A reference work, not a recommendation to use: this profile describes mechanism and evidence and does not replace medical advice. The claims come from marketing and forums and are tested here, not endorsed.

Claims checked

  • Better sleep

    Single unconfirmed finding

    Sleep · healthy (sleep complaints or shortened sleep) · Human, randomised small studiesEvery study behind this level and result had fewer than 100 participants. Small studies report larger effects on average than large ones, so the result is less certain.

    Small studies (19 and 11 participants in the two sleep studies according to the review), almost all from one Ajinomoto research group [5]; in the freely accessible study, only 7 analyzed Ajinomoto employees, single-blind [6]. Independent confirmation not found.

  • Less fatigue after sleep loss

    Single unconfirmed finding

    Cognition & focus · healthy · Human, randomised small studiesEvery study behind this level and result had fewer than 100 participants. Small studies report larger effects on average than large ones, so the result is less certain.

    After three nights of shortened sleep, less fatigue and better vigilance in 7 people in a single-blind study of Ajinomoto staff conducted on Ajinomoto employees [6].

  • Better cognition via the NMDA receptor

    No benefit

    Cognition & focus · Patients: schizophrenia · Human, randomised

    In the CONSIST trial (157 participants), no difference from placebo for cognitive deficits and negative symptoms [7]. Not studied in healthy people.

  • Longer life

    Not studied

    Longevity · healthy · Animal study

    Only in mice: 4–6% longer lifespan with glycine-rich feed [9]. Not studied in humans; GlyNAC data concern a combination [11].

  • Healthier joints and skin through more collagen

    Not studied

    Recovery & healing · healthy · Laboratory

    Only in cartilage cell cultures from cattle was collagen synthesis higher; the author group has applied for a patent [10].

small studies: Every study behind this level and result had fewer than 100 participants. Small studies report larger effects on average than large ones, so the result is less certain.

Mechanism of action

Evidence map: Glycine

Each line stands for a published finding; line style and color show where it comes from. The filter hides weaker evidence levels. Sources: see references.

Glycine is the simplest amino acid and acts in two directions in the nervous system: in the spinal cord and brainstem, it activates inhibitory glycine receptors, ligand-gated chloride channels [1]. At the NMDA receptor, by contrast, it is a co-agonist: as little as 10 nM glycine enhanced the NMDA response in mouse neurons, independent of the strychnine-sensitive glycine receptor [2].

In rats, orally administered glycine reached the cerebrospinal fluid, albeit at a concentration about a hundred times lower than in plasma; only very high doses raised the CSF level above the half-maximal effective concentration at the NMDA receptor, and serine rose as the main metabolite [3]. In sleep experiments in rats, glycine promoted non-REM sleep, shortened sleep latency, lowered core temperature and increased skin blood flow; NMDA antagonists, but not the glycine receptor blocker strychnine, abolished the blood flow effect, and destruction of the suprachiasmatic nucleus eliminated the sleep and temperature effects [4]. In animal experiments, the sleep effect thus runs via NMDA receptors, not via the inhibitory glycine receptors.

The sleep studies in humans come almost exclusively from one research group at the company Ajinomoto, which reports that glycine before bedtime improved subjective sleep quality in people with sleep complaints [5]. In the only freely accessible study from this group, 10 healthy men, all Ajinomoto employees, were examined in a randomized, single-blind crossover design and 7 were analyzed: after three nights with bedtime shortened by 25%, fatigue was lower and performance on the vigilance test was better; the authors declare no conflicts of interest [6]. Plasma melatonin and clock genes in the suprachiasmatic nucleus of rats did not change in the same paper [6]. According to this paper, the body produces itself a multiple of the amount of glycine taken in with food [6].

As an add-on to antipsychotics in schizophrenia, glycine was not effective against negative symptoms and cognitive deficits in the CONSIST trial with 157 participants [7]; together with clozapine, it even seemed to weaken the latter’s effect in a small study [8]. In genetically heterogeneous mice, glycine-rich feed extended lifespan by 4–6% [9]. In cartilage cell cultures from cattle, glycine increased collagen synthesis; the authors have applied for a patent on this [10]. The frequently cited human aging data come from a combination with N-acetylcysteine (GlyNAC), whose effects cannot be attributed to glycine alone [11]. As a ligand, glycine is also a component of the bisglycinates of magnesium, zinc and iron (see the profiles for magnesium glycinate, zinc bisglycinate and iron bisglycinate).

