Creatine! We’re Gonna Pump You Up!

Medical Disclaimer: This article is for medical education purposes only. It does not constitute medical advice. Supplement use should be discussed with your healthcare provider in the context of your personal health history. CardioAdvocate has no financial relationship with any supplement manufacturer.

Creatine! We’re Gonna Pump You Up!

What “the Best-Studied Supplement” Actually Means When You Hold It to a Real Evidentiary Standard

A Question from the Late ’90s

Before I went to medical school, I volunteered in a muscle physiology laboratory at the University of Washington in the late 1990s. Creatine supplements were starting to show up in locker rooms and GNC stores across the country. Mark McGwire had a jar of it in his locker. The supplement industry was booming. And I had a question for the professor who ran the lab — a man who understood skeletal muscle at the molecular level: Does this stuff actually work?

His answer was measured. He explained the phosphocreatine system — how creatine kinase catalyzes the transfer of a phosphate group from phosphocreatine to ADP, regenerating ATP during the first seconds of maximal effort. He thought supplementation might help in a situation like a sprint, where you need rapid ATP replenishment. But for longer efforts? The phosphagen system is depleted in roughly 10 seconds. After that, you’re running on glycolysis and oxidative phosphorylation. More creatine won’t help.

That made sense to me then. It still makes sense. But nearly three decades have passed, creatine has become a $2 billion global industry, and the claim I hear most often — from patients, from colleagues, from every fitness influencer with a ring light — is that creatine is “the best-studied supplement in existence.”

That claim deserves examination. Because “best-studied” is doing an enormous amount of work in that sentence, and almost nobody stops to ask: best-studied compared to what?

How Creatine Actually Works: The Phosphagen System

Let’s start with what is not controversial.

Your muscles store ATP in small quantities — roughly 2–5 millimoles per kilogram of muscle. At maximal exertion, that supply is exhausted in about 1–2 seconds. This is where the phosphocreatine (PCr) system comes in.

Phosphocreatine concentrations in skeletal muscle are much larger — 20–35 millimoles per kilogram. The enzyme creatine kinase (CK) catalyzes a beautifully simple reversible reaction: phosphocreatine donates its high-energy phosphate to ADP, regenerating ATP almost instantaneously. No oxygen required. No metabolic intermediates. It’s the fastest energy system in the body.

The catch: it’s also the shortest-lived. The phosphagen system sustains maximal effort for roughly 6–10 seconds before PCr stores are substantially depleted. After that, glycolysis and then oxidative phosphorylation take over — slower but sustainable.

Creatine supplementation increases intramuscular creatine and phosphocreatine stores by approximately 20–40% in people whose stores are not already saturated. The theory is simple: more PCr means more rapid ATP regeneration, which means a few more seconds of maximal power output, a few more reps before failure, and faster recovery of the phosphagen system between bouts.

That professor was right — mostly: The phosphocreatine system is fundamentally a sprint-speed energy buffer. It matters most in the first seconds of explosive effort. But what has become clearer since the late ’90s is that weight training is, repetition by repetition, a series of short maximal efforts with brief recovery periods. Each set is its own “sprint.” And the recovery of PCr between sets — which takes 3–5 minutes to fully replenish — is where supplemental creatine may provide its most practical benefit: faster PCr resynthesis, which means better performance in subsequent sets.

The “Best-Studied Supplement”: Grading on a Curve

Here is the claim you will encounter everywhere: creatine is the most-studied supplement in history, with hundreds of peer-reviewed studies supporting its efficacy and safety.

This is technically true. And profoundly misleading.

It is true in the same way that saying someone graduated first in their class is impressive — until you learn the class had four students. Creatine is the best-studied supplement in a category where the evidentiary bar is on the floor.

What Supplement Studies Look Like

The dietary supplement industry operates under the Dietary Supplement Health and Education Act of 1994 (DSHEA), which does not require manufacturers to prove efficacy before selling a product. No FDA approval. No phase III trials. No post-marketing surveillance. A supplement can make “structure/function” claims (“supports muscle health”) without a single human study. This is the regulatory environment that produced the evidence base we are about to evaluate.

