Creatine Monohydrate 1000mg | Micronized | Sarcopenia Prevention, Strength & Cognitive Longevity

Creatine is the most-researched supplement in human history — over 1,000 published trials — and it has quietly become one of the most-researched supplements in longevity as well. Skeletal-muscle mass is a stronger predictor of all-cause mortality after 60 than LDL cholesterol or systolic blood pressure (Srikanthan 2014, Am J Med). Creatine plus resistance training is the single most-validated nutritional intervention for slowing the muscle loss (sarcopenia) that drives frailty, falls, fractures, and the loss of independence. The cognitive evidence is now equally serious: creatine raises brain phosphocreatine stores, with the strongest effects in stressed, sleep-deprived, vegetarian, or aging populations whose ATP demand exceeds local supply. Five grams a day. The dose has not changed in thirty years because nothing has beaten it.

The 30-second answer

• 1000 mg micronized creatine monohydrate per capsule — 5 capsules = the 5 g/day dose used in the overwhelming majority of the human research, including the 2017 ISSN position stand.
• ≥99.9% pure, Creapure^®-grade equivalent — verified absent of creatinine, dicyandiamide, and dihydrotriazine, the three contaminants that show up in cheap creatine.
• Sarcopenia-grade evidence. Devries & Phillips 2014 meta-analysis (357 elderly subjects): creatine + resistance training added ~1.4 kg of lean mass and meaningfully improved chest-press and leg-press strength versus training alone (Devries & Phillips, Med Sci Sports Exerc).
• Cognitive-grade evidence. Rae 2003 (Proc Roy Soc B): 5 g/day for 6 weeks improved working memory and reasoning. McMorris 2007: creatine offset cognitive impairment from 24-hour sleep deprivation. Gordji-Nejad 2024 (Sci Rep): a single high-dose creatine load measurably improved cognition during 21 hours of sleep restriction.
• Bone-density evidence. Chilibeck 2015 (12-month RCT, 47 postmenopausal women): the creatine + training group preserved femoral-neck bone density while the placebo group lost it (Med Sci Sports Exerc).
• Methyl-pool sparing. Endogenous creatine synthesis consumes ~40% of the body's daily SAMe (S-adenosyl-methionine) budget. Supplementing creatine spares that methyl pool — lowering homocysteine and freeing methyl groups for DNA methylation, neurotransmitter synthesis, and epigenetic maintenance (Stead 2006, Am J Clin Nutr).
• Foundational, not exotic. Stacks with everything in this catalog — particularly the NMN / NAD+ precursor stack, the CoQ10 + PQQ + Urolithin A mitochondrial layer, TMG, and Magnesium Glycinate.

Why a sports supplement keeps appearing in longevity research

Every cell in the body uses ATP as its energy currency, but ATP cannot be stored in meaningful quantities — a typical cell holds only seconds of free ATP at peak demand. The phosphocreatine system is the buffer in front of mitochondrial ATP production: creatine binds a high-energy phosphate group, and when local ATP runs low (a muscle contraction, a neuron firing rapidly, a stressed cell trying to keep up with demand), the enzyme creatine kinase transfers that phosphate to ADP and regenerates ATP instantly — orders of magnitude faster than mitochondria can synthesize it from scratch. The effect is largest in tissues that demand short bursts of high power: skeletal muscle, the brain, and the heart.

The longevity-relevant question is what happens when that buffer runs low. Skeletal-muscle phosphocreatine stores fall with age. Brain creatine stores fall under sleep deprivation, hypoxia, hypoxic stress, depression, and aging. Without an adequate phosphocreatine pool, cells under load fall back on slower energy pathways, accumulate lactate, and signal stress — the same metabolic patterns that show up in frail elderly tissue and in sleep-deprived brains. Restoring the buffer to youthful levels is what supplementation does. It is not a stimulant, it is not a mitochondrial up-regulator, it is not a precursor to anything else — it is an energy reserve placed exactly where ATP is consumed, in the cytoplasm next to the contractile and synaptic machinery that needs it.

