Turkesterone increases testosterone and builds muscle

Turkesterone is an ecdysteroid from Ajuga turkestanica, sold as a "natural anabolic" on the claim that it builds muscle comparably to anabolic steroids while raising testosterone. Supplement marketing generally leans on rodent research and on a single human trial of a different compound — ecdysterone — while the mechanism literature indicates ecdysteroids do not act on the androgen receptor at all. Note also that WADA has placed ecdysterone on its Monitoring Program, not its Prohibited List: it is watched, not banned.

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7 studies weighed Updated

Evidence Breakdown

2 PRO
4 AGAINST
1 NEUTRAL

Based on 7 studies

THE BIGGER QUESTION

Whether this one statement holds is settled above. What to actually do about it is a wider question, weighed across every claim that bears on it.

Evidence map

For & against, at a glance

Pro Con Neutral
26.9% confidence
Claim
2 4 1
RCT Pro
Isenmann E et al. · 2019
Archives of Toxicology

The single most-cited human trial of an ecdysteroid: 46 young men were randomized across a 10-week supervised strength-training intervention to placebo, a lower ecdysterone dose (two capsules/day) or a higher dose (eight capsules/day), with a non-training arm as control. The abstract reports the result qualitatively and gives no figures at all: "significantly higher increases in muscle mass were observed in those participants that were dosed with ecdysterone", and "significantly more pronounced increases in one-repetition bench press performance were observed." The precise-sounding "+19 kg versus +6 kg" numbers that circulate for this trial **could not be traced to any accessible source** — the full text is paywalled and those figures appear only on supplement-retailer pages — so they are not repeated here. Parallel C2C12 myotube experiments in the same paper showed hypertrophic activity. No increase in liver or kidney toxicity biomarkers was seen. The authors were sufficiently convinced to recommend that ecdysterone be added to the WADA Prohibited List under S1.2 "other anabolic agents." Two caveats matter enormously: the compound tested was **ecdysterone (20-hydroxyecdysone), not turkesterone**, and the proposed mechanism was estrogen-receptor-mediated, not androgenic. The trial was small, has not been independently replicated, and analytical work found the ecdysterone content of the capsules used was far higher than the label stated.

0.44

The single most-cited human trial of an ecdysteroid: 46 young men were randomized across a 10-week supervised strength-training intervention to placebo, a lower ecdysterone dose (two capsules/day) or a higher dose (eight capsules/day), with a non-training arm as control. The abstract reports the result qualitatively and gives no figures at all: "significantly higher increases in muscle mass were observed in those participants that were dosed with ecdysterone", and "significantly more pronounced increases in one-repetition bench press performance were observed." The precise-sounding "+19 kg versus +6 kg" numbers that circulate for this trial **could not be traced to any accessible source** — the full text is paywalled and those figures appear only on supplement-retailer pages — so they are not repeated here. Parallel C2C12 myotube experiments in the same paper showed hypertrophic activity. No increase in liver or kidney toxicity biomarkers was seen. The authors were sufficiently convinced to recommend that ecdysterone be added to the WADA Prohibited List under S1.2 "other anabolic agents." Two caveats matter enormously: the compound tested was **ecdysterone (20-hydroxyecdysone), not turkesterone**, and the proposed mechanism was estrogen-receptor-mediated, not androgenic. The trial was small, has not been independently replicated, and analytical work found the ecdysterone content of the capsules used was far higher than the label stated.

Design RCT (0.8) × quality 0.55 = impact 0.44

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RCT Neutral
Dioh W et al. · 2023
Journal of Cachexia, Sarcopenia and Muscle

Phase 1 randomized, double-blind, placebo-controlled pharmacokinetic and safety study of BIO101, a pharmaceutical-grade 20-hydroxyecdysone (ecdysterone), in 54 healthy adults — a single-ascending-dose arm at 100–1400 mg in young adults and at 1400 mg in adults aged 65+, then a 14-day multiple-ascending-dose arm at 350 mg once daily up to 450 mg twice daily in older adults. Ecdysterone is orally absorbed and measurable in plasma, but the pharmacokinetics are unflattering for a supplement: Cmax and AUC rose **less than dose-proportionally** across 100–1400 mg (absorption appears saturable), mean half-life was short at 2.4–4.9 h, and only roughly 1.5–3% of the ingested dose was recovered in urine over 24 h. Safety was good (mild-to-moderate adverse events only). No sex hormones were measured; the biomarkers tracked were myostatin, renin, aldosterone, myoglobin and creatine kinase.