Here is what the typical creatine study looks like when you compare it to the standard we demand of a pharmaceutical:

Creatine studies vs. pharmaceutical trials:

• Sample size: The typical creatine RCT enrolls 10–54 participants. Many of the foundational studies had fewer than 20. A 1998 critical review noted that none of the studies it evaluated included a sample size calculation. Compare this to a statin trial like JUPITER (17,802 participants) or a CETP inhibitor trial like REVEAL (30,449).
• Duration: Most creatine trials last 4–12 weeks. The longest follow-up data cited by the ISSN position stand extends to about 5 years for safety. Compare this to statin studies with 5–10 years of hard-endpoint follow-up.
• Endpoints: Creatine studies measure 1-rep max, lean body mass by DEXA, and Wingate test power. These are surrogate endpoints. No creatine trial has ever measured cardiovascular events, fractures, falls, hospitalizations, or mortality as primary outcomes.
• Population: The majority of creatine RCTs have been conducted in young, healthy males. A 2025 systematic review in active females found that most studies showed no benefit compared to placebo, with an overall small evidence base.

A review by the Agency for Healthcare Research and Quality (AHRQ) described the creatine literature as “of small sample size and short duration.”

So when someone says creatine is “the best-studied supplement,” what they mean is: among products that face no regulatory requirement to prove they work, creatine has accumulated the largest pile of small, short studies using surrogate endpoints in mostly young men. That is a real distinction. It is not the same thing as “well-studied” by the standard we apply to any intervention we actually prescribe.

The honest framing: If the supplement industry’s evidence base is a D-minus, creatine is pulling a solid B. That makes it the valedictorian of a remedial class. The evidence is better than anything else in the supplement aisle. But it would not survive a New Drug Application at the FDA.

What the Data Actually Shows: Effect Sizes

Let’s be precise about what creatine does in controlled trials, because the gap between “statistically significant” and “practically meaningful” matters.

Strength

A 2025 meta-analysis of 69 RCTs (1,937 participants) found that creatine combined with resistance training significantly improved strength compared to placebo. The bench press gain averaged about 1.4 kg over placebo (weighted mean difference 1.43 kg, 95% CI: 0.53–2.34). Standardized effect sizes across various meta-analyses range from 0.265 to 0.677 — small to moderate by Cohen’s conventions.

A separate meta-analysis of adults under 50 reported upper-body strength gains of 4.43 kg and lower-body gains of 11.35 kg over placebo. These are larger numbers, but they represent the total gain difference over a training program, not the starting-point advantage.

Putting this in perspective: If you bench press 225 pounds, creatine might add 3–10 pounds to that over a training cycle compared to training without it. This is real. It is measurable. But it is not the difference between a productive training program and a “waste” — the claim that lifting without creatine is pointless is absurd on its face. The vast majority of the strength gain comes from the training itself.

Lean Mass

Creatine consistently increases lean body mass as measured by DEXA. But this finding comes with a substantial caveat: creatine pulls water into muscle cells. It is osmotically active, and raising intramuscular creatine concentrations increases intracellular osmotic pressure, drawing water into the cell. One study found that intracellular water rose by approximately 1.13 liters during a loading phase, accounting for roughly 55% of the total body weight gain.

DEXA cannot distinguish between intracellular water and contractile protein. When a study reports a “1.5 kg increase in lean mass,” a meaningful portion of that is water, not new muscle tissue. This does not mean creatine doesn’t support hypertrophy — but it means the lean mass numbers overstate the actual muscle protein accretion.

A 2026 meta-analysis in young men confirmed that lean mass gains were significant only when creatine was combined with resistance training. Without training, creatine does not build muscle. It fills muscle cells with water.

Power and Sprint Performance

This is where the phosphagen mechanism is most directly relevant, and the evidence is most consistent. Creatine improves short-duration, high-intensity power output — Wingate test peak power, repeated sprint performance, and short-burst activities. That prediction from the UW muscle lab holds up.

Endurance

For steady-state aerobic exercise — distance running, long cycling, sustained swimming — creatine does not improve performance. A 2023 systematic review in trained athletes found the evidence “controversial,” and a 2026 review in Nutrients concluded that creatine “may be most relevant in selected endurance and mixed-sport contexts involving repeated high-intensity efforts, sprint finishes, or power-endurance demands, rather than for endurance performance broadly.”

The 1–3 kg of water weight gain during loading may actually hurt weight-bearing endurance performance.