The sarcopenia argument (why this matters past 40)

Roughly 30% of skeletal-muscle mass is lost between ages 40 and 80 if nothing intervenes; the loss accelerates after 60 and again after 75. The endpoint is sarcopenia — clinical muscle wasting — and its consequences are not cosmetic. Skeletal-muscle index (lean mass divided by height squared) is one of the strongest single predictors of all-cause mortality in adults over 65, comparable to or exceeding the predictive power of LDL cholesterol or systolic blood pressure for that age group (Srikanthan 2014). Sarcopenia drives falls, fractures, hospitalization, loss of independence, metabolic dysfunction (muscle is the largest sink for postprandial glucose), and immune decline (skeletal muscle is the body's largest reservoir of glutamine, the immune system's preferred fuel).

The Devries & Phillips 2014 meta-analysis pooled 357 elderly subjects (mean age >57) across multiple resistance-training trials and found creatine plus training added ~1.4 kg of lean mass and improved chest-press and leg-press strength meaningfully versus training alone. Candow's 2014 and 2019 work confirms the effect is not training-day-only — daily 5 g works whether or not you trained that day, and creatine taken on training days only also works. The 2022 ISSN updated position stand reaffirms creatine as the most effective nutritional ergogenic for muscle mass and strength, with explicit elderly applications (Kreider 2017; Antonio 2021). Without resistance training, creatine helps less — the muscle has to be loaded for the buffer to matter. With training, the effect size roughly doubles versus training alone.

The cognitive evidence (which has caught up to the muscle evidence)

The brain runs on ATP at extraordinarily high turnover — neurons spike, glia clear neurotransmitter, ion gradients are restored, and the whole loop has to happen on a millisecond timescale. The brain has its own phosphocreatine system mirroring the one in muscle, and brain creatine concentrations can be measured by magnetic resonance spectroscopy (MRS). What that imaging shows: brain creatine falls with sleep deprivation, with chronic hypoxia, in major depression, and with age.

The trial set is now substantial. Rae 2003 (Proc Roy Soc B): 45 vegetarian subjects, 5 g/day for 6 weeks, double-blind crossover — significant improvement on Raven's Progressive Matrices and backward digit span. McMorris 2007: 5 g/day for 7 days, then 24-hour sleep deprivation — creatine subjects performed better than placebo on a battery of cognitive tasks. Benton 2011: vegetarian women, 5 g/day for 5 days — improved memory. Avgerinos 2018 systematic review of 6 trials: short-term memory and intelligence/reasoning improved consistently in creatine-supplemented subjects. Gordji-Nejad 2024 (Sci Rep): single oral dose of 0.35 g/kg creatine restored cognitive performance during 21 hours of sleep restriction — confirming a fast-acting central effect distinct from the slow muscle saturation timeline.

The pattern across trials: the cognitive benefit is largest in populations whose baseline brain creatine is lowest — vegetarians (lower meat-derived creatine intake), the sleep-deprived (creatine consumed faster than synthesized), the elderly (declining endogenous synthesis), and the depressed (depressive episodes are associated with low brain phosphocreatine on MRS imaging). For a healthy, well-rested, omnivorous 30-year-old, the cognitive effect is detectable but small. For everyone else, it is meaningful.

What the rest of the human research shows

Bone density. Chilibeck 2015 (Med Sci Sports Exerc) followed 47 postmenopausal women through 12 months of resistance training; the creatine group preserved femoral-neck bone-mineral density while the placebo group lost it. The mechanism is mechanotransduction — creatine-supported muscle pulls harder on bone, and bone remodels to load (Wolff's law).

Cardiovascular and metabolic. Smaller but consistent effects on insulin sensitivity (creatine improves muscle glucose uptake during training) and reductions in homocysteine via the methylation cycle that endogenous creatine synthesis would otherwise consume (Stead 2006). The methylation-sparing effect is mechanistically interesting: ~40% of the body's daily SAMe budget goes into making creatine de novo if you don't supplement, and chronically high methyl-group demand is a candidate driver of the elevated homocysteine seen in some aging adults.

Immune and recovery. Creatine supplementation reduces post-exercise muscle damage markers (creatine kinase, lactate dehydrogenase) and inflammatory cytokines after eccentric exercise (Cooke 2009). Older adults using creatine recover faster between resistance sessions, which is part of why long-term sarcopenia outcomes improve.