0.44

Phase 1 randomized, double-blind, placebo-controlled pharmacokinetic and safety study of BIO101, a pharmaceutical-grade 20-hydroxyecdysone (ecdysterone), in 54 healthy adults — a single-ascending-dose arm at 100–1400 mg in young adults and at 1400 mg in adults aged 65+, then a 14-day multiple-ascending-dose arm at 350 mg once daily up to 450 mg twice daily in older adults. Ecdysterone is orally absorbed and measurable in plasma, but the pharmacokinetics are unflattering for a supplement: Cmax and AUC rose **less than dose-proportionally** across 100–1400 mg (absorption appears saturable), mean half-life was short at 2.4–4.9 h, and only roughly 1.5–3% of the ingested dose was recovered in urine over 24 h. Safety was good (mild-to-moderate adverse events only). No sex hormones were measured; the biomarkers tracked were myostatin, renin, aldosterone, myoglobin and creatine kinase.

Design RCT (0.8) × quality 0.55 = impact 0.44

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Double-Blind RCT Con
Dissemond J et al. · 2025
Journal of the International Society of Sports Nutrition

Twelve-week randomized, double-blind, placebo-controlled trial in resistance-trained young men (24 completers) who trained with free weights three times per week while taking a commercial phytosteroid supplement (Weider Beta-Ecdysterone, labelled 25 mg 20-hydroxyecdysone + 50 mg diosgenin per capsule) or placebo. Both groups improved strength and body composition over time with **no group differences** — squat 1RM d=0.60, bench press 1RM d=0.16, fat-free mass d=0.13, all time effects only — and no significant changes in testosterone, estradiol, cortisol or IGF-1 in either group. Crucially, the researchers then chemically analysed the capsules and found **less than 1% of the labelled 20-hydroxyecdysone** (<10 µg against a claimed 25 mg) and only ~10–31% of the labelled diosgenin; the product also produced no hypertrophic activity in C2C12 muscle cells, whereas an earlier 2018 batch of the same product did. The null training result is therefore inseparable from the fact that the pills were essentially empty — which is itself a direct finding about the reliability of commercial ecdysteroid supplements.

0.47

Twelve-week randomized, double-blind, placebo-controlled trial in resistance-trained young men (24 completers) who trained with free weights three times per week while taking a commercial phytosteroid supplement (Weider Beta-Ecdysterone, labelled 25 mg 20-hydroxyecdysone + 50 mg diosgenin per capsule) or placebo. Both groups improved strength and body composition over time with **no group differences** — squat 1RM d=0.60, bench press 1RM d=0.16, fat-free mass d=0.13, all time effects only — and no significant changes in testosterone, estradiol, cortisol or IGF-1 in either group. Crucially, the researchers then chemically analysed the capsules and found **less than 1% of the labelled 20-hydroxyecdysone** (<10 µg against a claimed 25 mg) and only ~10–31% of the labelled diosgenin; the product also produced no hypertrophic activity in C2C12 muscle cells, whereas an earlier 2018 batch of the same product did. The null training result is therefore inseparable from the fact that the pills were essentially empty — which is itself a direct finding about the reliability of commercial ecdysteroid supplements.

Design Double-Blind RCT (0.85) × quality 0.55 = impact 0.47

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RCT Con
Antonio J et al. · 2024
Research Directs in Health Sciences

Randomized, placebo-controlled trial in 31 active adults (14 men, 17 women) given 500 mg/day of turkesterone (Ajuga turkestanica extract) or a rice-flour placebo for four weeks, with body composition measured by DXA. There were no between-group differences in any outcome: body mass (p=0.38), lean body mass (p=0.68), fat mass (p=0.06) or percent body fat (p=0.14). Numerically the turkesterone group actually *lost* slightly more lean mass than placebo (-0.6 ± 1.4 kg vs -0.3 ± 1.7 kg). The authors — who titled the paper "It's Not Deca" — concluded that four weeks of 500 mg turkesterone "did not affect body composition in active, healthy males and females." Limitations: short duration, no supervised resistance-training programme, no strength testing, and no verification of the capsules' actual turkesterone content.

0.44

Randomized, placebo-controlled trial in 31 active adults (14 men, 17 women) given 500 mg/day of turkesterone (Ajuga turkestanica extract) or a rice-flour placebo for four weeks, with body composition measured by DXA. There were no between-group differences in any outcome: body mass (p=0.38), lean body mass (p=0.68), fat mass (p=0.06) or percent body fat (p=0.14). Numerically the turkesterone group actually *lost* slightly more lean mass than placebo (-0.6 ± 1.4 kg vs -0.3 ± 1.7 kg). The authors — who titled the paper "It's Not Deca" — concluded that four weeks of 500 mg turkesterone "did not affect body composition in active, healthy males and females." Limitations: short duration, no supervised resistance-training programme, no strength testing, and no verification of the capsules' actual turkesterone content.

