Bone Broth for Sleep and Glycine

Table of Contents

1. How Much Glycine Is in a Cup of Broth
2. Glycine's Pharmacology — N-Methyl-D-Aspartate Co-Agonist and Inhibitory Neurotransmitter
3. The Bannai / Ajinomoto Sleep Trials
4. Core Body Temperature and Sleep Onset
5. Sleep Architecture — Slow-Wave vs REM
6. The "Cup Before Bed" Protocol
7. Bone Broth vs Powdered Glycine for Sleep
8. Glycine vs Other Sleep Aids (Melatonin, Magnesium, L-Theanine)
9. Downstream Benefits Beyond Sleep
10. Cautions and Drug Interactions
11. Key Research Papers
12. Connections
13. Featured Videos

How Much Glycine Is in a Cup of Broth

Gelatin — the protein matrix extracted from bones during a long simmer — is approximately 33% glycine by amino-acid composition, which is the highest glycine content of any common dietary protein source. For comparison: beef muscle protein is roughly 6% glycine, casein in milk is 2%, whey is 1.7%, and egg white is 4%. Gelatin's glycine content is several-fold higher than any other dietary protein.

A well-made cup of bone broth that gels firmly when chilled contains approximately 9-15 g of total protein, almost all of which is gelatin. USDA FoodData Central lists 19.0 g of glycine in 100 g of dry gelatin powder (85.6 g of protein), so most of a cup's glycine is bound in the gelatin matrix rather than free and immediately available. A smaller part is in free form (already broken down during the long simmer); the remainder is released as the body digests the gelatin over the following hours.

For the sleep application, the key question is how much glycine arrives in the bloodstream within the 30-60 minute window before bedtime when serum glycine elevation would be expected to influence sleep onset. Free glycine in the broth reaches peak serum concentration in 30-60 minutes. Glycine released from gelatin digestion arrives more gradually over 1-4 hours. The combined kinetics deliver a meaningful glycine bolus over the typical sleep window.

The published Bannai sleep trials used 3 g of free glycine in water as the test dose. A cup of bone broth delivers some free glycine and more over the digestion window — so the kinetics are different from the supplement, and the total varies with how much gelatin the broth holds. People following the Weston A. Price Foundation (WAPF) / nourishing-traditions "cup of broth before bed" protocol report sleep improvement comparable to powdered glycine.

Back to Table of Contents

Glycine's Pharmacology — N-Methyl-D-Aspartate Co-Agonist and Inhibitory Neurotransmitter

Glycine is unusual among amino acids in having direct, well-characterized neurotransmitter activity. It operates through two distinct receptor systems with opposite effects:

• Inhibitory glycine receptors — ligand-gated chloride channels expressed in the brainstem and spinal cord. Glycine binding opens the channel, allowing chloride influx, which hyperpolarizes the neuron and inhibits its firing. This is glycine's "diazepam-like" inhibitory effect — the same mechanism by which strychnine causes lethal convulsions (strychnine blocks the glycine receptor, leaving brainstem motor neurons unopposed in their firing). The inhibitory glycine receptor is concentrated in motor control circuits and contributes to the modest muscle-relaxant effect of glycine.
• N-methyl-D-aspartate receptor co-agonist site — the N-methyl-D-aspartate glutamate receptor requires both glutamate and a co-agonist (glycine or D-serine) for full activation. Glycine binds at the "glycine site" on the N-methyl-D-aspartate receptor and modulates its function. The N-methyl-D-aspartate receptor is the principal substrate for synaptic plasticity (long-term potentiation, the cellular basis of memory) and is the target of psychiatric drugs including ketamine, memantine, and phencyclidine (PCP). Glycine's role at this site is more complex than the brainstem inhibitory effect — it is a permissive modulator rather than a direct agonist or antagonist.

For the sleep application specifically, the relevant mechanism appears to be a combination of:

1. Modest brainstem inhibition — reduced sensory and motor drive, helping the transition to sleep
2. Suprachiasmatic nucleus (SCN) effects — lowering of core body temperature, which is an essential sleep-onset signal (see below)
3. N-methyl-D-aspartate modulation in cortical circuits — possibly contributing to slow-wave sleep enhancement
4. Reduction of sympathetic nervous system tone — small reduction in heart rate and blood pressure during the hour after dosing

The combined effect is a gentle "lights down" signal to the central nervous system without the strong receptor agonism that produces the cognitive impairment, dependence, and rebound insomnia of benzodiazepines and z-drugs (zolpidem, eszopiclone). Glycine is essentially the inverse of these drugs — weak effect, no addictive potential, no morning grogginess, no dependency.