Safety. Creatine is one of the most-studied supplements in human history. Long-term trials at 5 g/day in healthy adults — including trials specifically designed to detect kidney function changes — show no signal for kidney damage, liver damage, or any other organ effect (Gualano 2012; Kim 2011; Lugaresi 2013). The persistent rumor that creatine harms kidneys traces to a single 1998 case report in a person with pre-existing kidney disease and has been repeatedly disproved in subsequent controlled trials. Creatine raises serum creatinine in routine lab work — but creatinine is the breakdown product of creatine itself, not a kidney-damage marker; the rise is expected and harmless.

Where creatine fits in this catalog

The longevity stack we sell already addresses NAD⁺ production (NMN, NMN 1000mg, NR, Liposomal NAD+), mitochondrial function (CoQ10, PQQ, Urolithin A), antioxidant cover (Glutathione, Vitamin C, Astaxanthin, ALA, NAC), inflammation (Curcumin, Quercetin, Fisetin), sirtuin activation (Resveratrol, Pterostilbene, Apigenin), epigenetic age (CaAKG), autophagy (Spermidine), and foundational nutrients (Magnesium, D3+K2, Omega-3, Taurine, Glycine).

What it didn't address until creatine sat in the catalog is tissue-level energy buffering: the phosphocreatine pool that determines how cells respond to short-term high-demand events — a muscle contraction, a cognitive task under stress, a heart beat under load. NMN and the NAD⁺ precursors raise the production ceiling of mitochondrial ATP. CoQ10 and PQQ optimize how mitochondria run. Creatine is the immediate-availability layer in front of all of that — the energy reserve that lets cells respond to demand at the timescale demand actually arrives at, rather than waiting for mitochondrial throughput to ramp.

What's in the bottle

• Creatine Monohydrate, micronized — 1000 mg per capsule. Monohydrate is the form used in over 90% of the published research, including every one of the trials cited above. Micronization reduces particle size for faster dissolution, lower GI side effects, and slightly better solubility in cool water than standard creatine.
• 5 capsules per serving = 5 g daily — the dose that has been the standard since the early 1990s and remains the recommendation in the 2017 ISSN position stand and the 2022 update. Loading phase (20 g/day for 5–7 days) is optional and only accelerates the speed at which intramuscular creatine reaches saturation; the long-term outcome at 5 g/day daily without loading is the same.
• Pharmaceutical-grade Creapure^®-equivalent purity — verified ≥99.9% creatine monohydrate by HPLC, with documented absence of creatinine (the inert breakdown product), dicyandiamide, and dihydrotriazine. The cheap creatine sold globally — particularly product sourced from non-regulated synthesis routes — is where those three impurities concentrate; ask any reputable supplement distributor and they will tell you the same.
• 90 capsules per bottle — 18-day supply at the 5 g/day saturation dose, or one month at the 3 g/day minimum-effective long-term dose. Designed to be taken alongside a meal.
• Capsules, not powder, intentionally. Powder is more economical per gram, but capsules eliminate the slight compliance friction of mixing — the people who fail at creatine usually fail because the powder sat unmixed on the counter, not because the dose was wrong.
• Vegetable cellulose capsule. No magnesium stearate, no titanium dioxide, no artificial colorants, no SLS, no proprietary blends. The label discloses the entire formula.
• Manufactured in cGMP-certified facilities with third-party batch testing for identity, potency, and purity.

How to take it

• Daily standard dose (recommended for 95% of people): 5 capsules (5 g) once per day, with a meal. Timing relative to training matters less than total daily intake; pick whichever time you'll actually remember. Adherence is the lever, not chronobiology.
• Optional loading protocol: 20 g/day (split into 4 doses of 5 g across the day) for 5–7 days, then drop to 5 g/day. Reaches intramuscular saturation in about a week instead of about a month. Eventual outcome is identical; loading is purely about speed-to-effect for athletes with a competition timeline.
• Long-term maintenance dose (post-saturation): 3 g/day (3 capsules) is the lowest dose with reliable evidence for maintaining elevated muscle creatine once the pool is full. Some people use this dose during deload weeks or periods when they're not training hard.
• Training-days-only pattern: Candow 2019 showed that taking 5 g only on training days (e.g., 3–5 days/week) produces gains comparable to daily dosing in resistance-trained subjects. Reasonable for cost-conscious or pill-fatigued users; for sarcopenia or cognitive applications, daily is still preferred.
• Hydration: creatine pulls water into muscle cells (this is partly the mechanism — cell volumization is itself an anabolic signal). Drink to thirst. Expect ~1–2 lb of intracellular water gain in the first 2–4 weeks; this is not fat and is not bloating in the gastrointestinal sense.
• Pair with carbohydrate or protein for slightly better uptake — insulin signaling drives muscle creatine transport via the SLC6A8 transporter. Not required; the effect is small.
• Coffee is fine. The early "caffeine blunts creatine" claim came from a single 1996 trial that did not replicate; subsequent work shows no antagonism at normal coffee doses.