The 20–30% Problem: Non-Responders

Here is a fact the supplement industry rarely advertises: approximately 20–30% of people who take creatine do not respond meaningfully.

The responder/non-responder classification was formalized by Syrotuik and Bell (2004), building on earlier work by Greenhaff. They defined non-response as an increase of less than 10 mmol/kg dry weight in resting total muscle creatine after 5 days of loading at 20 g/day. Non-responders tend to have higher baseline creatine stores, fewer type II muscle fibers, and less muscle mass to begin with.

Think about what this means: if you already eat a creatine-rich diet (red meat, fish) and have naturally high intramuscular creatine, supplementation may do nothing for you. Your stores are already near saturation. The supplement has nowhere to go.

The uncomfortable caveat: The responder/non-responder data come from very small studies — the original classification was based on 11 men. We are making population-level claims about response rates from samples that would not survive peer review in any other field. The 20–30% non-responder figure is widely cited but weakly supported, which is a microcosm of the broader problem with creatine research.

Creatine for Your Brain: Where the Hype Outpaces the Science

The brain is metabolically voracious — it consumes roughly 20% of the body’s ATP despite being 2% of body weight. The brain synthesizes and stores its own creatine, and the phosphocreatine system operates in neurons just as it does in muscle. In theory, supplemental creatine could improve brain bioenergetics.

In practice, the evidence is thin.

A 2024 systematic review and meta-analysis of 16 trials found a small positive effect on memory (standardized mean difference of 0.31) — roughly comparable to the difference between a good night’s sleep and a mediocre one. It found no significant effect on overall cognitive function or executive function. A corrigendum to the paper walked back some of the attention and processing speed claims.

The age pattern is uncertain: one analysis found the strongest cognitive effect in older adults (66–76 years), while another subgroup analysis pointed to larger benefits in younger adults. When two meta-analyses of the same data point in opposite directions on the same question, the answer is: we don’t know.

What about 10–15 grams for cognition? The claim that higher doses (10–15 g/day) produce cognitive benefits circulates widely in the longevity and biohacking communities. Here is where it comes from: a critical review in The Journal of Nutrition (2025) found that only 5 of the 16 trials in the cognitive meta-analysis used the standard 3–5 g/day dose. The working-memory effect seen at 20 g/day did not appear at lower doses. The “10 gram” figure comes from a single 8-week dose-ranging study in adolescent females with SSRI-resistant depression. This is the foundation upon which influencers are building dosing recommendations for the general population. The European Food Safety Authority (EFSA) has not established a cause-and-effect relationship between creatine supplementation and cognitive function.

The Journal of Nutrition critique put it bluntly: the marketing has outpaced the science, and “cognitive and structural biases shape how the evidence is interpreted and communicated.”

Dosing: What the Evidence Actually Supports

Loading vs. Daily Dosing

The traditional loading protocol is 20–25 g/day for 5–7 days, split into 4–5 doses, followed by a maintenance dose of 3–5 g/day. This saturates muscle creatine stores in about a week.

Alternatively, taking 3–5 g/day without loading reaches the same saturation point in approximately 3–4 weeks. The endpoint is identical; loading just gets you there faster. Loading also causes more GI discomfort and more acute water retention (1–3 kg of body weight gain).

There is no evidence that cycling creatine (taking breaks) provides any benefit. Once stores are saturated, a daily maintenance dose keeps them there. If you stop, stores return to baseline over 4–6 weeks.

Timing: Before, During, or After?

The evidence for workout timing is surprisingly thin. Most studies find that daily consistency matters more than when you take it. One meta-analysis suggested a slight advantage for post-workout dosing, but the effect was small and the studies were heterogeneous. Taking creatine with a meal or with carbohydrates may modestly improve uptake via insulin-mediated muscle creatine transport, but this has not been shown to produce meaningfully different outcomes.

The honest answer: take it whenever you’ll actually remember to take it.

Which Form?

Creatine monohydrate is the only form with a substantial evidence base. Period.

Creatine HCl is marketed as more soluble and requiring lower doses. The solubility claim is true. The efficacy claim is unsupported — no large, independent trial has shown HCl is superior to monohydrate for muscle uptake or performance.

