Glycine 1500mg | GlyNAC Partner | Glutathione Precursor, Slow-Wave Sleep & Healthy-Aging Substrate

The 30-second answer

Glycine is the smallest amino acid in the body and the second substrate the cell uses to build glutathione, the body's master endogenous antioxidant. Cysteine is the famous rate-limiter — that's why NAC works — but in older adults glycine becomes a co-bottleneck. Older bodies have a quietly worsening glycine deficit relative to demand, and pairing glycine with NAC (the GlyNAC combination) is the precise intervention Baylor College of Medicine's Rajagopal Sekhar group ran through 14-day, 24-week, and 36-week clinical trials in older adults — restoring red-blood-cell glutathione to youthful levels and moving oxidative-stress, mitochondrial-fuel-handling, insulin-sensitivity, body-composition, walking-speed, cognition, and inflammation markers in a single intervention. Glycine also has a second life as the cheapest, safest evidence-based sleep aid in longevity medicine: 3 grams 30–60 minutes before bed lowers core body temperature, deepens slow-wave sleep, and improves next-day subjective alertness in published Japanese trials. Our Glycine 1500mg formula delivers 500mg of pharma-grade glycine per capsule, 60 vegan HPMC capsules per bottle, with a 1500mg / 3-cap serving sized to the GlyNAC clinical literature and a 1000mg / 2-cap serving sized to foundational daily use. No fillers, no stearates, no titanium dioxide, no synthetic glycine isomers — just unflavored, unsweetened, third-party-tested glycine.

Why glycine moved from "nutrition-class footnote" to longevity headline

For decades glycine was the amino acid you skimmed past in biochemistry textbooks — small, simple, formally "non-essential" because the body can technically synthesize it from serine via the SHMT enzyme system. The textbook framing was wrong about the part that matters most for adults over 40. "Non-essential" in nutrition has a very specific meaning: an amino acid your body can synthesize from other amino acids, given adequate substrate, energy, and enzymatic capacity. It does not mean "your body has unlimited supply" or even "your body has enough to meet demand." Glycine has now been studied carefully enough that two parallel lines of research have flipped its status from nutritional afterthought to one of the most-discussed amino acids in clinical aging biology.

The first line is the glutathione collapse story. Glutathione (GSH) is a tripeptide: γ-glutamyl-cysteinyl-glycine. The enzyme glutamate-cysteine ligase joins glutamate to cysteine, and then glutathione synthetase adds the glycine. Without all three amino acids present in adequate intracellular concentration, the cell cannot manufacture glutathione no matter how much oxidative-stress demand it is facing. Sekhar's group at Baylor was the first to systematically demonstrate, in human older adults, that the cells of aged individuals have markedly reduced glutathione — and that the deficit traces to inadequate glycine and cysteine substrate, not to broken enzymatic machinery. The corollary follow-up was the obvious one: replace the missing substrate, restore the missing glutathione, and see what happens to the rest of the aging picture. Multiple things, it turned out.

The second line is the glycine-deficit-of-aging story, an independent observation that older adults have lower plasma and intracellular glycine relative to demand. The collagen-turnover side of glycine biology consumes a non-trivial fraction of the body's daily production, and age-related changes in collagen turnover combined with reductions in renal recycling and shifts in hepatic one-carbon metabolism appear to compound the gap. Several groups have published on this independently of the GlyNAC literature, and the upshot is the same: older adults consistently show reduced glycine availability relative to physiological need, and supplementation closes the gap dose-dependently with no risk profile of any clinical concern.

If you have been reading the longevity literature and watching the same precursor names appear in NAD+ posts, glutathione posts, sleep posts, collagen posts, and methylation posts and wondering why one amino acid keeps showing up, this is why. Glycine sits at six different metabolic intersections, and unlike most amino acids where excess is neutral or slightly harmful, the human evidence on supraphysiological oral glycine is unusually clean.