What it pairs with in this catalog

Creatine is foundational rather than mechanism-specific, so it stacks cleanly with every supplement we sell. The strongest pairings:

• NMN + NAD⁺ precursors. NMN raises NAD⁺, which feeds mitochondrial ATP production. Creatine buffers the ATP that production yields. The two operate at different timescales — NAD⁺ raises the steady-state energy ceiling; phosphocreatine handles the transient spikes — and people running NMN protocols who add creatine often report a step-change in muscular endurance and recovery that NMN alone does not produce. Same logic for the Liposomal NAD+ Ultimate stack.
• CoQ10 + PQQ + Urolithin A — the mitochondrial-quality stack. CoQ10 shuttles electrons in Complex III of the mitochondrial chain. PQQ drives biogenesis (more mitochondria via PGC-1α/NRF1/TFAM). Urolithin A drives mitophagy (clearing the damaged ones via PINK1/Parkin). Creatine works downstream of all three — in the cytoplasm, where ATP is actually consumed. Better mitochondria + a fuller phosphocreatine buffer is the cleanest mechanistic case for combining all four.
• TMG (Trimethylglycine). Endogenous creatine synthesis burns ~40% of the body's daily methyl-group budget; supplementing creatine spares that pool, lowering homocysteine and freeing methyl groups for DNA methylation, neurotransmitter synthesis, and the work TMG already supports. The two pair particularly well in NMN protocols, where the methylation demand of NMN itself stacks on top.
• Magnesium Glycinate. Creatine kinase — the enzyme that actually uses phosphocreatine to regenerate ATP — is magnesium-dependent. Without sufficient elemental magnesium, the phosphocreatine system runs slower regardless of how saturated the creatine pool is. Magnesium Glycinate is the chelated form with the cleanest absorption profile and no laxative effect at the 400 mg elemental dose.
• Glycine. Glycine is the rate-limiting amino acid for endogenous creatine synthesis (creatine = guanidinoacetate + methyl group, and guanidinoacetate is built from glycine + arginine via AGAT). Glycine 1500mg supports the synthesis pathway and additionally improves slow-wave sleep, which is when creatine pool replenishment is most efficient.
• Resveratrol / Pterostilbene / Apigenin (sirtuin layer). Sirtuins use the NAD⁺ creatine helps cells make use of. Resveratrol activates SIRT1; Pterostilbene is the higher-bioavailability stilbenoid; Apigenin protects the NAD⁺ pool from CD38 degradation. Creatine indirectly supports the entire sirtuin layer by sparing methyl groups that the methylation reactions of healthy aging depend on.
• Vitamin D3 + K2. Vitamin D3+K2 independently improves muscle protein synthesis and bone density; combined with creatine + resistance training the bone-density signal in postmenopausal women (Chilibeck 2015) is meaningfully larger.
• Whey or plant protein (food, not in this catalog). Creatine plus adequate protein (≥1.6 g/kg/day) plus resistance training is the maximally-validated muscle-preservation protocol in adults over 60. Creatine without adequate protein still works; the reverse is also true; combined the effect is largest.