Design RCT (0.8) × quality 0.55 = impact 0.44

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+3 more studies View all ↓

Showing the 4 strongest of 7 studies. Tap any node to expand its detail.

Evidence

PRO (2)

PRO RCTn=460.55 Isenmann E, Ambrosio G et al. (2019)

Ecdysterone (NOT turkesterone) produced 'significantly higher increases in muscle mass' and 'significantly more pronounced increases in one-repetition bench press performance' over 10 weeks. The abstract reports no numeric values, and the full text is paywalled -- the widely-quoted '+19 kg vs +6 kg' figures could not be traced to any accessible source and have been removed

The single most-cited human trial of an ecdysteroid: 46 young men were randomized across a 10-week supervised strength-training intervention to placebo, a lower ecdysterone dose (two capsules/day) or a higher dose (eight capsules/day), with a non-training arm as control. The abstract reports the result qualitatively and gives no figures at all: "significantly higher increases in muscle mass were observed in those participants that were dosed with ecdysterone", and "significantly more pronounced increases in one-repetition bench press performance were observed." The precise-sounding "+19 kg versus +6 kg" numbers that circulate for this trial could not be traced to any accessible source — the full text is paywalled and those figures appear only on supplement-retailer pages — so they are not repeated here. Parallel C2C12 myotube experiments in the same paper showed hypertrophic activity. No increase in liver or kidney toxicity biomarkers was seen. The authors were sufficiently convinced to recommend that ecdysterone be added to the WADA Prohibited List under S1.2 "other anabolic agents." Two caveats matter enormously: the compound tested was ecdysterone (20-hydroxyecdysone), not turkesterone, and the proposed mechanism was estrogen-receptor-mediated, not androgenic. The trial was small, has not been independently replicated, and analytical work found the ecdysterone content of the capsules used was far higher than the label stated.

Weighted 0.55 — n=46 split across four arms leaves only ~11-12 per group, so every comparison is underpowered. Never independently replicated, and the capsules assayed far above their labelled ecdysterone content, so the dose actually administered is uncertain. Tests ecdysterone (20-hydroxyecdysone), NOT turkesterone -- serious indirectness for any turkesterone claim. WADA funding carries no commercial stake, though the funder had an interest in a positive anabolic finding (it underpins a scheduling recommendation).

Funding: World Anti-Doping Agency (grant 15C18MP)

Archives of Toxicology

DOI: 10.1007/s00204-019-02490-x

PRO Animal Study0.15 Syrov VN, Kurmukov AG (1976)

Reported anabolic effects of turkesterone and turkesterone tetraacetate on muscle tissue, protein synthesis, organ mass and blood proteins in male rats; doses, controls and effect sizes are not recoverable

The original Soviet rodent work that turkesterone's entire reputation rests on: a 1976 Russian-language study (Probl Endokrinol (Mosk) 22(3):107-12) reporting anabolic properties of the phytoecdysone turkesterone and of turkesterone tetraacetate in male rats, with effects on muscle tissue, protein synthesis, organ mass and blood proteins. PubMed indexes the citation but carries no abstract, and the full text is not accessible in English, so the doses, controls and effect sizes cannot be independently checked. Secondary sources routinely cite it as showing turkesterone outperforming methandrostenolone (Dianabol) for weight gain in rats — a comparison this evidence card cannot verify. Treat it as what it is: a fifty-year-old, non-replicated, unverifiable rat study, in rats, with no human follow-up.

Weighted 0.15 — Male rats; the number of animals cannot be determined. PubMed and Europe PMC index the citation but carry NO abstract, and the Russian-language full text is not accessible, so sample size, funding, doses and controls are all unverifiable -- every one is omitted rather than guessed. A fifty-year-old, non-replicated, unauditable Soviet rodent study with no human follow-up, routinely cited second-hand for a methandrostenolone comparison this record cannot confirm. Floor of the animal class: the limitation is not that it is small but that it cannot be checked at all.