The Sekhar Baylor trial progression — what GlyNAC actually did in humans

The clinical case for glycine supplementation in older adults is anchored in a multi-stage RCT program from Dr. Rajagopal Sekhar's lab at Baylor College of Medicine, run from roughly 2011 onward and culminating in 2021–2022 with the longest-running and most carefully phenotyped trials. The progression matters because each trial extended both duration and outcome panel:

2011 — Sekhar et al., American Journal of Clinical Nutrition. The foundational paper. HIV-positive adults with documented glutathione deficiency received cysteine + glycine supplementation for 14 days. Erythrocyte glutathione concentration was restored, and oxidative-stress and mitochondrial-fuel-handling markers improved alongside it. The proof-of-concept finding was that a substrate-only intervention — no drug, no enzyme — could restore intracellular glutathione in adults with established deficits.

2018 — Sekhar et al., Journals of Gerontology Series A: Biological Sciences and Medical Sciences. The first dedicated older-adult trial. Older adults received GlyNAC (glycine + N-acetylcysteine) for 14 days. The published outcomes included restored erythrocyte glutathione concentrations, decreased oxidative stress, improved mitochondrial fuel oxidation, decreased insulin resistance, decreased endothelial dysfunction, decreased genotoxicity, decreased waist circumference, and improvements in body composition. Two weeks. One amino acid pair.

2021 — Kumar et al., Clinical and Translational Medicine. The 24-week randomized clinical trial. Older adults vs. younger comparator. GlyNAC supplementation for 24 weeks. Outcomes spanned eight aging-relevant domains: oxidative stress, glutathione deficiency, mitochondrial dysfunction, inflammation, insulin resistance, endothelial dysfunction, genotoxicity, body composition. Plus pre-specified functional outcomes: gait speed, exercise capacity, strength, cognition. The 24-week intervention moved every domain meaningfully in the older-adult cohort. The clearest single takeaway was that a six-month substrate intervention closed the gap on multiple aging-of-aging biomarkers simultaneously.

2022 — Kumar et al., Nutrients. The 36-week extension and longevity-protocol formalization. The continued-use cohort maintained gains; the discontinuation cohort regressed on most markers within weeks of stopping, confirming the gains were maintained pharmacology rather than durable epigenetic change. The implication is straightforward: GlyNAC is a daily-use longevity intervention, not a fixed-course one.

None of this is a small claim, and the supplement industry has, predictably, run with versions of "GlyNAC reverses aging" that overshoot what the literature actually supports. The careful summary is this: in older adults with measured glutathione deficiency, replacing the substrate with adequate glycine and cysteine restores intracellular glutathione, and that restoration appears to drive measurable improvements across a panel of aging biomarkers in randomized, controlled, multi-month human trials. That is rare in aging biology. It is the precise reason glycine — boring, "non-essential", textbook footnote — became one of the most-discussed amino acids in clinical longevity over the last five years.

Six jobs glycine does that the longevity catalog cares about

Glutathione synthesis is the headline mechanism but not the only one. Glycine is unusually multifunctional even by amino-acid standards — most amino acids do one or two jobs in the body; glycine does at least six that matter for healthy aging.

1. Glutathione tripeptide assembly

Glutathione is γ-glutamyl-cysteinyl-glycine. The cell makes it in two steps: γ-glutamylcysteine first (rate-limited by cysteine via NAC or whole-protein dietary cysteine), then glutathione synthetase ligates the terminal glycine. Without adequate glycine substrate, the second step is rate-limited regardless of how much cysteine you provide. This is the precise pharmacology behind the GlyNAC pair: NAC supplies the cysteine bottleneck, glycine supplies the second bottleneck, and the cell's glutathione synthesis runs at capacity again. Glutathione is recycled rather than consumed when it neutralizes a reactive oxygen species — but recycling capacity itself depends on NADPH and the GSH/GSSG ratio, both of which deteriorate under chronic oxidative load. Restoring substrate availability is the most direct intervention to keep the recycling pool topped up.

