Nervous-system changes were clearest in psychiatric illness at high oral doses for several weeks. Healthy-adult sleep findings used 3 g before bed for a few nights and were small studies at high risk of bias. A large single dose worsened sensorimotor gating and cognitive performance. Combined supplements were outside the review.

[2] Polekhina et al. (1999). Molecular basis of glutathione synthetase deficiency and a rare gene permutation event. Human glutathione synthetase adds glycine in the second step of glutathione assembly and binds one magnesium ion per subunit. Enzyme structure, not a food trial.

[3] Sekhar et al. (2011). Deficient synthesis of glutathione underlies oxidative stress in aging and can be corrected by dietary cysteine and glycine supplementation. Older adults had lower red-cell glutathione synthesis than younger adults. Two weeks of N-acetylcysteine together with glycine raised that synthesis. The trial does not isolate glycine, does not measure the brain, and is not an ordinary-food result.

[4] Lyons et al. (2000). Blood glutathione synthesis rates in healthy adults receiving a sulfur amino acid-free diet. A diet containing neither methionine nor cysteine slowed whole-blood glutathione synthesis in healthy young men. Glycine in that formula was increased, so the slowdown is not a glycine deficit. Whole blood, not brain.

BRS matrix — individual KC inputs

BRS / PM	Relationship	Biological role and limitation
BRS3 · BRS3-FM1-PM1 BRS3(KC1)	Supported upstream supply	Glycine supplies a constituent of glutathione. Glutathione participates in the redox regulation of NF-κB kinase activity and DNA binding; this is upstream resource supply, not a direct NF-κB reaction substrate. Limitation: This is supported upstream supply, not a demonstrated dietary constraint on NF-κB. Human precursor supplementation measured red-cell glutathione, not NF-κB; cysteine was supplied as N-acetylcysteine together with glycine. Cellular redox studies show context-dependent effects, including inhibition after glutathione depletion or increased extracellular cysteine. Neither individual dietary limitation, brain transfer nor benefit from additional intake is established. Reynaert et al. (2006) [11] Mihm et al. (1995) [12] Sekhar et al. (2011) [13]
BRS3 · BRS3-FM1-PM2 BRS3(KC1)	Supported upstream supply	Glycine supplies a constituent of glutathione used in epithelial redox protection. Glutathione prevented oxidant-induced paracellular permeability in a cell model; this supports upstream supply to a barrier-protection route, not a proven dietary reduction in endotoxin spillover. Limitation: Supported upstream supply through glutathione-dependent epithelial redox protection, not an established dietary constraint on endotoxin spillover. Human precursor tracing measured red-cell glutathione after combined glycine and N-acetylcysteine; epithelial experiments measured oxidant-induced paracellular permeability. In Salmonella-infected rats, glutathione depletion did not increase permeability or bacterial translocation. Neither intestinal precursor inadequacy, individual constituent limitation, human LPS reduction nor benefit from additional intake is established. Sekhar et al. (2011) [11] Rao et al. (2000) [12] van Ampting et al. (2009) [13]