Problemy Endokrinologii (Moskva)

https://pubmed.ncbi.nlm.nih.gov/935080/

AGAINST (4)

AGAINST Animal Study0.65 Parr MK, Zhao P et al. (2014)

Ecdysterone increased muscle fibre size in rats; the hypertrophy was blocked by an antiestrogen but not by an antiandrogen, and was reproduced by a selective ERβ ligand (not an ERα ligand) — the pathway is estrogen receptor beta, not the androgen receptor

Mechanistic study in male Wistar rats plus differentiated C2C12 muscle cells and HEK293 transactivation assays, testing how ecdysterone (20-hydroxyecdysone) produces muscle hypertrophy. Ecdysterone did increase fibre size, but the decisive finding is how: the hypertrophy it induced could be blocked by an antiestrogen and not by an antiandrogen, and a selective estrogen-receptor-beta (ERβ) ligand reproduced the effect while an ERα ligand did not. Ecdysterone therefore appears to act through estrogen receptor beta, not through the androgen receptor — the pathway that testosterone and anabolic steroids use. This is the primary experimental basis for the conclusion that ecdysteroids are not androgenic and are not a mechanism by which testosterone would rise.

Weighted 0.65 — Male Wistar rats plus differentiated C2C12 myotubes and HEK293 transactivation assays; the number of animals is not reported in the accessible record. Strong for its class — the receptor attribution is supported by three independent lines of evidence (selective ligands, selective antagonists, reporter-gene transactivation) rather than a single assay. It stays below 0.7 because the animal count is unverifiable and the funding statement could not be retrieved (paywalled). Note the weight is a quality multiplier only; the indirectness of rodent and cell-line evidence for humans is already carried by the animal-study base weight.

Molecular Nutrition & Food Research

DOI: 10.1002/mnfr.201300806

AGAINST RCTn=31AGAINST FUNDER0.55 Antonio J, Silver TA et al. (2024)

No between-group differences after 4 weeks of 500 mg/day turkesterone vs placebo: body mass p = 0.38, lean body mass p = 0.68, fat mass p = 0.06, percent body fat p = 0.14; the turkesterone group numerically lost more lean mass (-0.6 +/- 1.4 kg vs -0.3 +/- 1.7 kg)

Randomized, placebo-controlled trial in 31 active adults (14 men, 17 women) given 500 mg/day of turkesterone (Ajuga turkestanica extract) or a rice-flour placebo for four weeks, with body composition measured by DXA. There were no between-group differences in any outcome: body mass (p=0.38), lean body mass (p=0.68), fat mass (p=0.06) or percent body fat (p=0.14). Numerically the turkesterone group actually lost slightly more lean mass than placebo (-0.6 ± 1.4 kg vs -0.3 ± 1.7 kg). The authors — who titled the paper "It's Not Deca" — concluded that four weeks of 500 mg turkesterone "did not affect body composition in active, healthy males and females." Limitations: short duration, no supervised resistance-training programme, no strength testing, and no verification of the capsules' actual turkesterone content.

Weighted 0.55 — n=31 analysed (14 M, 17 F), randomised and placebo-controlled with DXA. An industry-supplied null result, which makes the null more rather than less credible. Held to 0.55 by real limitations the authors admit: only 4 weeks, no supervised resistance-training programme, no strength testing, and no independent assay confirming the capsules actually contained turkesterone. The lead author is also CEO of the ISSN, which is sponsor-funded.

Funding: Nutrition Formulators, Miramar FL (in-kind donation of the product and placebo) — this result runs against the funder's own interest, which strengthens it.

Research Directs in Health Sciences

DOI: 10.53520/rdhs2024.104126

AGAINST Double-Blind RCTn=240.55 Dissemond J, Havers T et al. (2025)

No group differences over 12 weeks (squat 1RM d=0.60, bench 1RM d=0.16, fat-free mass d=0.13 — time effects only) and no change in testosterone, estradiol, cortisol or IGF-1; chemical assay found LESS THAN 1% of the labelled 20-hydroxyecdysone (<10 ug against a claimed 25 mg) and only ~10-31% of the labelled diosgenin

Twelve-week randomized, double-blind, placebo-controlled trial in resistance-trained young men (24 completers) who trained with free weights three times per week while taking a commercial phytosteroid supplement (Weider Beta-Ecdysterone, labelled 25 mg 20-hydroxyecdysone + 50 mg diosgenin per capsule) or placebo. Both groups improved strength and body composition over time with no group differences — squat 1RM d=0.60, bench press 1RM d=0.16, fat-free mass d=0.13, all time effects only — and no significant changes in testosterone, estradiol, cortisol or IGF-1 in either group. Crucially, the researchers then chemically analysed the capsules and found less than 1% of the labelled 20-hydroxyecdysone (<10 µg against a claimed 25 mg) and only ~10–31% of the labelled diosgenin; the product also produced no hypertrophic activity in C2C12 muscle cells, whereas an earlier 2018 batch of the same product did. The null training result is therefore inseparable from the fact that the pills were essentially empty — which is itself a direct finding about the reliability of commercial ecdysteroid supplements.