2. Heme biosynthesis

The first step of heme synthesis — the molecule at the center of hemoglobin, myoglobin, cytochrome P450, mitochondrial cytochromes, and the electron transport chain — is the condensation of glycine with succinyl-CoA to form δ-aminolevulinic acid (ALA). Glycine is not a cofactor here; it is the literal carbon-and-nitrogen substrate. Mitochondrial cytochrome turnover, hepatic CYP enzyme synthesis, and red-blood-cell production all draw on this pathway daily. Inadequate glycine availability is a small but persistent drag on cellular energy machinery that compounds over years.

3. Collagen — the dominant amino acid in the triple helix

Collagen is roughly one-third glycine by residue count. Every third amino acid in the canonical Gly-X-Y collagen repeat is glycine — it has to be, because glycine is the only amino acid small enough to fit in the inner position of the collagen triple helix without disrupting the structure. The body's daily collagen turnover is large (skin, bone matrix, tendon, ligament, joint cartilage, vascular intima, gut lining, fascia), and glycine is a quantitatively dominant amino-acid demand for that turnover. The classical longevity-skin pairing is glycine + Vitamin C (the rate-limiting cofactor for prolyl/lysyl hydroxylase, which crosslinks the collagen triple helix into mature fiber). If you are running our Marine Collagen Peptides or Multi Collagen Peptides Powder, glycine is the residue that compounds you are taking the most of in the supplement. Adding free glycine on top is the inexpensive way to keep the substrate floor high.

4. Sleep architecture — NMDA inhibitory co-agonism

Glycine is a co-agonist of central nervous system NMDA receptors at the glycine-binding site (separate from the glutamate-binding site), and an inhibitory neurotransmitter at glycine receptors in the brainstem and spinal cord. Three Japanese clinical trials run between roughly 2006 and 2012 (Yamadera et al. 2007, Bannai et al. 2012, plus related work from the Ajinomoto group) demonstrated that 3 grams of oral glycine taken 30–60 minutes before bed lowered core body temperature, increased delivered slow-wave sleep, reduced subjective fatigue the next morning, and improved next-day cognitive performance — without producing a benzodiazepine-style residual sedation, without altering total sleep time meaningfully, and without producing the dependency or rebound profile of GABA-acting hypnotics. The proposed mechanism is peripheral (cutaneous vasodilation lowers core temperature, which is the body's own signal to initiate sleep onset and deepen slow-wave architecture) more than direct central sedation. The dose ceiling in the Japanese literature is essentially safety-only; the trials used 3g and saw clean signal at that dose with no adverse effects.

5. One-carbon methylation — a quiet contribution

Glycine is a substrate for the glycine cleavage system, which donates one-carbon units to the folate-mediated methyl pool. That methyl pool is the same pool that drives DNA methylation, neurotransmitter synthesis, creatine biosynthesis, phosphatidylcholine production, and the disposal of methylated NAD+ metabolites (the reason TMG is in every serious NMN protocol). Glycine is a smaller, slower contributor than methionine or TMG, but it feeds the same methylation pool and it does so without homocysteine accumulation. For longevity protocol-builders running NMN at 500–1000mg/day, glycine contributes to methylation buffer in addition to its glutathione job.

6. Bile-acid conjugation, creatine synthesis, neurotransmitter buffering

Three smaller but real downstream demands on the daily glycine pool: bile-acid conjugation (most glycine-conjugated bile acids in the enterohepatic loop are physically that — bile acid + glycine), creatine biosynthesis (glycine + arginine → guanidinoacetate → creatine, the molecule any user of creatine monohydrate is supplementing the end-product of), and CNS inhibitory tone (glycine is the dominant inhibitory neurotransmitter in the spinal cord and brainstem; glycine receptor agonism damps the muscle-tone and startle-response circuits). Each of these is a small persistent draw on the daily glycine pool. None alone is a strong reason to supplement. Together they explain why oral glycine demand in older adults exceeds what the textbook "non-essential" framing assumes.

Why older adults specifically run short on glycine

Three contributing factors, additive:

(a) Reduced de-novo synthesis capacity. The dominant biosynthetic route is from serine via the serine-hydroxymethyltransferase (SHMT) enzyme system, which depends on adequate folate, B6, and one-carbon flux. All three of those tend to drift suboptimal with age, mild B-vitamin status decline, age-related kidney function decline, and the methylation-pool draw of high-protein diets. Less de-novo synthesis at the same daily turnover demand equals a slow chronic deficit.