Synaptik serves solely to explain biochemistry and pharmacology and is not medical advice or a recommendation to take anything.

Mechanism of action only. Schematic section through an excitatory synapse, not to scale: of the NMDA receptor (a tetramer of two GluN1 and two GluN2B subunits) the two rear subunits are drawn and the front two are cut away to expose the pore. The sequence repeats in three beats: glutamate with depolarisation, glutamate alone, depolarisation alone. Particle numbers, timings, openings and the Ca²⁺ influx are outputs of this figure's model, not measurements, and are not shown as numbers. The numbers in the bottom-right readout come from laboratory and animal experiments and are not comparable with each other.
Drug
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Glutamate  Glycine / D-serine  Mg²⁺  Ca²⁺  Na⁺  K⁺  red = drug, shown in the scene as a miniature skeletal formula · shapes as in the figure

Glycine is a co-agonist at the NMDA receptor: in cultured mouse neurons as little as 10 nM potentiated the NMDA response, independently of the inhibitory glycine receptor [4]. At some synapses, however, D-serine already fully occupies the site [5], and extra glycine then adds little. In the model the site is mostly occupied at baseline and always with glycine (illustrative). Whether orally taken glycine reaches the site in the brain is not shown.

Tap or focus a labelled part for a one-line explanation.

Also acting here, not drawn

  • CX-717: ampakine; NMDA effect only indirect, no action on the receptor itself
  • Huperzine A: NMDA inhibition only in a review by the developers’ group, without a binding site
  • L-theanine: only very weak binding to glutamate receptors
  • Phenylpiracetam: no displacement of ligands at NMDA receptors
  • Piracetam: only changed receptor numbers (mice)
  • Selank: only changed numbers of binding sites (mice)

What the figure shows, and how sure we are

Mechanism-of-action explainer only. Not medical advice, and no statement about benefit, risk, amount or use. Ketamine, esketamine, memantine and atomoxetine are medicines; most of the other substances have been studied at the NMDA receptor only in the lab or in animals.

What was simplified. One receptor stands for many; sizes, cleft width, membrane thickness, ion numbers and all timings are illustrative. The rear two subunits of a GluN1-GluN2B receptor are drawn; NMDA receptors with GluN2A and other subunits, and the AMPA receptors that help produce the depolarisation, are left out. The positions of Mg²⁺ in the filter and of ketamine in the vestibule follow [2] and [8]; for atomoxetine and crocetin the position in the pore has not been determined, and for agmatine the binding site at all. The numbers in [3], [4], [9], [11] to [18], [20] to [22], [24] and [26] to [32] come from the Synaptik drug profiles, where they were checked against the abstracts; [1], [5] to [8], [19], [23] and [25] were checked against their PubMed abstracts (25 Oct 2026), and the statements taken from the review [2] (M1, M3, M4 and the pore loop M2, M3 as the gate, the Mg²⁺ site at the tip of M2, Na⁺, K⁺ and Ca²⁺ as charge carriers, kinases and scaffold proteins at the C-terminal domain of GluN2B) against the relevant sections of the full text.

If medicines, alcohol or other substances are causing problems, a GP or a local addiction counselling service can help.

Synaptik serves solely to explain biochemistry and pharmacology and is not medical advice or a recommendation to take anything.

Mechanism of action only. Schematic cross-section of a GABAergic synapse, not to scale; below, the GABA-A receptor α1β2γ2 seen from above with its binding sites. Particle numbers, opening times, speeds and the bars of the live readout are outputs of an illustrative model, not measurements. In the side view the binding sites are placed schematically; the top view shows the interfaces.
Drug
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GABA  Cl⁻  K⁺  drug (shape per site)  rings = binding sites

Glycine activates the glycine receptor, a chloride channel from the same family as the GABA-A receptor that mediates inhibition mainly in the spinal cord and brainstem [34]. In rats, oral glycine reached the cerebrospinal fluid only at about a hundredth of its plasma concentration [35], and its sleep-promoting effect in animals ran through NMDA receptors, not the glycine receptor [36]. The side panel therefore shows the mechanism at the receptor, not an effect of taking glycine.

Tap or focus a labelled part for a short explanation.

