Brain Food? New Study Ties Creatine Intake to Mental Health

Written by John O'Sullivan CEO Principia Scientific International (using ChatGPT) on October 3, 2025. Posted in Current News

A fascinating new study out of Korea looked at over 5,000 people and found that those eating the least dietary creatine (remember, this is from food only — no supplements) had roughly double the risk of depression compared to those eating more.

They also had higher rates of suicidal thoughts, plans, and attempts, plus elevated anxiety scores. Creatine comes almost entirely from meat and fish, so this isn’t just a “supplement story” — it’s about what’s on your plate. Now, big caveat: this was a cross-sectional study, so we can’t prove cause and effect, and the mental health benefits might also be due to other nutrients in animal foods.

But taken together with a growing body of literature linking creatine to better brain and mental health, it’s another reason to think twice before skimping on this key nutrient. Read the study here.

Here is a summary of the Ostojic et al. (2025) paper plus a broader overview of evidence around creatine (its benefits, mechanisms, caveats) from other scientific sources.

Summary of the Ostojic et al. (2025) study

Title: Dietary creatine intake and mental health among the Korean population PubMed+1

Objective & design

• The aim was to examine associations between habitual dietary creatine intake (i.e. from non-supplement sources) and mental health indicators (depression, anxiety, suicidality) in a large Korean population sample. PubMed

• The study used data from the 2022 Korean National Health and Nutrition Examination Survey (KNHANES). PubMed

• Sample: 5,257 individuals (56% female, mean age ~51.1 years) with dietary intake data and at least one mental health assessment. PubMed

• Mean creatine intake was ~10.3 ± 9.5 mg per kg body weight (~0.7 g to ~1.0 g/day, depending on body weight). PubMed

Key findings

• Participants in the lowest quartile of creatine intake had higher depression scores than those in higher quartiles (ANOVA F = 4.003, p = 0.007). PubMed

• The prevalence of depression was highest in Q1 (6.9%) vs Q2 (3.3%), Q3 (4.3%), Q4 (3.6%) (p ≤ 0.05). PubMed

• Those in the lowest creatine quartile also reported more suicidal thoughts, plans, and attempts relative to other quartiles (p ≤ 0.05). PubMed

• Higher creatine intake was associated with lower odds of generalized anxiety disorder, after controlling for biomarkers of creatine turnover and demographic covariates (p ≤ 0.05). However, this relationship lost statistical significance when lifestyle factors (e.g. physical activity, smoking, alcohol) were also included in the model. PubMed

• The authors interpret these findings to suggest that higher dietary creatine intake may exert modest protective effects against depression, suicidality, and anxiety. PubMed

Limitations & caveats (as per authors / inferred)

• The design is cross-sectional, so directionality / causality cannot be established (i.e. we can’t tell whether low creatine intake contributes to depression or depressed individuals eat differently).

• Dietary intake is self-reported, which is subject to recall bias and measurement error.

• Creatine intake from diet is relatively modest compared to supplemental dosing; hence, effects are expected to be small.

• The anxiety-creatine association was attenuated when adjusting for lifestyle covariates, indicating the possibility of confounding.

• The findings are in a Korean (East Asian) population; generalizability to other populations may be limited.

Broader evidence for creatine: mechanisms, efficacy, safety

Below is a structured overview of what is known (and what remains uncertain) regarding creatine supplementation, with key references. (Note: some evidence is from supplementation, which provides larger doses than typically found in diet.)

How the Ostojic et al. study fits into this landscape & critical perspective

• The Ostojic et al. paper focuses on dietary creatine (i.e. from food) rather than supplementation. Its findings align with the broader hypothesis that creatine availability (whether endogenous, dietary, or supplemental) may influence brain/mental health outcomes.

• However, supplementation studies typically use much higher creatine doses (e.g. 3–5 g/day maintenance, or loading protocols) than the ~0.5–1 g/day range of dietary intake. Thus, effect sizes and mechanistic exposure differ.

• The cross-sectional and observational nature means that confounding (diet, lifestyle, health status) may bias associations. The attenuation of the anxiety relationship when including lifestyle covariates underscores this risk.

• Nonetheless, the observed associations are consistent with mechanistic plausibility (creatine’s role in brain energy metabolism) and complement experimental data.

Gaps, uncertainties, and future directions

• Causality and interventional trials: Observational studies (like Ostojic et al.) are hypothesis-generating. More randomized controlled trials (RCTs) are needed to test whether creatine supplementation (in various doses) can reduce depression, anxiety, or suicidality in vulnerable populations.

• Optimal dosing for brain effects: The dosing regimens needed to raise brain creatine (vs muscle creatine) and elicit cognitive or mood benefits are not fully established. MDPI+2MDPI+2

• Population heterogeneity: Effects may differ by age, baseline diet (e.g. vegetarians may respond differently), sex, baseline cognitive / mood status, and underlying pathology.

• Long-term safety in diverse groups: While short- to medium-term studies in healthy adults are reassuring, safety in populations with renal disease, psychiatric conditions, or long-term high-dose use warrants further study.

• Mechanistic clarity in brain / mood: More studies combining brain imaging / spectroscopy (e.g. ^31P-NMR) with cognitive / mood measures could help clarify causal pathways (i.e. does increasing brain creatine translate to functional changes?).

Reference: https://www.tandfonline.com/doi/full/10.1080/1028415X.2025.2558118

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