(b) Increased glycine demand for collagen turnover at the same time the body is replacing more collagen than it is making. Collagen catabolism in older adults exceeds new collagen deposition (this is the "aging connective tissue" picture clinically: thinner skin, less elastic vasculature, more fragile bone matrix). Glycine is the residue most consumed by this turnover, and the body cannot reincorporate the glycine from broken-down collagen as efficiently as it produced it.

(c) Reduced glutathione recycling efficiency. The recycling of GSSG back to GSH is NADPH-dependent, and NADPH availability declines with mitochondrial dysfunction. As recycling drops, daily new-synthesis demand rises — and that new-synthesis demand pulls more glycine off the limited pool.

The result is a chronic, slowly-worsening, asymptomatic glycine deficit relative to physiological demand, exactly the type of deficit that responds well to substrate-only oral supplementation. Sekhar's group estimated that older-adult plasma glycine is roughly 25–30% lower than young-adult plasma glycine, and that the additional intracellular deficit is larger still because the cell is drawing from the same depleted pool.

Sleep mechanism — the part everyone wants to know about

The glycine-as-sleep-aid finding is the most replicable practical effect of high-dose oral glycine, and the mechanism is unusually well-characterized for an over-the-counter compound:

The temperature pathway. Sleep onset and slow-wave sleep depth are physiologically gated by core body temperature drop. The body initiates sleep when peripheral skin vessels dilate, releasing heat and dropping core temperature roughly 0.4–0.7°C below daytime baseline. Glycine ingestion 30–60 minutes pre-bed appears to cause cutaneous vasodilation through a brain-mediated mechanism (the suprachiasmatic and preoptic regions), accelerating the core-temperature drop. Yamadera et al. 2007 in Sleep and Biological Rhythms measured this directly with thermistors and showed glycine subjects reached sleep-onset core temperature faster and stayed there longer. Bannai et al. 2012 in Frontiers in Neurology extended the finding with EEG, showing increased slow-wave sleep without total sleep time change.

The NMDA inhibitory co-agonism pathway. Separately, glycine is a positive modulator of NMDA receptors via the glycine-binding site, and an inhibitory neurotransmitter at strychnine-sensitive glycine receptors. Whether central glycinergic inhibition contributes to the sleep effect at oral doses (which produce only modest CNS glycine increases) remains debated. The temperature pathway is generally considered the dominant clinical mechanism.

Why this matters in the longevity stack. Slow-wave sleep is when growth hormone is released, when the glymphatic clearance of brain metabolic waste runs (including beta-amyloid clearance), when peripheral immune-cell trafficking peaks, and when much of the body's daily protein turnover and tissue repair happens. A 2g–3g pre-bed glycine dose is the cheapest, safest evidence-based intervention to preserve slow-wave architecture without the residual-sedation tail of GABA-acting hypnotics or the receptor-downregulation profile of long-term sleep-aid use.

The trial dose to replicate is 3g (six of our 500mg capsules) 30–60 minutes before bed. Most users report a noticeable next-morning subjective freshness within the first week. Long-term users typically settle on 1.5–3g pre-bed as a daily protocol, often stacked with magnesium glycinate (our 400mg version is dosed for this) since the magnesium-glycinate chelate delivers both the magnesium GABA-A potentiation and additional glycine.

Glycine vs. GlyNAC vs. whey vs. gelatin — what's actually different

You can get glycine from several places. They are not interchangeable for the longevity protocol use case.

Free glycine (this product). Pharma-grade crystalline glycine, ~80–90% bioavailable orally, with predictable plasma kinetics and clean per-dose math. The Sekhar trials used pharma-grade free glycine. The sleep trials used pharma-grade free glycine. If you are trying to replicate clinical protocols, free glycine is what was studied.

