Hormones
What does it do to testosterone?
Measured hormone levels, and separately whether anything changed as a result.
12,336
people in trials
15
human studies
6
compounds, animal or cell only
1
trials found nothing
Measured in people
Ranked by how many people, which is a fact about the evidence and not a judgement about the compound. The one at the top is the most studied, which is not the same as the best. Counts are never added across compounds, because the same person can appear in more than one trial.
- 5,246 people2 human studies1 found nothing
TRAVERSE. 5,246 men aged 45 to 80 with preexisting or high risk of cardiovascular disease, symptoms of hypogonadism and two fasting testosterone levels below 300 ng/dL, randomised double-blind to transdermal testosterone gel titrated to 350 to 750 ng/dL or placebo. Mean treatment 21.7 months, mean follow-up 33.0 months. Primary composite of cardiovascular death, non-fatal myocardial infarction or non-fatal stroke occurred in 182 (7.0%) on testosterone and 190 (7.3%) on placebo, hazard ratio 0.96 (95% CI 0.78 to 1.17), p < 0.001 for non-inferiority.
New England Journal of Medicine, 2023 · 5,246 people
found nothingThe T-Trials. Treatment raised testosterone into the mid-normal range for men aged 19 to 40. Sexual activity, sexual desire and erectile function all improved significantly. Vitality did not improve on the fatigue scale. The proportion improving 6-minute walking distance by at least 50 m did not differ in the Physical Function Trial but did when all three trials were pooled, 20.5% against 12.6%, p = 0.003. Mood and depressive symptoms were slightly better. Adverse event rates were similar.
New England Journal of Medicine, 2016 · no headcount in the line
- 5,246 people1 human study
TRAVERSE, 5,246 men, no excess of cardiovascular death, heart attack or stroke against placebo. Included because it is the safety context for any testosterone ester, with the qualifier that TRAVERSE used a transdermal gel titrated to a defined range rather than an injectable.
New England Journal of Medicine, 2023 · 5,246 people
- 964 people3 human studies
Pooled analysis of 920 men from nine prospective studies, with testosterone as the primary endpoint. The proportion reaching testosterone below 20 ng/dL was 79 percent at month 1, then 92, 93, 90 and 91 percent at months 3, 6, 9 and 12. This is a pooled analysis of prospective studies, not itself a randomised trial, despite how PubMed indexes it, and it should not be cited as one.
Advances in Therapy, 2017 · 920 people
International phase 3 study at 18 centres in the United States, Chile and Mexico, in 44 treatment-naive children, 39 girls and five boys. 41 of 44 (93.2 percent) had prepubertal stimulated luteinising hormone at or below 5 IU/L at month 6, rising to 97.7 percent at month 12. Note the design: non-comparative and open-label, with no control group, and the endpoint is hormone suppression rather than adult height.
Journal of Pediatric Endocrinology and Metabolism, 2016 · 44 people
A randomised phase 3 trial in which triptorelin is the background androgen deprivation given to both arms while the randomisation tests immediate versus early salvage radiotherapy. Included here as the correction it represents: trials like this are frequently listed as triptorelin evidence, and they tell you about radiotherapy timing, not about the hormone drug.
The Lancet Oncology, 2020 · no headcount in the line
- 610 people1 human study
610 men with prostate adenocarcinoma, median age 72, randomised to two degarelix regimens or monthly intramuscular leuprolide. Testosterone at or below 0.5 ng/mL at every monthly measurement from day 28 to day 364 in 97.2, 98.3 and 96.4 percent respectively, meeting non-inferiority. At day 3, testosterone was at or below 0.5 ng/mL in 96.1 and 95.5 percent of degarelix patients and in none on leuprolide. Injection site reactions 40 percent with subcutaneous degarelix versus under 1 percent with intramuscular leuprolide, P below 0.001.
BJU International, 2008 · 610 people
- 199 people1 human study
199 patients: leuprolide suppressed testosterone comparably to DES with far fewer gynecomastia, nausea, edema and thromboembolic events.
New England Journal of Medicine, 1984 · 199 people
- 30 people1 human study
30 men with BMI at or above 26, randomised double-blind to 250 mg of a 10 percent forskolin extract twice daily or placebo for 12 weeks. Body fat percentage and fat mass on DXA fell significantly against placebo, bone mass changed significantly, serum free testosterone rose significantly, and lean body mass showed a non-significant trend upward (p equals 0.097). Fifteen participants per arm.
Obesity Research, 2005 · 30 people
- 29 people1 human study
Randomized study in 29 men: low-dose hCG every other day preserved intratesticular testosterone during exogenous testosterone.
Journal of Clinical Endocrinology and Metabolism, 2005 · 29 people
- 6 people2 human studies
Kisspeptin-54, not kisspeptin-10. First human kisspeptin study: a 90-minute infusion significantly raised LH, FSH and testosterone in six men.
Journal of Clinical Endocrinology and Metabolism, 2005 · 6 people
IV bolus kisspeptin-10 tripled LH in healthy men within 30 minutes; a 22.5-hour infusion raised LH and testosterone and increased LH pulse frequency.