Buffered creatine (Kre-Alkalyn) was tested head-to-head against monohydrate in a 2012 JISSN study. The conclusion was definitive: “neither manufacturer’s recommended doses of Kre-Alkalyn promoted greater changes in muscle creatine content, body composition, strength, or anaerobic capacity than creatine monohydrate.” There was also “no evidence that supplementing the diet with a buffered form of creatine resulted in fewer side effects.”

Micronized creatine monohydrate is chemically identical to standard monohydrate, processed into smaller particles for better mixability. It may be easier on the stomach for some people. It is not a different molecule.

The supplement industry math: Creatine monohydrate costs roughly $0.03–0.05 per gram. Creatine HCl costs 5–10 times more. Buffered creatine costs even more. There is no evidence that any of them outperforms the cheapest option. The price premium is a marketing achievement, not a scientific one.

Creatine and Aging: Sarcopenia, Bone, and the Longevity Angle

This is where creatine advocacy has expanded most aggressively in recent years, driven by the longevity medicine and functional medicine communities. The argument: if creatine helps muscles, it should help fight sarcopenia (age-related muscle loss), preserve bone density, and extend healthspan.

Muscle

A 2025 meta-analysis of 11 RCTs in adults over 60 found that creatine plus resistance training probably adds a small strength benefit over resistance training alone. The effect size was small (Hedges’ g = 0.31, 95% CI 0.18–0.45), and the evidence was rated moderate certainty. This is not nothing. But it is a modest effect, and it requires the training — creatine alone does not preserve muscle in aging.

Bone

A 2025 review in Current Osteoporosis Reports by Candow and Moriarty concluded that the majority of research points to creatine being more “hype” than “hope” for bone mass. Creatine does not appear to increase areal bone mineral density (BMD). Some work suggests it may preserve regional bone structure when combined with exercise, but the evidence is insufficient to recommend it for bone health.

The Longevity Claim

No study has examined whether creatine supplementation extends lifespan or reduces all-cause mortality. The longevity community’s enthusiasm for creatine is built on extrapolation from short-term surrogate endpoints, not clinical outcomes. This is the same inferential leap we criticize in every other domain of medicine — assuming that moving a biomarker will move the clinical needle. It is the HDL hypothesis applied to a supplement.

Related: Too Much of a GOOD Thing? — Dysfunctional HDL — Why raising a number on a lab report is not the same as improving a clinical outcome. The $10 billion CETP inhibitor lesson applies to surrogate-endpoint reasoning everywhere.

Side Effects: What to Expect and What to Watch For

Water Retention and Weight Gain

This is the most predictable side effect, and it is not subtle. Creatine is osmotically active. When intramuscular creatine concentrations rise, water follows — drawn into the cell by osmotic pressure. During a loading phase (20–25 g/day for 5–7 days), expect a weight gain of 1–3 kg (2–6 pounds), virtually all of it water. Even at maintenance dosing (3–5 g/day without loading), most users gain 1–2 kg once stores are saturated.

This water is primarily intracellular — roughly 55% of the total weight gain in one study. It is inside the muscle cell, not subcutaneous bloating. Some researchers have speculated that this cell swelling may itself act as an anabolic signal, promoting protein synthesis. That is biologically plausible but far from proven.

For lifters, the water retention is cosmetically neutral or even favorable — muscles look fuller. For endurance athletes, runners, or anyone competing in a weight-class sport, 2–6 extra pounds of water is not nothing. It increases the metabolic cost of weight-bearing movement. This is one reason creatine has not caught on in distance running or competitive swimming.

Gastrointestinal Effects

GI complaints — nausea, bloating, diarrhea, cramping — are common during the loading phase and are clearly dose-dependent. Taking 20 grams in a single dose is substantially more likely to cause GI distress than splitting it into four 5-gram servings with meals. At maintenance doses (3–5 g/day), GI side effects are uncommon and not clearly above placebo rates in controlled trials.

The practical advice: if you choose to load, split your doses across the day and take them with food. Or skip loading entirely and take 3–5 g/day — you reach the same saturation point in 3–4 weeks with far less GI trouble.

Muscle Cramping

Creatine has a reputation for causing muscle cramps. The evidence does not support this. A critical review of creatine side effects found that cramping was inconsistently reported across studies and not clearly above placebo rates. The International Society of Sports Nutrition’s position stand specifically states that creatine does not increase the incidence of cramping or dehydration. This appears to be gym folklore that has persisted despite the evidence.