GlyNAC (glycine + NAC together). Not a separate molecule — just the co-administration of glycine and N-acetylcysteine. The trials used roughly 100mg/kg/day of each. For a 70kg adult that's ~7g/day of glycine and ~7g/day of NAC, taken in divided doses morning and evening. We sell the two as separate SKUs because they have different shelf-life and palatability profiles, but they are designed to be co-stacked. Three of these capsules + one 600mg NAC capsule, twice a day, gives you the same 1500mg + 1200mg foundational GlyNAC dose at half the trial volume — appropriate for users not in clinically diagnosed glutathione deficiency.

Hydrolyzed collagen (collagen peptides). Collagen peptides are roughly 22–28% glycine by mass. A 10g collagen-peptide serving delivers 2–2.5g glycine — coincidentally in the same range as a glycine-as-sleep-aid dose. This is the cleanest food-based way to get foundational glycine, and the reason traditional broth-and-stew diets historically delivered far more glycine than modern muscle-meat-dominant diets. Marine Collagen at 5000mg/day delivers ~1.1–1.4g glycine — useful but below GlyNAC trial doses without additional free glycine.

Whey protein. Whey is glycine-poor relative to collagen — typically 1.7–2.2% glycine by mass. A 30g whey serving delivers only ~600mg glycine. Whey is excellent for leucine-driven mTOR / muscle-protein-synthesis but is not a substantial glycine source. Older adults running whey-only daily protein and assuming "I'm getting plenty of amino acids" are usually still glycine-short.

Plant proteins. Highly variable. Soy is ~4% glycine by mass; legumes 3–5%; nuts 4–6%. A varied plant-protein-rich diet provides a moderate glycine baseline but rarely reaches GlyNAC trial doses without supplemental free glycine.

The recommendation we would give a typical longevity-protocol-builder adult: keep dietary collagen or broth at floor (1–2 servings/day if possible), and supplement free glycine on top to hit your clinical-protocol target.

How to dose this product

Each capsule is 500mg pure glycine. Below are the three dosing protocols that map cleanly onto the trial literature.

Foundational longevity dose — 1000–1500mg/day

2–3 capsules daily. The "I run a longevity protocol but am not specifically targeting glutathione restoration" dose. Take with the morning longevity stack (NMN, resveratrol, etc.) for amino-acid pool support, or split AM/PM. At 60 caps/bottle, 2 caps/day is a 30-day supply — the standard catalog re-up cadence.

Sleep-aid protocol — 1500–3000mg pre-bed

3–6 capsules taken 30–60 minutes before sleep, with water or a small carbohydrate. The trial dose is 3g (6 caps) — this is the most replicable target if you are specifically using glycine for slow-wave sleep restoration. Most users find 3g produces a clear subjective freshness effect within the first 5–7 nights. Some find the effect modest at 1.5g and substantial only at 3g; some find the reverse. Start at 1.5g for a week; titrate up.

GlyNAC protocol — 1500mg with NAC, twice daily

3 capsules of glycine + 2 capsules of NAC 600mg (= 1200mg NAC), morning and evening. This is roughly 40% of the Sekhar trial dose of 100mg/kg/day for each compound — a sustainable foundational maintenance dose for adults in the 60–80kg range who are not in measured deficiency. Adults in measured glutathione deficiency, or those replicating Sekhar's protocols closely with physician oversight, can dose-escalate toward 100mg/kg/day. The Sekhar trials had no adverse-event signal at 100mg/kg/day in adults aged 65–80 over 36 weeks.

Co-supplemental considerations

Glycine is exceptionally well-tolerated and stacks cleanly with essentially every other supplement in the catalog. The most common combinations are:

• NAC. The other GlyNAC half. Co-administration is the entire trial design.
• TMG. Both contribute methyl pool support. Methylation pool buffer for high-dose NMN protocols benefits from co-supplementation of both. Glycine indirectly via the cleavage-system one-carbon contribution; TMG directly via betaine-homocysteine methyltransferase.
• Vitamin C. Collagen synthesis cofactor. If you take glycine for collagen turnover support, liposomal Vitamin C 500–1000mg/day is the rate-limiting cofactor for prolyl/lysyl hydroxylation.
• Magnesium glycinate. The chelate delivers both magnesium (GABA-A potentiation, deep-sleep and recovery support) and additional glycine. Dose-stack-additive for the sleep protocol. Our 400mg magnesium glycinate delivers ~50mg additional glycine alongside 400mg elemental magnesium.
• Collagen peptides. Substrate-stacking. The combination is essentially "free glycine for the longevity-protocol target dose, collagen peptides for connective-tissue substrate breadth (proline, hydroxyproline, glycine, lysine)." See our Marine Collagen and Multi Collagen Powder.