Also acting here, not drawn

  • Ashwagandha: extract; partial agonist only in frog oocytes, binding site unresolved
  • Cortexin: only a binding screen
  • Fasoracetam: only changed receptor expression
  • IDRA-21: GABA currents enhanced only in cell culture; mainly an AMPA modulator
  • Magnesium glycinate: concerns only the glycine part; the only evidence is a review on glycine
  • Nefiracetam: affinity reported only in a review
  • Selank: binding site unresolved

Targets

TargetTypeActionKey dataEvidence
Glycine receptor (chloride channel)Ion channelAgonistmainly spinal cord and brainstem Laboratory[1]
NMDA receptor, glycine binding siteReceptorAgonistCo-agonist; enhancement from 10 nM (mouse neurons) Laboratory[2]
NMDA receptors in the suprachiasmatic nucleusReceptorAgonistEffect abolished by NMDA antagonists, not by strychnine (rat) Animal study[4]

Effect profile

Which signaling systems the compound affects according to current data. ↑ enhanced, ↓ dampened, ≈ modulated, ○ no effect; dots = evidence level.

  • Dopamineno data
  • Noradrenalineno data
  • Serotoninno data
  • Acetylcholineno data
  • Glutamate · AMPAno data
  • Glutamate · NMDA↑ · Co-agonist at the NMDA receptor (laboratory); sleep and temperature effect via NMDA receptors in the suprachiasmatic nucleus (rat)[2][4]
  • GABAno data
  • Histamineno data
  • Orexinno data
  • Adenosineno data
  • Opioidsno data
  • Melatoninno effect · Plasma melatonin unchanged in rats[6]
  • Neurotrophinsno data
  • Blood flow↑ · Skin blood flow increased, thereby heat loss and lower core temperature (rat)[4]
  • Nitric oxideno data
  • Energy metabolismno data
  • Insulin · glucoseno data
  • Inflammation · oxidativeunclear · Studied in humans only as a combination with N-acetylcysteine (GlyNAC); contribution of glycine unknown[11]
  • Stress axisno data
  • Testosterone axisno data
  • Endocannabinoidsno data
  • Autophagy · senescenceno data
  • Immune systemno data
  • Lipid metabolismno data
  • Coagulation · fibrinolysisno data
  • Methylationno data

Routes of administration and bioavailability

How much of a compound reaches the blood or target tissue depends on the route into the body and on the dosage form. All routes of administration explained

  • Oral (swallowed) · free glycine

    In rats, glycine reached the cerebrospinal fluid at a concentration about a hundred times lower than in plasma, presumably by passive diffusion [3]. Pharmacokinetics in humans not verified.

    Animal study

Human studies

  • Daytime well-being after sleep restriction

    randomized, single-blind, crossover, placebo-controlled · healthy (men, Ajinomoto employees) · n = 10 · 3 nights per phase

    Measured: Fatigue and sleepiness (VAS), vigilance test

    Result: Less fatigue, trend toward less sleepiness, better vigilance; 7 analyzed.[6]

    Human, randomised

  • CONSIST: glycine in schizophrenia

    RCT, double-blind, double-dummy, placebo-controlled · Patients: schizophrenia with negative symptoms · n = 157 · 16 weeks

    Measured: SANS, composite cognitive score

    Result: No difference from placebo.[7]

    Human, randomised

  • Glycine in addition to clozapine

    RCT, double-blind, placebo-controlled · Patients: treatment-resistant schizophrenia on clozapine · n = 19 · 12 weeks

    Measured: BPRS, SANS

    Result: Glycine ineffective; only the placebo group improved in positive symptoms, by 35%.[8]

    Human, randomised

  • GlyNAC in older adults

    RCT, placebo-controlled (alanine), combination with N-acetylcysteine · healthy (older adults; plus 12 young adults, open-label) · n = 36 · 16 weeks

    Measured: Glutathione, oxidative stress, mitochondria, physical function

    Result: Improvements with GlyNAC, not with placebo; glycine alone not tested.[11]

    Human, randomised

Risks and warnings

  • Company-dependent body of evidence

    The sleep data come almost entirely from one Ajinomoto research group [5]; the freely accessible study examined Ajinomoto employees without declaring a conflict of interest [6].

    Human, randomised

  • Limited safety data

    No systematic safety data on glycine alone were found; the GlyNAC combination was well tolerated over 16 weeks [11].

    Human, randomised

Interactions

  • Clozapine: In a small RCT, glycine as an add-on to clozapine was ineffective, and the authors suspect a weakening of the antipsychotic effect [8].