What to expect — realistic timeline

• Week 1. If you load (20 g/day): intramuscular saturation reached by day 5–7; mild GI sensitivity in some users (mitigated by splitting doses and taking with meals); ~1–2 lb of intracellular water weight. If you don't load: nothing perceptible yet.
• Weeks 2–4. Saturation reached without loading. Strength improves measurably in the gym — typically 5–15% on compound lifts versus the same training program without creatine. Recovery between hard sessions improves. Body weight up ~1–2 lb (water).
• Months 2–3. Lean mass gains accumulate: roughly 1–1.5 kg above what training alone would have delivered, per the Devries & Phillips meta-analysis. Cognitive effects, when present, become apparent — particularly during sleep restriction or stressful weeks.
• Months 3–6. Sarcopenia-relevant strength gains compound — measurable improvements in chest press, leg press, and grip strength. People over 60 begin to see meaningful functional changes (climbing stairs without breath, easier carrying, better balance).
• Months 6–12+. Bone-density signal in postmenopausal women becomes measurable on DEXA. Long-term cognitive and mood signals stabilize. The lean-mass gain plateaus — additional creatine does not push past the saturation ceiling — but the gains are maintained as long as supplementation continues.
• What NOT to expect. Acute energy. Stimulant feel. Sleep changes. Mood changes within the first week. Creatine is a slow-onset structural intervention; if you feel something dramatic in the first 48 hours, it's a placebo or it's the water shift. The signal you're looking for is in your training log over weeks, not in subjective feel on day 3.

Who this is for

• Anyone over 40 — sarcopenia begins quietly in the 40s and accelerates after 60. Earlier intervention is cheaper than later remediation.
• Anyone over 60, especially with concerns about frailty, falls, or grip strength — creatine + resistance training is the highest-evidence intervention available.
• Postmenopausal women — the bone-density preservation signal (Chilibeck 2015) is one of the cleanest creatine outcomes in the literature.
• Vegetarians and vegans — baseline muscle and brain creatine are lower because dietary creatine comes almost entirely from animal flesh; the cognitive trial effect sizes are largest in this group.
• People running an NMN or NAD+ protocol who want the energy buffer downstream of the production capacity NMN delivers.
• Athletes and lifters across all ages — the original use case; the strength and recovery effect remains the most-replicated finding in sports nutrition.
• People with high cognitive demand and poor sleep hygiene — students, parents of newborns, shift workers, founders, anyone whose week regularly contains a sub-6-hour-sleep night.
• People in or recovering from depression — small but consistent literature on creatine as adjunct for depressive symptoms (Lyoo 2012; Roitman 2007), particularly in women.

Who this is NOT for (or who should ask a doctor first)

• Pre-existing kidney disease. Creatine raises serum creatinine in routine kidney-function lab work — not because it harms kidneys, but because creatinine is the breakdown product of creatine itself. People with diagnosed CKD, on renal-replacement therapy, or with single-kidney status should clear creatine with their nephrologist before starting; healthy adults have repeatedly shown no kidney impact in long-term controlled trials.
• Diuretic use. Creatine pulls water intracellularly and can affect overall hydration status; coordinate with your prescribing physician.
• Bipolar disorder. A small case-report literature describes creatine triggering hypomanic or manic episodes in bipolar individuals (Roitman 2007 reported one such case during a depression trial); not contraindicated but warrants caution and ideally psychiatric monitoring in the first weeks.
• Pregnancy and breastfeeding. Safety not formally established despite long-standing use; conservative recommendation is to wait. Endogenous creatine demand is elevated during pregnancy and the maternal-fetal creatine system is an active research area, but supplementation has not been formally studied in this population.
• Under 18. Despite widespread use among adolescent athletes, formal long-term safety in growing humans is not established; conservative recommendation is to wait until skeletal maturity.
• People expecting a stimulant feel. Creatine is not pre-workout. If you want acute energy, look elsewhere; this is the structural buffer, not the pharmacological kick.

Frequently asked

Why not just eat red meat? A pound of raw red meat contains roughly 2 g of creatine. To hit 5 g/day from food alone you'd be eating ~2.5 lb of meat daily — a saturated-fat, methionine, and IGF-1-stimulating load that defeats the longevity goal. Creatine in meat also degrades with cooking; heat converts a portion of it to creatinine (biologically inert). For vegetarians and vegans the food gap is even more severe; vegetarian baseline muscle creatine is meaningfully lower than omnivore baseline, which is why cognitive trials show some of the largest effects in vegetarian populations.