For deeper treatment of glycine biochemistry — including its roles in methylation, glutathione synthesis, and aspirin detoxification — see our Glycine page.

Back to Table of Contents

The Bannai / Ajinomoto Sleep Trials

The systematic clinical investigation of glycine for sleep was led by Makoto Bannai and Nobuhiro Kawai in Japan, beginning in the mid-2000s; the papers list the authors' affiliation as the Institute for Innovation of Ajinomoto Co., Inc., a producer of amino acids. The glycine sleep program produced a series of placebo-controlled trials that established the basic dosing and efficacy:

• Inagawa et al. 2006 (Sleep and Biological Rhythms) — the first report, on the subjective effects of glycine taken before bedtime. Volunteers rated how they felt on waking; glycine improved their ratings of fatigue, "liveliness and peppiness" and clear-headedness.
• Yamadera et al. 2007 (Sleep and Biological Rhythms) — the follow-up with polysomnographic (overnight sleep-recording) measurement. In volunteers with continuing unsatisfactory sleep, 3 g of glycine before bedtime improved subjective sleep quality and sleep efficiency (sleep time divided by time in bed), shortened the time to sleep onset and to slow-wave sleep without changing the sleep architecture, lessened daytime sleepiness, and improved performance on memory recognition tasks.
• Bannai & Kawai 2012 (Journal of Pharmacological Sciences) — the consolidated review of the program. Confirmed the 3 g dose, the approximately 60-minute pre-bed timing, the safety profile, and the mechanism hypothesis involving core body temperature reduction.
• Bannai et al. 2012 (Frontiers in Neurology) — tested 3 g of glycine against placebo in healthy volunteers under sleep restriction (25% less sleep than usual for 3 nights), measuring next-day sleepiness, fatigue and computer-test performance. The glycine group reported significantly less fatigue and a trend toward less sleepiness, and scored significantly better on a psychomotor vigilance test. The same paper measured circadian clock genes and neuropeptides in the rat suprachiasmatic nucleus: glycine raised two neuropeptides (arginine vasopressin and vasoactive intestinal polypeptide) without changing the clock genes.
• Kawai et al. 2015 (Neuropsychopharmacology) — investigated the mechanism in rats. Oral glycine induced non-REM sleep, shortened the time to fall asleep and lowered core temperature by increasing blood flow to the skin, which releases heat. N-methyl-D-aspartate receptor blockers (AP5 and CGP78608) stopped that rise in skin blood flow when glycine was injected into the brain, and destroying the suprachiasmatic nucleus completely abolished glycine's sleep-promoting and temperature-lowering effects.

The trial data are consistent: 3 g of glycine taken approximately 1 hour before bed produces measurable sleep-architecture improvements that translate to subjective benefit and to next-day cognitive protection, with no significant adverse effects. Effect size is modest but consistent; the trials studied volunteers with ongoing unsatisfactory sleep and healthy volunteers under sleep restriction, not people with severe insomnia.

Back to Table of Contents

Core Body Temperature and Sleep Onset

The body's core temperature follows a clear circadian rhythm, peaking in late afternoon and reaching its nadir approximately 2 hours after sleep onset. The transition from waking to sleep is preceded by an active drop in core temperature of 0.5-1.0°C, driven by peripheral vasodilation (the warm hands and feet that often precede sleep onset) that dissipates body heat. This temperature drop is not just a correlate of sleep onset — it appears to be a causally required signal. Interventions that prevent the temperature drop (warm room, electric blanket, heated room) delay sleep onset; interventions that accelerate it (warm bath 1-2 hours before bed, which causes initial vasoconstriction followed by rebound vasodilation) accelerate sleep onset.

In rats, the Bannai team found that oral glycine produces a modest reduction in core body temperature, together with an increase in blood flow to the skin that releases heat (Bannai & Kawai 2012; Kawai 2015). The proposed mechanism is glycine's effect on the suprachiasmatic nucleus, the brain's master circadian pacemaker, which modulates the autonomic nervous system signals controlling peripheral vasodilation. By lowering core temperature, glycine produces or enhances the signal that the body interprets as "time for sleep."