Fact check: common claims

  • partly supported

    “Glycine improves sleep”

    Plausible mechanism in rats [4] and positive small human studies, which, however, almost all come from one Ajinomoto research group [5][6].

  • partly supported

    “Glycine lowers body temperature and thereby makes it easier to fall asleep”

    Shown in rats via skin blood flow and NMDA receptors in the suprachiasmatic nucleus [4]; temperature data in humans were not checked.

  • not supported

    “Glycine calms because it is an inhibitory neurotransmitter”

    Inhibitory glycine receptors are located mainly in the spinal cord and brainstem [1]; in rats, the sleep effect ran via NMDA receptors, not via glycine receptors [4].

  • not supported

    “As an NMDA co-agonist, glycine improves mental performance”

    In schizophrenia, no benefit for cognitive deficits [7]; not studied in healthy people.

  • not supported

    “Glycine extends life”

    Only in mice (4–6%) [9]; one co-author is affiliated with a company that sells glycine [9]. Human data are lacking.

  • not supported

    “Glycine strengthens collagen in skin and joints”

    Cell culture with cartilage cells from cattle only [10].

Pharmacokinetics

Absorption
By mouth; not verified in humans. In rats, rise in plasma, cerebrospinal fluid and brain tissue [3].
Half-life
Not verified.
Metabolism
Serine increased as the main metabolite in plasma, cerebrospinal fluid and brain of rats [3].
Entry into the brain
CSF level about a hundred times lower than in plasma, uptake into brain tissue presumably passive (rat) [3].

Legal status

Germany
Not verified.
EU
Not verified.
USA
Not verified.

Related compounds

Magnesium glycinatesame classZinkbisglycinatsame class (German only)Eisenbisglycinatsame class (German only)GlyNAC (Glycin + N-Acetylcystein)contains this component (German only)

Open questions

  • Do independent, sufficiently large studies with polysomnography confirm the sleep effect?
  • How much does glycine rise in human cerebrospinal fluid after ingestion?
  • Which part of the GlyNAC effects is due to glycine?

References

  1. Lynch JW. Molecular structure and function of the glycine receptor chloride channel. Physiol Rev. 2004;84(4):1051–95. doi:10.1152/physrev.00042.2003 · PubMed
  2. Johnson JW, Ascher P. Glycine potentiates the NMDA response in cultured mouse brain neurons. Nature. 1987;325(6104):529–31. doi:10.1038/325529a0 · PubMed
  3. Kawai N, Bannai M, Seki S, Koizumi T, Shinkai K, Nagao K, et al. Pharmacokinetics and cerebral distribution of glycine administered to rats. Amino Acids. 2012;42(6):2129–37. doi:10.1007/s00726-011-0950-y · PubMed
  4. Kawai N, Sakai N, Okuro M, Karakawa S, Tsuneyoshi Y, Kawasaki N, et al. The sleep-promoting and hypothermic effects of glycine are mediated by NMDA receptors in the suprachiasmatic nucleus. Neuropsychopharmacology. 2015;40(6):1405–16. doi:10.1038/npp.2014.326 · PubMed
  5. Bannai M, Kawai N. New therapeutic strategy for amino acid medicine: glycine improves the quality of sleep. J Pharmacol Sci. 2012;118(2):145–8. doi:10.1254/jphs.11r04fm · PubMed
  6. Bannai M, Kawai N, Ono K, Nakahara K, Murakami N. The effects of glycine on subjective daytime performance in partially sleep-restricted healthy volunteers. Front Neurol. 2012;3:61. doi:10.3389/fneur.2012.00061 · PubMed
  7. Buchanan RW, Javitt DC, Marder SR, Schooler NR, Gold JM, McMahon RP, et al. The Cognitive and Negative Symptoms in Schizophrenia Trial (CONSIST): the efficacy of glutamatergic agents for negative symptoms and cognitive impairments. Am J Psychiatry. 2007;164(10):1593–602. doi:10.1176/appi.ajp.2007.06081358 · PubMed
  8. Potkin SG, Jin Y, Bunney BG, Costa J, Gulasekaram B. Effect of clozapine and adjunctive high-dose glycine in treatment-resistant schizophrenia. Am J Psychiatry. 1999;156(1):145–7. doi:10.1176/ajp.156.1.145 · PubMed
  9. Miller RA, Harrison DE, Astle CM, Bogue MA, Brind J, Fernandez E, et al. Glycine supplementation extends lifespan of male and female mice. Aging Cell. 2019;18(3):e12953. doi:10.1111/acel.12953 · PubMed
  10. de Paz-Lugo P, Lupiáñez JA, Meléndez-Hevia E. High glycine concentration increases collagen synthesis by articular chondrocytes in vitro: acute glycine deficiency could be an important cause of osteoarthritis. Amino Acids. 2018;50(10):1357–65. doi:10.1007/s00726-018-2611-x · PubMed
  11. Kumar P, Liu C, Suliburk J, Hsu JW, Muthupillai R, Jahoor F, et al. Supplementing glycine and N-acetylcysteine (GlyNAC) in older adults improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, physical function, and aging hallmarks: a randomized clinical trial. J Gerontol A Biol Sci Med Sci. 2023;78(1):75–89. doi:10.1093/gerona/glac135 · PubMed
How this profile was checked