Will I gain weight? Yes — typically 1–2 lb (0.5–1 kg) in the first 2–4 weeks, almost entirely intracellular water. Muscle cells become slightly fuller, which is itself part of the mechanism (cell volumization is an anabolic signal). The scale change is water, not fat. If you are training, the lean-mass gain that follows over months 2–6 is on top of this.

What about creatine HCL, magnesium chelate, ethyl ester, buffered, or "nitrate" forms? Each has been marketed as superior to monohydrate. None has produced a head-to-head trial showing meaningful clinical advantage. Monohydrate has the deepest evidence base, the lowest cost per gram, the highest documented purity standards, and the longest safety record. The other forms typically solve for marginal GI tolerance differences — which micronization addresses without abandoning the most-studied molecule. Save the money for more grams.

Do I need to cycle off? No. Long-term continuous-use trials at 5 g/day show no decline in benefit and no need for washout. Some people prefer training-days-only dosing (Candow 2019); that works too. There is no biological "tolerance" to creatine — the muscle is either saturated or it is not.

How long until I notice anything? Strength and recovery effects typically appear in 2–4 weeks (faster with loading). Cognitive effects, when present, tend to show in 4–8 weeks. Sarcopenia and bone-density benefits are longer arcs — 6–12 months of training plus creatine before the bone-density effect is measurable on DEXA.

Is timing important? Less than the supplement industry suggests. Daily total intake is what matters; pre- vs post-workout timing differences in trials are small and inconsistent. With a meal is a small absorption advantage via insulin-driven SLC6A8 transport; without a meal still works.

Does creatine cause hair loss? A single 2009 trial in rugby players showed an increase in serum DHT after a high-dose loading phase; the result has not replicated in subsequent studies, no trial has linked creatine supplementation to actual hair loss, and the meta-analytic literature finds no signal. If you are already on finasteride/dutasteride for male-pattern baldness or are concerned about androgenic acceleration, the practical recommendation is unchanged: monohydrate at 5 g/day is fine.

Does creatine cause kidney damage? No. Long-term controlled trials at 5 g/day in healthy adults show no kidney impact. The persistent concern traces to a 1998 case report in a person with pre-existing kidney disease and has been disproved in subsequent prospective trials including Gualano 2012, Kim 2011, and Lugaresi 2013. The serum creatinine elevation that creatine produces in lab work is the breakdown product of creatine itself, not a kidney-damage signal.

Does creatine cause cramping or dehydration? The opposite. Creatine pulls water intracellularly (which means slightly more total body water, not less) and football and rugby trials in heat have actually shown fewer cramps in creatine-supplemented athletes (Greenwood 2003). The 1990s-era concern came from anecdote, not from controlled work.

Can I open the capsules and put them in a smoothie? Yes. Micronized monohydrate dissolves better in cool water than coarse standard creatine; a few minutes of stirring or a brief shake is enough. Capsule shells are vegetable cellulose and pose no issue if discarded.

Does coffee blunt creatine? No. The 1996 single-trial finding never replicated; subsequent work shows no antagonism at normal coffee doses (1–4 cups/day). Take them together if convenient.

Vegetarian or vegan — bigger effect? Yes. Baseline intramuscular and intracerebral creatine are lower in plant-based eaters because dietary creatine is concentrated in animal flesh. The cognitive trial effect sizes (Rae 2003, Benton 2011) are among the largest in the literature precisely because the baseline was low. If you are vegetarian or vegan, creatine should arguably be your first supplement.

Is creatine an anabolic steroid? No. Creatine does not interact with the androgen receptor and does not affect endogenous testosterone production. It is an amino-acid-derived molecule that participates in cellular energy metabolism. The "supplement" categorization in the FDA framework is appropriate.

Why 1000 mg per capsule and not 2500 mg? Capsule swallowing limits — 1000 mg of micronized creatine fits a standard size-00 vegetable capsule reliably; pushing beyond that produces capsules that some users find difficult. Five 1000 mg capsules deliver the standard 5 g dose; users who prefer 3 g maintenance take three. Larger capsule sizes are achievable but increase swallowing-friction non-compliance — and adherence is the lever.