What we put in the capsule (and what we left out)

Each capsule contains 500mg pharma-grade L-glycine (the only natural isomer; we do not use D-glycine or racemic mixtures, neither of which is metabolically active). The capsule shell is plant-derived hydroxypropyl methylcellulose (HPMC) — vegan, no gelatin, no porcine or bovine source. We do not add magnesium stearate, silicon dioxide, titanium dioxide, soy oil flowing agents, sucralose, sorbitol, or maltodextrin fillers. Each lot is third-party tested for identity (HPLC), microbial limits, heavy metals (lead, mercury, cadmium, arsenic) below USP and California Prop 65 thresholds, and PAH/melamine residue.

The 500mg-per-cap fill is intentional: it lets a single bottle cover three different dosing protocols (foundational at 2 caps/day = 30-day supply, sleep at 3–6 caps pre-bed = 10–20-night supply, GlyNAC at 3 caps × 2/day = 10-day supply). Higher per-cap doses (1g+) reduce flexibility; lower per-cap doses (250mg) waste shell mass and increase swallow burden. 500mg is the dose that maps cleanly onto the published trial dosing arithmetic.

Frequently asked questions

Why not just take collagen powder for the glycine?

You can — and we recommend it as part of the protocol for connective-tissue substrate breadth. But collagen alone caps out at roughly 1–2.5g glycine per typical 5–10g serving, which is below the GlyNAC trial dose and at the floor of the sleep-aid trial dose. If your goal is GlyNAC-style glutathione restoration or sleep-aid effect, free glycine is a more practical way to hit the dose. If your goal is connective-tissue substrate, collagen peptides are denser in proline and hydroxyproline (the other dominant collagen residues) and worth pairing.

Does glycine cause sedation during the day?

Daytime glycine in foundational doses (1–1.5g) does not produce subjective sedation in published trials. The sleep-aid effect is timing-dependent and dose-dependent, requiring a higher pre-bed dose (~3g) on top of the temperature-drop window. We have not seen daytime drowsiness reported in the Sekhar trials at 100mg/kg/day taken in divided doses. Some users describe a calm or "low-noise" subjective effect at higher daytime doses (3g+), generally interpreted as the inhibitory-tone CNS contribution.

Is it safe with antidepressants or other psychiatric medications?

Glycine has a clean profile in trials with psychiatric populations and is even being investigated as an adjunctive agent in schizophrenia (where higher doses show some benefit on negative symptoms). Standard combination with SSRIs, SNRIs, bupropion, or anti-anxiety medications has not produced clinically significant interactions in published reports. That said, anyone on prescription psychiatric medication should clear new supplements with their prescriber. Avoid combination with clozapine specifically: there is one case report of clozapine efficacy attenuation with high-dose glycine, attributed to the NMDA co-agonist mechanism.

I'm taking high-dose NMN. Do I need glycine for the methylation pool?

Glycine is a smaller methyl-pool contributor than TMG (which donates three methyl groups directly via betaine-homocysteine methyltransferase). For NMN protocols, TMG at 500–1000mg/day is the more direct methyl-buffer support. Glycine contributes additional buffer through the one-carbon system and is worth co-stacking, but is not a substitute for TMG in this role.

Does it taste like anything?

Free glycine is famously sweet — Greek glykys, "sweet". You will not taste anything from a swallowed capsule, but if you open one onto your tongue you will get a subtly sweet, slightly cooling profile (the same "free amino acid" taste signature as MSG-glutamate but without the savory/umami axis). Some users dissolve 1–3 caps in warm water before bed instead of swallowing capsules; this works fine and the dissolved glycine has a not-unpleasant mildly-sweet character.