Weighted 0.55 — 24 completers (12 per group) of 28 randomised — underpowered for between-group strength differences. Methodologically strong for its size: double-blind, 12 weeks of supervised free-weight training, independently funded, product bought off the shelf, and unusually the researchers assayed the capsules afterwards. That assay is what caps the multiplier for any claim ABOUT ECDYSTERONE: the pills were essentially empty, so the null tells you about commercial supplement labelling rather than about the compound. As evidence on label reliability it would rate far higher.

Funding: none declared (no external funding; the supplement was purchased commercially, not donated by the manufacturer)

Journal of the International Society of Sports Nutrition

DOI: 10.1080/15502783.2025.2540408

AGAINST Crossover Trialn=110.30 Harris DR, Chapman-Lopez T et al. (2024)

No condition, time or interaction effects (p>0.05) on IGF-1, resting metabolic rate or substrate oxidation at either 1000 or 2000 mg

Randomized, single-blinded, placebo-controlled crossover trial in 11 recreationally active men (23.3 ± 2.2 y) who each completed three conditions separated by at least seven days: 1000 mg turkesterone, 2000 mg turkesterone, or placebo. Serum IGF-1, resting metabolic rate and substrate oxidation were measured pre-ingestion and at 1 h, 3 h and 24 h post-ingestion. There were no significant condition, time or interaction effects (p > 0.05) for IGF-1, resting metabolic rate, or carbohydrate/fat oxidation at either dose — i.e. acute turkesterone, even at 2 g, did not move the anabolic signalling or metabolic markers the supplement is marketed on. No adverse cardiovascular or gastrointestinal effects were observed. This is an acute-dose mechanistic study, not a training trial, and the sample is small.

Weighted 0.30 — Only 11 men, and an acute single-dose design tracking surrogate markers over 24 hours - not a training study, so it cannot speak to hypertrophy directly and is seriously indirect for the claims turkesterone is marketed on. The null is genuine but underpowered. Independently funded, with no supplement-company involvement declared.

Funding: Baylor University departmental thesis research grant and the Texas Chapter of the American College of Sports Medicine

Muscles

DOI: 10.3390/muscles3040031

NEUTRAL (1)

NEUTRAL RCTn=54INDUSTRY0.55 Dioh W, Tourette C et al. (2023)

Cmax and AUC rose LESS than dose-proportionally across 100-1400 mg (absorption appears saturable); mean half-life only 2.4-4.9 h; roughly 1.5-3% of the ingested dose recovered in urine over 24 h; only mild-to-moderate adverse events

Phase 1 randomized, double-blind, placebo-controlled pharmacokinetic and safety study of BIO101, a pharmaceutical-grade 20-hydroxyecdysone (ecdysterone), in 54 healthy adults — a single-ascending-dose arm at 100–1400 mg in young adults and at 1400 mg in adults aged 65+, then a 14-day multiple-ascending-dose arm at 350 mg once daily up to 450 mg twice daily in older adults. Ecdysterone is orally absorbed and measurable in plasma, but the pharmacokinetics are unflattering for a supplement: Cmax and AUC rose less than dose-proportionally across 100–1400 mg (absorption appears saturable), mean half-life was short at 2.4–4.9 h, and only roughly 1.5–3% of the ingested dose was recovered in urine over 24 h. Safety was good (mild-to-moderate adverse events only). No sex hormones were measured; the biomarkers tracked were myostatin, renin, aldosterone, myoglobin and creatine kinase.

Weighted 0.55 — 54 healthy volunteers in a Phase 1 dose-ranging study. Run entirely by the manufacturer of the compound, which normally warrants heavy discounting — but the pharmacokinetic findings are unflattering to the sponsor's own product (saturable absorption, short half-life, poor recovery), which cuts against reporting bias. Mid-band mainly for indirectness: this measures PK and safety of a pharmaceutical-grade compound in healthy adults, not the efficacy of an ecdysterone supplement, and no sex hormones were measured.

Funding: Biophytis (five authors are Biophytis employees and three are former employees; BIO101 is the company's own drug candidate — there is no separate funding statement)

Journal of Cachexia, Sarcopenia and Muscle

DOI: 10.1002/jcsm.13195