This mechanism is shared with several other modest sleep interventions:

• Warm bath 1-2 hours before bed — produces the temperature drop via rebound vasodilation after initial warming
• Cool bedroom (65-68°F / 18-20°C) — supports the natural temperature drop by removing the environmental heat barrier
• Exercise timing — exercise raises core temperature and can delay the evening cooling phase by 1-2 hours when done late in the evening
• Melatonin — produces a modest peripheral vasodilation that enhances the temperature drop
• Glycine 3 g pre-bed — produces a similar modest temperature drop via SCN-mediated peripheral vasodilation

Combining glycine with the environmental temperature interventions (cool bedroom, no late workout, optional warm bath 90 minutes pre-bed) appears to produce additive effects greater than glycine alone — an important practical point for patients trying to optimize sleep without pharmaceutical intervention.

Back to Table of Contents

Sleep Architecture — Slow-Wave vs REM

Polysomnographic measurement of sleep distinguishes several distinct sleep stages, each with characteristic electroencephalogram (EEG) patterns and physiologic correlates:

• N1 (light sleep) — transition phase, easily disrupted, 5-10% of total sleep
• N2 (intermediate sleep) — the largest sleep stage, 45-55% of total sleep, characterized by sleep spindles and K-complexes
• N3 (slow-wave / deep sleep) — the most physiologically restorative stage, 15-25% of total sleep in young adults declining to 5-10% in older adults, characterized by high-amplitude delta-wave electroencephalogram activity. This is the sleep stage during which growth hormone secretion peaks, glymphatic clearance of brain metabolic waste is most active, and memory consolidation occurs.
• REM (rapid eye movement / dream sleep) — 20-25% of total sleep, characterized by skeletal muscle atonia and intense brain activity. The principal stage for emotional processing and procedural memory consolidation.

The Bannai team's polysomnographic data (Yamadera 2007) showed that 3 g of pre-bed glycine shortened the time to reach slow-wave (N3) sleep without changing the sleep architecture, so the share of each stage, REM included, stayed the same. This is an important distinction because most sleep aids — benzodiazepines, z-drugs, alcohol, sedating antihistamines — suppress both slow-wave and REM sleep. The user feels more deeply asleep (because of the receptor sedation) but the actual restorative sleep architecture is degraded. Morning grogginess, "hangover" effect, and impaired memory consolidation are downstream consequences.

Glycine's preservation of sleep architecture without REM suppression is its key difference from sedative sleep aids. In the trials, volunteers reported improved subjective sleep quality, reached slow-wave sleep sooner on objective measurement, and showed improved next-day performance — without the architecture distortion that comes with pharmaceutical sedation. The trade-off is that the magnitude of subjective effect is modest, and the trials did not test glycine in severe insomnia.

Back to Table of Contents

The "Cup Before Bed" Protocol

The Weston A. Price Foundation / nourishing-traditions practitioner community has converged on a "cup of warm bone broth approximately 60-90 minutes before bed" protocol as the practical translation of the glycine-for-sleep literature. The protocol is:

1. 1 cup of well-made (gelling) bone broth, warmed in a saucepan or microwave to drinking temperature (about 140-160°F / 60-70°C, hot enough to be soothing but not scalding)
2. Drunk slowly over 5-10 minutes, seated in a relaxed setting (not standing at the kitchen counter)
3. 60-90 minutes before getting into bed, the time practitioners allow for the glycine bolus to begin influencing core body temperature and the broader sleep onset signal
4. Combined with other sleep hygiene measures (cool bedroom, dim lights, no screens for the hour before bed) for additive effect
5. Taken nightly, not just occasionally — practitioners describe the effect building over the first 1-2 weeks of consistent use, similar to other gentle sleep aids

People who use this protocol commonly report that it helps, among those who tolerate the broth flavor and have access to well-made broth. The warm-liquid ritual itself has a sleep-inducing effect independent of the glycine content (similar to the bedtime cup of chamomile tea or warm milk traditions), and the slow drinking pace creates a natural slowdown that aids the transition to sleep.