Can I take this on an empty stomach?

Yes. Free glycine is well-absorbed without food. The amino-acid transporters that handle glycine (system gly, system A) are constitutively expressed and saturate at much higher doses than typical supplemental ones. There is no bioavailability advantage to dosing with food, though a small amount of water with the capsules helps with capsule transit.

What's the maximum safe dose?

The published clinical doses go up to roughly 100mg/kg/day in older adults (~7g/day for a 70kg person) over 36 weeks with no adverse-event signal. Acute single doses up to 9g have been used in psychiatric research without adverse effect. The practical ceiling for most users is set by GI tolerance — at very high single doses (>5g) some users report mild GI looseness, which is osmotic and resolves with split dosing. There is no toxicity ceiling of clinical concern for healthy adults at typical supplemental doses.

Why only 60 capsules per bottle?

To match the catalog re-up cadence at the foundational dose (2 caps/day = 30-day supply) while keeping per-bottle freshness and shelf-life predictable. Heavy GlyNAC protocol users cycle through 2–3 bottles per month and typically subscribe.

How does this compare to the cheap bulk glycine on the big online retailers?

Glycine is a low-cost commodity raw material. The differences in supplement-grade products are: (1) identity verification — pharma-grade L-glycine vs. unverified bulk that may include D-glycine isomer mass; (2) filler load — many cheap brands cut with magnesium stearate (5–15% of capsule mass), silicon dioxide, or titanium dioxide; (3) heavy-metal testing — bulk-grade glycine has historically been a route for arsenic and lead contamination; (4) capsule shell quality — gelatin vs. HPMC, with associated allergen/source concerns. We test every lot and source from facilities GMP-certified for human dietary use, not livestock-feed-grade.

Who should not take this

Standard supplement caveats apply. Adults under 18, pregnancy, and breastfeeding: clear with a prescriber. Anyone with diagnosed kidney disease at stage 3 or worse should clear protein-loading supplements (including amino acids) with their nephrologist, since renal handling of nitrogen waste from amino acid catabolism is a relevant load. Anyone on clozapine specifically should avoid high-dose glycine due to a published interaction case report. Anyone with a known glycine-metabolism inborn error (non-ketotic hyperglycinemia is the relevant rare condition) is already under clinical management and should not self-supplement glycine without their physician.

The longevity-protocol short version

Glycine is the most under-rated amino acid in the longevity catalog. It's the second substrate for the glutathione tripeptide (NAC supplies the first), the literal building block of heme and the one-third residue density in collagen, an inhibitory co-agonist that deepens slow-wave sleep, a one-carbon methyl-pool contributor that supports NMN protocols, and the cleanest, cheapest, most well-tolerated single ingredient on the longevity shelf. The Sekhar Baylor trials made GlyNAC the most clinically-supported aging intervention in the substrate-replacement class. Older adults are the demographic with the largest glycine-supply-vs-demand gap, and the gap closes dose-dependently with oral free glycine. We made ours the way the trials used it: pure pharma-grade L-glycine, 500mg per capsule, 60 caps per bottle, no fillers, no stearates, no titanium dioxide, vegan HPMC shell, third-party-tested every lot. 1500mg / 3 caps maps to the GlyNAC partner dose. 3000mg / 6 caps maps to the sleep-aid trial dose. 1000mg / 2 caps is the foundational floor.

Stack pairing recommendations: Glycine + NAC for GlyNAC glutathione restoration. Glycine + Magnesium Glycinate for the sleep protocol. Glycine + Marine Collagen + Liposomal Vitamin C for connective-tissue substrate. Glycine + TMG for methylation-pool buffering on high-dose NMN protocols. Glycine + reduced glutathione if you want both substrate-precursor and direct-supplementation strategies running in parallel.

These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider before starting any new supplement, particularly if you are pregnant, breastfeeding, taking prescription medications, or have a diagnosed medical condition. Individual results vary; clinical-trial outcomes apply at population level and are not guarantees for any individual user.