Journal of Clinical Endocrinology and Metabolism, 2011 · no headcount in the line
- 6 people1 human study
Pulsatile subcutaneous GnRH by pump normalized gonadotropins within a week, raised testosterone from 77 to 520 ng/dL in one month and produced spermatogenesis in three of six hypogonadotropic men.
New England Journal of Medicine, 1982 · 6 people
- no headcount stated1 human study
Cetrorelix prevented premature LH surges (1.6% LH rise) with fewer gonadotropin ampoules and stimulation days than buserelin.
Human Reproduction, 2000 · no headcount in the line
- no headcount stated1 human study
Raised testosterone while preserving sperm concentration.
Fertility and Sterility, 2014 · no headcount in the line
Measured in animals or cells, not yet in people
These are separated from the trials above rather than ranked against them, because they answer a different question. A result in a rat is a real result and a reason somebody ran the study; it is not a measurement of what happens in you. Where the human work is missing, the reason is usually money rather than failure, and that is set out at the bottom of this page.
- 1 preclinical study
Measured in animals or cells
Independent replication of the mechanism: FOXO4-DRI induced p53 nuclear exclusion and apoptosis in senescent Leydig cells and improved testosterone secretion in naturally aged mice.
Aging, 2020 · animal
- 1 preclinical study
Measured in animals or cells
Interventions Testing Program. 17-alpha-estradiol at a threefold higher dose than previously tested robustly extended both median and maximal lifespan, still only in males. The same paper reports nordihydroguaiaretic acid replicated in males at the original dose and at threefold lower and higher doses, dose-dependently and without an effect on maximal lifespan, and that Protandim extended median lifespan in males only. It also reports that neither fish oil nor ursodeoxycholic acid extended lifespan, and that metformin alone at 0.1 percent of diet did not significantly extend lifespan while metformin combined with rapamycin robustly did.
Aging Cell, 2016 · animal
- 1 preclinical study
Measured in animals or cells
The original report of the male-preferential lifespan effect, alongside acarbose and 17-alpha-estradiol.
Aging Cell, 2014 · animal
- 1 preclinical study
Measured in animals or cells
found nothingThe relevant lifespan null for the nicotinamide riboside half of this product. In the National Institute on Aging Interventions Testing Program, genetically heterogeneous UM-HET3 mice fed nicotinamide riboside from 8 months of age showed no significant effect on lifespan in either sex in the pooled three-site dataset, the programme's primary endpoint. In the same cohort and the same three sites, 17-alpha-estradiol extended median male lifespan by 19 percent, demonstrating the experiment could detect a large effect. Funded by the National Institute on Aging, conflicts declared as none.
Aging Cell, 2021 · animal
- 1 preclinical study
Measured in animals or cells
A new osteocalcin-deficient mouse made by deleting Bglap and Bglap2. Bone quantity, glucose metabolism, testosterone synthesis and muscle mass were all normal. What was abnormal was the crystallographic orientation of bone apatite, and bone strength fell as a result. The authors conclude osteocalcin does not function as a hormone.
PLoS Genetics, 2020 · animal
- 1 preclinical study
Measured in animals or cells
C2C12 myotubes treated with 15 micromolar urolithin B for 24 hours grew and differentiated more, through increased protein synthesis and repression of the ubiquitin-proteasome pathway, with the androgen receptor implicated. In mice, 10 micrograms a day delivered continuously by implanted mini-osmotic pump for 28 days induced muscle hypertrophy and reduced atrophy after sciatic nerve section. Cells and mice, by continuous infusion, not an oral human dose.
Why the trial record looks like this
A missing trial is usually a missing sponsor. Nobody runs a nine-figure programme on a molecule they cannot own, so the compounds with the thinnest human records are often the oldest and most freely available ones rather than the weakest. Taking 17-alpha-estradiol as the example, because it states the problem most clearly:
The male-specific pattern is the most under-discussed finding in this whole field. Several of the programme's most reliable positives extend lifespan in male mice and not in female mice, and the effect is not a matter of statistical power: the female curves simply do not move. Nobody has established why. Proposed explanations include differences in drug metabolism, in baseline mortality causes between the sexes in this strain, and in hormonal context. What it means practically is that a headline reading a compound extends lifespan in mice is frequently describing an effect in half the animals, and that half is usually not stated.
The Interventions Testing Program is run by the National Institute on Aging at three independent sites, using UM-HET3 mice, a genetically heterogeneous four-way cross, so a result cannot be an artefact of one inbred strain. Both sexes are tested, cohorts are large enough to detect roughly a 10 percent change in lifespan, and nulls are published alongside positives. Nothing else in ageing research has that combination, which is why its results carry more weight than a single-laboratory finding and why its failures to replicate are worth as much attention as its successes.
A compound appears here only when a citation on its own page states this outcome and reports a result for it; naming it is not enough. Human, animal and cell work are counted separately and never merged. Participant counts are read from the study lines and deliberately undercount. Nothing here is advice, and nothing here is a recommendation to take or to avoid anything.