Hair Loss

A single 2009 study in college-age rugby players found that creatine loading increased levels of dihydrotestosterone (DHT), which is associated with androgenetic alopecia. This finding has never been replicated. The ISSN position stand does not list hair loss as a side effect. But the claim circulates widely, and patients ask about it. The honest answer: one small, unreplicated study does not establish causation, but we cannot rule it out either.

The Creatinine Trap: A Clinical Problem Hiding in Your Lab Results

This is the section I am writing for clinicians — and for patients who need to understand what their doctor may be seeing on their lab work.

Creatine is non-enzymatically and irreversibly converted to creatinine through spontaneous dehydration in skeletal muscle. This is normal physiology. Creatinine is then filtered by the kidneys, and we measure serum creatinine to estimate glomerular filtration rate (eGFR). The equations we use — CKD-EPI, MDRD — assume that serum creatinine production is relatively stable. Creatine supplementation violates that assumption.

When you increase the total body pool of creatine by 20–40%, you increase the rate of creatinine production. Serum creatinine rises. eGFR falls. Not because the kidney is filtering less, but because there is more creatinine to filter.

How Much Does Creatinine Actually Rise?

A 2025 systematic review and meta-analysis in BMC Nephrology pooled 12 randomized trials and found a statistically significant but small increase in serum creatinine: a mean difference of approximately 0.07 mg/dL (95% CI: 0.01–0.12). This is the pooled average. Individual variation is wider — some patients will see a rise of 0.1–0.3 mg/dL, especially during loading or at higher doses. The rise was largest in studies of one week or less (during loading) and persisted at lower levels with chronic use.

Critically, the same meta-analysis found no significant change in GFR when measured by gold-standard methods (inulin clearance, ⁵¹Cr-EDTA, or cystatin C–based equations). The kidney is fine. The lab test is misleading.

What this looks like in practice: A patient with a baseline creatinine of 1.0 mg/dL and an eGFR of 90 starts taking creatine. Their creatinine rises to 1.15 mg/dL. Their eGFR drops to 78. On paper, they have just crossed from CKD stage 1 to stage 2. In reality, nothing has changed about their kidney function. The equation was fed a higher input and produced a lower output. This is a mathematical artifact, not a clinical event.

The Dangerous Scenario: Older Patients with Borderline Kidney Function

Here is the clinical trap I see in my practice, and it should concern every primary care physician, nephrologist, and longevity medicine doctor who has patients on creatine:

An older patient — perhaps 65 or 70 — starts taking creatine. Maybe they lift. Maybe they were told it helps cognition. Maybe their functional medicine doctor recommended it. Their baseline eGFR was already marginal — say, 55–65, reflecting mild CKD stage 3a. They start creatine. Their next lab shows creatinine has crept up and eGFR has dropped to 48. The patient says: “Oh, that’s just the creatine.”

Maybe it is. Maybe it isn’t. And that is the problem.

Creatine supplementation gives patients — and sometimes their doctors — a ready-made excuse to dismiss a worsening creatinine. “It’s just the supplement.” But CKD is progressive. Diabetic nephropathy is progressive. Hypertensive nephrosclerosis is progressive. A rising creatinine in a 70-year-old with diabetes and hypertension may very well reflect real kidney decline, and attributing it to creatine without verification is dangerous.

The clinical rule: A rising creatinine in a patient taking creatine must be verified, not assumed to be an artifact. The verification is straightforward:

• Cystatin C: Order a cystatin C–based eGFR. Cystatin C is produced at a constant rate by all nucleated cells and is not affected by creatine supplementation, muscle mass, diet, or exercise. If the cystatin C eGFR is stable while the creatinine-based eGFR has dropped, the creatinine rise is likely an artifact of supplementation. If both are declining, you have a real problem.
• Combined CKD-EPI equation: The 2021 CKD-EPI equation that uses both creatinine and cystatin C provides the most accurate eGFR estimate and is less susceptible to being thrown off by creatine.
• Stop and recheck: If cystatin C is unavailable, have the patient discontinue creatine for 2–4 weeks, then recheck serum creatinine. If it returns to baseline, the elevation was an artifact. If it does not, the decline is real.

A 2025 literature review concluded that “robust trials show no adverse renal effects in healthy individuals, even with long-term or high-dose use,” and a comprehensive narrative review in Nutrients agreed. But both reviews explicitly flag that these data come from healthy populations. Patients with pre-existing CKD, diabetic nephropathy, or other renal disease were largely excluded from these studies. We do not have safety data in the populations that need it most.