For patients who do not want to drink savory broth before bed, alternative formats that deliver similar glycine load include:

• 3 g of powdered glycine dissolved in warm water with a small amount of stevia or honey for palatability — this is the supplement version of the Bannai trial dose
• 1 cup of warm milk with 1 scoop (10 g) of collagen peptides stirred in — delivers roughly 3 g of glycine plus other gelatin amino acids in a sweet rather than savory format
• "Bone broth + collagen peptide" combination — a half cup of broth plus a half scoop of collagen peptides, for those who tolerate some broth but want supplementary glycine

Back to Table of Contents

Bone Broth vs Powdered Glycine for Sleep

For the specific outcome of pre-bed glycine dosing for sleep, powdered glycine has several advantages:

• Dose precision — a precisely measured 3 g (one teaspoon of glycine powder) matches the Bannai trial dose exactly; broth varies batch to batch
• Convenience — powder dissolves in any liquid; broth requires heating and a willingness to drink savory liquid before bed
• Cost — pharmaceutical-grade glycine powder costs approximately $0.05 per 3 g dose; bone broth costs $1-2 per cup homemade or $5-8 per cup commercial
• Travel and shelf stability — powder lasts years and travels anywhere
• Histamine-free — relevant for the mast cell activation syndrome (MCAS) / postural orthostatic tachycardia syndrome (POTS) / small intestinal bacterial overgrowth (SIBO) population, for whom broth's histamine content can be a sleep disruptor
• Sweet rather than savory taste profile — glycine has a mildly sweet taste (it is one of the few sweet amino acids), pleasant in warm water with a little honey

Broth has its own advantages in the sleep context:

• Whole-food matrix — the additional amino acids, modest minerals, and small amount of fat (if not skimmed) in broth produce a more complex pre-bed nutritional input than isolated glycine
• Ritual — the warm-cup-before-bed ritual is itself sleep-promoting independent of the glycine content
• Combined with caloric value — for patients who tend to wake hungry, a cup of broth is a small "before bed snack" that quiets the appetite without the blood-sugar disruption of carbohydrate-heavy snacks
• Integration with broader gut-healing / nourishing-traditions practice — if the patient is already drinking broth daily for gut healing or convalescence, the bedtime cup is just a continuation of an existing practice rather than a new intervention

Practitioners describe people trying both and keeping whichever they will use consistently; many settle on powder for travel and weeknights, broth for weekends or when the broth is fresh.

Back to Table of Contents

Glycine vs Other Sleep Aids (Melatonin, Magnesium, L-Theanine)

Glycine is one of several "gentle" sleep aids that occupy the space between basic sleep hygiene and pharmaceutical hypnotics. Each has a distinct mechanism, evidence profile, and ideal patient population:

• Melatonin (0.3-3 mg, taken 30-60 min before bed) — the strongest evidence base of the gentle interventions. Works principally on circadian timing rather than sleep depth, so most effective for jet lag, shift work, delayed sleep phase syndrome, and elderly patients with declining endogenous melatonin. Lower doses (0.3-0.5 mg) appear to be more physiological and often more effective than the 3-5 mg doses commonly sold; megadose melatonin (10+ mg) is increasingly common in supplement stores but has weaker evidence and more next-day grogginess.
• Magnesium glycinate (200-400 mg before bed) — the magnesium component supports relaxation via N-methyl-D-aspartate modulation, gamma-aminobutyric acid (GABA) support, and muscle relaxation; the glycine component contributes the sleep effects discussed on this page. Magnesium glycinate is the "two-for-one" approach to gentle sleep aid that targets multiple mechanisms in one supplement. See our Magnesium page.
• L-theanine (100-400 mg, often combined with magnesium) — the amino acid abundant in green tea. Increases alpha brain waves, promotes calm wakefulness during the day and gentler transition to sleep at night. Particularly useful for patients whose sleep onset difficulty is driven by ruminative anxiety.
• Apigenin (50 mg from chamomile or as isolated supplement) — flavonoid in chamomile that binds gamma-aminobutyric acid receptors with modest sedative effect. Used in some popular sleep stacks including the Andrew Huberman protocol.
• Glycine (3 g pre-bed) — the focus of this page. Best for patients whose primary issue is sleep depth (frequent awakenings, light sleep, poor next-day recovery) rather than initial sleep onset latency. Often combined with melatonin for patients with both onset and maintenance issues.