Will it interact with my medications? Likely not. Creatine has no significant CYP450 interactions and does not bind plasma proteins competitively. The known cautions are diuretics (hydration), lithium (mechanism unclear, theoretical), and renal-affecting drugs (NSAIDs in renal compromise). Always disclose all supplements to your prescriber.

Why does the bottle say 18-day supply at 5 g/day? Because 90 capsules × 1000 mg = 90 g, divided by 5 g/day = 18 days. The 90-capsule format is an entry-tier bottle suited to a first cycle, a saturation phase, or to running creatine on training days only (where a bottle lasts noticeably longer). For continuous daily 5 g/day users, two bottles per month is the typical reorder cadence; a multi-bottle subscription is the lowest-friction option.

Quality and purity

The creatine market has well-documented purity issues. Cheap creatine sourced from non-regulated synthesis routes can contain creatinine (the breakdown product, biologically inert — present means less actual creatine per gram), dicyandiamide (a cyanamide-derived synthesis intermediate), or dihydrotriazine (a synthesis-route contaminant of regulatory concern). Independent surveys of unbranded global creatine have found varying levels of all three.

Our creatine is verified ≥99.9% creatine monohydrate by HPLC, with documented absence of those three contaminants — Creapure^®-grade equivalent. Manufactured in cGMP-certified facilities with third-party verification on each batch (identity, potency, purity, and microbial safety). The certificate of analysis is available on request for any batch. The label discloses the entire formulation; there are no proprietary blends, no undeclared additives, no fillers beyond the vegetable cellulose capsule shell.

The science (selected references)

• Devries MC, Phillips SM. Creatine supplementation during resistance training in older adults — a meta-analysis. Med Sci Sports Exerc. 2014.
• Kreider RB, et al. International Society of Sports Nutrition position stand: safety and efficacy of creatine supplementation in exercise, sport, and medicine. J Int Soc Sports Nutr. 2017.
• Antonio J, et al. Common questions and misconceptions about creatine supplementation. J Int Soc Sports Nutr. 2021.
• Candow DG, et al. Effectiveness of creatine supplementation on aging muscle and bone: focus on falls prevention and inflammation. J Clin Med. 2019.
• Chilibeck PD, et al. Creatine monohydrate and resistance training increase bone mineral content and density in older men. Med Sci Sports Exerc. 2015.
• Rae C, et al. Oral creatine monohydrate supplementation improves brain performance: a double-blind, placebo-controlled, cross-over trial. Proc Roy Soc B. 2003.
• McMorris T, et al. Creatine supplementation and cognitive performance in elderly individuals. Aging Neuropsychol Cogn. 2007.
• Avgerinos KI, et al. Effects of creatine supplementation on cognitive function of healthy individuals: a systematic review of randomized controlled trials. Exp Gerontol. 2018.
• Gordji-Nejad A, et al. Single dose creatine improves cognitive performance and induces changes in cerebral high-energy phosphates during sleep deprivation. Sci Rep. 2024.
• Stead LM, et al. Methylation demand and homocysteine metabolism: effects of dietary provision of creatine and guanidinoacetate. Am J Clin Nutr. 2006.
• Srikanthan P, Karlamangla AS. Muscle mass index as a predictor of longevity in older adults. Am J Med. 2014.
• Gualano B, et al. Effects of creatine supplementation on renal function: a randomized, double-blind, placebo-controlled clinical trial. Eur J Appl Physiol. 2008/2012.
• Lyoo IK, et al. A randomized, double-blind placebo-controlled trial of oral creatine monohydrate augmentation for enhanced response to a selective serotonin reuptake inhibitor in women with major depressive disorder. Am J Psychiatry. 2012.
• Roitman S, et al. Creatine monohydrate in resistant depression: a preliminary study. Bipolar Disord. 2007.
• Cooke MB, et al. Creatine supplementation enhances muscle force recovery after eccentrically-induced muscle damage in healthy individuals. J Int Soc Sports Nutr. 2009.

Disclaimer

These statements have not been evaluated by the FDA. This product is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider before starting any supplement, particularly if you have kidney disease, are taking diuretics or lithium, are pregnant or breastfeeding, or are under 18. Creatine raises serum creatinine in routine lab work without indicating kidney harm — let your physician know you take creatine before any kidney-function test so that the result is interpreted correctly.