Last reviewed: 2026-10-25. All sources with a DOI or PMID were resolved automatically via Crossref or doi.org and PubMed.

Translated from the German profile (version of 2026-10-25); translation checked on 2026-10-26.

Checked

  • DOIs checked via Crossref and PMIDs via PubMed (checking script).
  • Checked against the abstract: glycine receptor in spinal cord and brainstem [1]; enhancement from 10 nM, strychnine-independent [2]; CSF 100-fold lower, passive diffusion, serine [3]; NREM, core temperature, skin blood flow, AP5/CGP78608 vs. strychnine, SCN lesion [4]; Ajinomoto affiliation [5][6]; melatonin and clock genes unchanged [6]; 157 participants, no difference [7]; 19 participants, 35% only under placebo [8]; +4–6%, conflict of interest Brind [9]; collagen +60–75%, patent application [10]; 24 older adults plus 12 young adults, 16 weeks [11].
  • Checked in the full text of [6]: 10 Ajinomoto employees, 7 analyzed, randomized, single-blind, crossover; statement “no conflicts of interest”; endogenous synthesis a multiple of dietary intake.
  • ClinicalTrials.gov: 25 hits for “glycine sleep” (October 23, 2026).
  • Cross-references according to guideline K1/G1/G12 on October 24, 2026: related zinc-bisglycinate and iron-bisglycinate added as “same class” (reverse links; both link to glycine), plus a reference sentence at the end of wirkweise_text without a new reference.
  • October 25, 2026: decision q098/E-8: back-reference glycine → glynac “component” present, no change. q012: full text read [6]; all other study findings checked against the abstract only.
  • Precision flags (m004, rules provisional, pending confirmation by Tilman), checked against the sources on October 26, 2026 (PubMed efetch, full texts as stated): “Less fatigue after sleep loss” → “kleine_studien”: [6] 10 enrolled, 7 analyzed (full text PMC3328957); herstellerfinanziert not set: according to the full text, all three first authors are at Ajinomoto, participants were Ajinomoto employees, ethics approval came from Ajinomoto, funding “in part” by PROBRAIN, conflict-of-interest statement without commercial relationships; the origin of the glycine is not stated, and no source in the profile names Ajinomoto as the manufacturer of the glycine (in the rat experiment [4] it came from Sigma). Cross-check on October 26, 2026: texts therefore say “Ajinomoto” instead of “manufacturer” (rule “manufacturer status” in the guideline); “Better sleep” → “kleine_studien”: [5] gives 19 and 11 participants for the two sleep studies (both crossover; full text J-STAGE), [6] 10 enrolled, 7 analyzed; herstellerfinanziert not set for the same reason.

Not verified

  • The Japanese sleep studies (Inagawa 2006, Yamadera 2007, Sleep Biol Rhythms) could not be read in the original (not in PubMed, publisher page blocked); they are therefore reported only via the review [5] and the description in [6] and are not listed as separate references.
  • Legal status (dietary supplement, additive) not checked.
  • Pharmacokinetics and cerebrospinal fluid levels in humans not found.
  • Conflicts of interest of the GlyNAC study leadership [11] are checked in the glynac profile (the study declares no conflicts of interest; the principal investigator is an inventor on the patents US 9,084,760 B2 and US 11,730,711 B2, according to Google Patents). Only referenced in this profile, not checked again.

No dosages, no sources of supply. This information does not replace medical advice.

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