A common "stack" used by sleep-optimization practitioners: 0.5 mg melatonin + 200 mg magnesium glycinate + 100 mg apigenin + 3 g glycine, all 60-90 minutes before bed. Each component has modest individual effect; the combination targets multiple mechanisms (circadian timing, gamma-aminobutyric acid, N-methyl-D-aspartate, core temperature) and often produces meaningful additive benefit.

Pharmaceutical hypnotics (zolpidem, eszopiclone, suvorexant, trazodone) are prescribed for severe established insomnia or for time-limited use during acute stressors. The gentle interventions discussed here are not replacements for these drugs in those uses — they are used by the much larger population of people with mild-to-moderate sleep complaints who do not need or want pharmaceutical intervention.

Back to Table of Contents

Downstream Benefits Beyond Sleep

One of the appealing features of nightly glycine intake (whether from broth or supplement) is that the same glycine bolus has multiple downstream effects beyond sleep:

• Methylation buffer — glycine N-methyltransferase (GNMT) is one of the body's major buffers against excess methylation. Patients on high-methyl-donor regimens (B12 + methylfolate for methylenetetrahydrofolate reductase (MTHFR) polymorphisms, S-adenosylmethionine (SAM-e) for depression, betaine for homocysteine) can develop "methyl trapping" anxiety symptoms. 3 g of glycine acts as a methyl acceptor and can blunt these effects. See our Glycine and Aspirin Metabolism page for related discussion.
• Glutathione synthesis substrate — glycine is one of the three amino acids in glutathione (glutamate + cysteine + glycine). Glutathione synthesis is often glycine-limited rather than cysteine-limited in patients on long-term N-acetylcysteine (NAC) supplementation. Adequate glycine supports the full glutathione cycle.
• Bile acid conjugation — the liver conjugates bile acids to glycocholate and glycochenodeoxycholate using glycine. Adequate glycine supports the enterohepatic bile circulation that recycles 95% of bile acids each day.
• Collagen synthesis — glycine occupies every third position in the collagen triple helix. Repleting glycine supports the collagen-related effects discussed on the Joints and Collagen page.
• Insulin sensitivity — some evidence suggests that glycine supports insulin sensitivity through effects on the glycine receptor in pancreatic beta cells and through methylation buffering. Several small trials have tested glycine as adjunct in type 2 diabetes management.
• Aspirin metabolism — the liver clears salicylate by conjugation to salicyluric acid, which uses glycine. Patients on chronic low-dose aspirin can become glycine-depleted; nightly glycine supports this detoxification pathway. See Glycine and Aspirin Metabolism.
• Anti-inflammatory effect via glycine-gated chloride channels — macrophages, T cells, and Kupffer cells express glycine receptors; glycine binding modestly suppresses pro-inflammatory cytokine output

The multi-pathway benefit profile is part of what makes nightly glycine such a low-risk high-leverage intervention. A patient drinking a cup of bone broth before bed for sleep gets these additional benefits at no additional cost. For patients using powdered glycine, the same applies.

Back to Table of Contents

Cautions and Drug Interactions

Glycine has a near-perfect safety profile, but a few considerations:

• Clozapine — in a placebo-controlled trial, 60 g/day of glycine added to clozapine for 8 weeks in 30 adults with schizophrenia produced no significant change in symptoms or cognitive function, and no one's ratings worsened significantly; the authors concluded that glycine-site agonists may be less effective combined with clozapine than with conventional antipsychotics (Evins 2000).
• Ketamine therapy — for patients undergoing low-dose ketamine therapy for depression or chronic pain, glycine may modify N-methyl-D-aspartate receptor function and alter the ketamine response; this interaction is theoretical, based on the shared receptor.
• Anticonvulsants — theoretical interaction at the inhibitory glycine receptor; not commonly reported as clinically meaningful
• Schizophrenia spectrum disorders — some clinical trials have used 30-60 g/day of glycine as adjunct in schizophrenia. The data on whether this helps or hinders is mixed. The 3 g/day sleep dose is far below the 30-60 g/day used in those trials.
• Bone broth specific — histamine intolerance — the histamine content of long-simmered broth can disrupt sleep in mast cell activation syndrome / small intestinal bacterial overgrowth / postural orthostatic tachycardia syndrome patients who are histamine-reactive. Short-simmer broth (4-6 hours) and pressure-cooker broth (2-3 hours) carry less histamine, and powdered glycine carries none.
• Sodium load — for patients on sodium restriction (heart failure, advanced chronic kidney disease), salted commercial broth may contribute too much sodium for nightly use; unsalted homemade broth or powdered glycine are alternatives.
• Diabetic patients — broth contributes minimal carbohydrate but does have some calorie load; powdered glycine is essentially zero calorie. Both are compatible with most diabetic dietary approaches.
• Pregnancy and lactation — bone broth is a traditional postpartum food across cultures. Powdered glycine has not been systematically tested in pregnancy at the 3 g dose.