For clinicians: Do not tell your patient creatine is “fine for kidneys” without qualification. It is probably fine for healthy kidneys. For a patient with CKD stage 3 or worse, the honest answer is: we do not know, the safety data do not include you, and the lab artifact problem makes monitoring harder. If your patient insists on continuing creatine, order cystatin C at baseline and at each follow-up so you can separate signal from noise. And never let “it’s just the creatine” become a substitute for clinical vigilance.

For patients: If you are taking creatine and your doctor tells you your kidney function has declined, do not dismiss it. Ask: “Can we check a cystatin C to see if this is real or just the creatine?” That single question could be the difference between catching early kidney disease and missing it.

So Should You Take It?

Here is my honest assessment, applying the same evidentiary standard I apply to everything on this site:

The Bottom Line

What the evidence supports:

• Creatine monohydrate, at 3–5 g/day, increases intramuscular phosphocreatine stores and improves short-duration, high-intensity performance. The mechanism is well understood and undisputed.
• When combined with resistance training, creatine produces small but statistically significant strength gains over placebo — roughly a standardized effect of 0.3–0.7, or 1–10 additional pounds on your big lifts over a training cycle.
• Creatine monohydrate is the only form supported by substantial evidence. No alternative form has demonstrated superiority.
• Safety in healthy adults appears well-established, with no evidence of kidney harm at standard doses. The creatinine elevation is a lab artifact, not nephrotoxicity.
• Loading (20 g/day for 5–7 days) saturates stores faster but is not necessary. Daily dosing of 3–5 g reaches the same endpoint in 3–4 weeks.

What the evidence does not support:

• The claim that creatine is “well-studied” by the standard we apply to pharmaceuticals. The evidence base consists of hundreds of small, short trials using surrogate endpoints, mostly in young men. No creatine study has measured hard clinical outcomes.
• The claim that lifting without creatine is a “waste.” The vast majority of training adaptation comes from the training itself. Creatine provides a modest marginal benefit.
• Cognitive benefits at any dose. The meta-analytic evidence shows a small effect on memory (SMD 0.31), no effect on executive function, and the higher-dose cognitive claims rest on individual small studies. EFSA has not established a cause-and-effect relationship.
• Benefits for bone density. The literature is more “hype than hope.”
• Benefits for steady-state endurance performance. The mechanism does not support it, and the data confirm it.
• Superiority of any form over monohydrate. The price premium for HCl, buffered, and other forms is marketing, not science.

What I tell patients:

• If you’re doing serious resistance training and want to optimize a marginal gain, creatine monohydrate at 3–5 g/day is a reasonable choice. It works for what the mechanism predicts: short-burst power, recovery between sets, and possibly training volume.
• If you’re not training, creatine will do nothing for you except add water weight.
• If someone tells you creatine is essential, that lifting without it is pointless, or that you need 10–15 grams for brain health — ask them to show you the trial. A real one, with adequate power, appropriate endpoints, and independent funding. They won’t be able to.
• 20–30% of people may not respond at all. If you try it for 4–6 weeks and notice nothing, your stores may already be saturated from dietary intake.
• Buy monohydrate. The cheapest option is the best-studied one. Everything else is a premium for marketing.
• If you have kidney disease, talk to your nephrologist first.

Questions to Ask Your Doctor

• Is creatine supplementation appropriate given my kidney function and current medications?
• My creatinine level went up after starting creatine — is this a real kidney problem or a lab artifact?
• I’m being told to take 10–15 g/day for cognitive benefits — what does the evidence actually say?
• I’m over 60 and interested in creatine for sarcopenia — is the evidence strong enough to justify it?
• How do I know if I’m a responder or non-responder?

“Because an informed patient is a healthier patient.”
— CardioAdvocate.com

Disclaimer: CardioAdvocate.com provides science-based cardiovascular and metabolic education for patients and their families. This content is authored and reviewed by a board-certified cardiologist but does not establish a doctor–patient relationship. CardioAdvocate has no financial relationship with any supplement manufacturer. Always consult your own physician before starting any supplement. If you have kidney disease or other chronic conditions, discuss creatine supplementation with your specialist before use.