The overall risk profile is essentially benign — nightly glycine is one of the safest sleep interventions available and has none of the dependency or cognitive-impairment concerns of pharmaceutical sedatives.

Back to Table of Contents

Key Research Papers

1. Bannai M, Kawai N (2012). New therapeutic strategy for amino acid medicine: glycine improves the quality of sleep. Journal of Pharmacological Sciences. — PubMed PMID: 22293292
2. Yamadera W et al. (2007). Glycine ingestion improves subjective sleep quality in human volunteers, correlating with polysomnographic changes. Sleep and Biological Rhythms. — doi:10.1111/j.1479-8425.2007.00262.x
3. Inagawa K et al. (2006). Subjective effects of glycine ingestion before bedtime on sleep quality. Sleep and Biological Rhythms. — doi:10.1111/j.1479-8425.2006.00193.x
4. Bannai M et al. (2012). The effects of glycine on subjective daytime performance in partially sleep-restricted healthy volunteers. Frontiers in Neurology. — PubMed PMID: 22529837
5. Kawai N et al. (2015). The sleep-promoting and hypothermic effects of glycine are mediated by NMDA receptors in the suprachiasmatic nucleus. Neuropsychopharmacology. — PubMed PMID: 25533534
6. Meléndez-Hevia E et al. (2009). A weak link in metabolism: the metabolic capacity for glycine biosynthesis does not satisfy the need for collagen synthesis. Journal of Biosciences. — PubMed PMID: 20093739
7. File SE, Fluck E, Fernandes C (1999). Beneficial effects of glycine (bioglycin) on memory and attention in young and middle-aged adults. Journal of Clinical Psychopharmacology. — PubMed PMID: 10587285
8. Kräuchi K, Cajochen C, Wirz-Justice A (2004). Waking up properly: is there a role of thermoregulation in sleep inertia? Journal of Sleep Research. — PubMed PMID: 15175091
9. Zhong Z et al. (2003). L-glycine: a novel antiinflammatory, immunomodulatory, and cytoprotective agent. Current Opinion in Clinical Nutrition and Metabolic Care. — PubMed PMID: 12589194
10. Díaz-Flores M et al. (2013). Oral supplementation with glycine reduces oxidative stress in patients with metabolic syndrome. Canadian Journal of Physiology and Pharmacology. — PubMed PMID: 24144057
11. Razak MA et al. (2017). Multifarious beneficial effect of nonessential amino acid, glycine: a review. Oxidative Medicine and Cellular Longevity. — PubMed PMID: 28337245
12. Evins AE, Fitzgerald SM, Wine L, Rosselli R, Goff DC (2000). Placebo-controlled trial of glycine added to clozapine in schizophrenia. American Journal of Psychiatry. — PubMed PMID: 10784481

PubMed Topic Searches

1. PubMed: Glycine sleep latency
2. PubMed: Glycine slow-wave sleep
3. PubMed: Core body temperature sleep onset
4. PubMed: NMDA glycine suprachiasmatic
5. PubMed: Gelatin amino acid glycine

Back to Table of Contents

Connections

• All Food
• Bone Broth Overview
• Bone Broth Benefits Hub
• Bone Broth for Gut Healing
• Bone Broth for Joints & Collagen
• Bone Broth for Mineral Repletion
• Glycine
• Glycine & Aspirin Metabolism
• Proline
• Glutamine
• Magnesium (Glycinate)
• Collagen
• Gut Healing
• Gut-Brain Axis
• Joint Pain
• History

Back to Table of Contents

Featured Videos