Literature index · testosterone & AAS
Testosterone & Anabolic-Androgenic Steroid Literature Index
A cited bibliography of the trials, guidelines, and harm literature that define what is — and is not — established about testosterone therapy and non-prescribed anabolic-androgenic steroid use.
This is a reading list of published science on testosterone therapy and anabolic-androgenic steroids — not clinical guidance. Every entry links to a primary source (peer-reviewed journal, regulatory document, or government reference) that was fetched and verified during research. Items are grouped by theme and tagged with an evidence tier reflecting the strength of the underlying study design.
Evidence tiers
- Approvedregulator-licensed / approved indication
- Clinicalpublished human data, unapproved
- Preclinicalanimal / tissue / cell only
- Unverifiedno peer-reviewed literature
Landmark randomized trials
The trials that established the modern evidence base for testosterone therapy in men with hypogonadism.
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Clinical
A multicenter, randomized, double-blind, placebo-controlled noninferiority trial in 5,246 men with hypogonadism and preexisting or high cardiovascular risk. Testosterone replacement was noninferior to placebo for the composite of cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke.
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Clinical
The coordinated Testosterone Trials evaluated 790 men aged 65 or older with low serum testosterone. Sexual function improved significantly; vitality and walking distance did not improve in their primary trials, and adverse-event rates were similar between groups.
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Clinical
Measured spine and hip volumetric bone mineral density and estimated bone strength by finite element analysis. Volumetric bone density and estimated strength increased with testosterone treatment, more in trabecular than peripheral bone and more in spine than hip.
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Clinical
The placebo-controlled Cognitive Function Trial measured delayed paragraph recall, visual memory, executive function, and spatial ability. No significant improvement in memory or other cognitive domains was observed versus placebo.
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Clinical
Tested whether testosterone treatment raised hemoglobin in men aged 65 and older with unexplained anemia. Hemoglobin increases and correction of anemia were greater with testosterone than placebo, including in participants with anemia of known cause.
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Clinical
A two-year, double-blind, placebo-controlled trial. Testosterone treatment reduced the proportion of participants with type 2 diabetes beyond the lifestyle programme effect; increases in haematocrit were noted as a potential limitation.
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Clinical
Measured adjudicated clinical fractures in men with hypogonadism randomized to testosterone or placebo. Testosterone did not lower fracture incidence, and fracture counts were numerically higher with testosterone over a median 3.19 years of follow-up.
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Clinical
The foundational dose-response study. In 61 eugonadal men, graded doses of testosterone produced dose-dependent increases in fat-free mass, muscle strength and volume, hemoglobin, and IGF-I, while HDL cholesterol and fat mass decreased with dose. This established that testosterone's anabolic effects are dose-dependent in healthy men. The study quantifies doses only to characterize its design; no dosing recommendation is made or implied here.
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Clinical
In 88 hypogonadal men aged 60 and older, daily anastrozole normalized androgen production and modestly decreased estradiol production, but did not improve body composition or strength. Aromatase inhibitors are not FDA-approved for male hypogonadism and are used off-label.
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Guidelines and regulatory documents
Clinical practice guidelines and FDA regulatory actions that define approved use, contraindications, and monitoring.
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Approved
Recommends diagnosing hypogonadism only in men with consistent symptoms and signs plus unequivocally and consistently low serum testosterone. Sets out recommendations for diagnostic testing, evaluation of cause, appropriate use of therapy, contraindications, treatment targets, and monitoring of adverse effects including hematocrit and prostate cancer risk.
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Approved
Provides evidence-based guidance on diagnosing, treating, and monitoring adult men with testosterone deficiency. The underlying systematic review covered literature from 1980 through February 2017 (546 studies of approximately 350,000 men), with an updated evidence search through February 2022.
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Approved
States that functional hypogonadism should be diagnosed from clinical symptoms plus repeatedly low morning fasting total testosterone measured with a well-validated assay, after excluding organic causes. Notes short-term improvement in sexual function while long-term benefit and safety in functional hypogonadism remain incompletely documented.
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Approved
Based on review of the TRAVERSE trial and required postmarket ambulatory blood pressure monitoring studies, FDA required class-wide labeling changes: adding TRAVERSE results, retaining the Limitation of Use language regarding age-related hypogonadism, removing prior Boxed Warning language on adverse cardiovascular outcomes, and adding blood-pressure information. Completed ABPM studies confirmed a class-wide increase in blood pressure.
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Approved
States that testosterone products are FDA-approved only for men with absent or low testosterone in conjunction with an associated medical condition, and that no approved product is indicated for low testosterone without an associated medical condition. In June 2026, FDA requested prescribing-information updates following review and reanalysis of the evidence.
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Approved
Assesses the analytical accuracy and reliability of testosterone and estradiol tests in clinical, research, and public-health laboratories through reference measurement procedures, performance assessment, certification, and ongoing accuracy monitoring. Addresses the well-documented variability between immunoassay and LC-MS/MS testosterone measurements.
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Unverified
The FDA warns that SARMs are not FDA-approved, cannot legally be marketed in the U.S. as dietary supplements or drugs, and have been associated with serious or life-threatening problems including heart attack, stroke, psychosis, liver injury and acute liver failure, infertility, and testicular shrinkage.
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Measurement and physiology
How testosterone is measured accurately and what the foundational dose-response literature established.
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Approved
Assesses the analytical accuracy and reliability of testosterone and estradiol tests in clinical, research, and public-health laboratories through reference measurement procedures, performance assessment, certification, and ongoing accuracy monitoring. Addresses the well-documented variability between immunoassay and LC-MS/MS testosterone measurements.
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Clinical
The foundational dose-response study. In 61 eugonadal men, graded doses of testosterone produced dose-dependent increases in fat-free mass, muscle strength and volume, hemoglobin, and IGF-I, while HDL cholesterol and fat mass decreased with dose. This established that testosterone's anabolic effects are dose-dependent in healthy men. The study quantifies doses only to characterize its design; no dosing recommendation is made or implied here.
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Anabolic-androgenic steroid harm literature
What the published literature documents about the harms of non-prescribed and illicit AAS use — cardiomyopathy, hypogonadism, lipid derangement, hepatotoxicity, psychiatric morbidity, and prevalence.
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Clinical
The first large controlled study of its type. Long-term illicit AAS use was associated with left ventricular systolic and diastolic dysfunction, left ventricular hypertrophy, and increased coronary atherosclerosis. Coronary atherosclerotic burden was strongly associated with cumulative lifetime duration of use. Systolic deficits appeared to recover after discontinuation; diastolic dysfunction appeared less reversible.
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Clinical
Recovery from anabolic steroid-induced hypogonadism (ASIH) is highly variable and depends on age and degree of AAS use. Testicular function and spermatogenesis generally recover over months to years; gynaecomastia is unlikely to recover; psychological recovery data are insufficient and conflicting. The review notes a paucity of prospective controlled data.
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Clinical
AAS abuse was associated with elevated LDL, reduced HDL, elevated blood pressure, left ventricular hypertrophy that may persist after cessation, acute myocardial infarction, and fatal ventricular arrhythmias.
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Approved
C-17α alkylated androgenic steroids have been implicated in prolonged cholestasis, peliosis hepatis, nodular regeneration, hepatic adenomas, and hepatocellular carcinoma. Non-alkylated injectable testosterone produces this hepatotoxic profile far less frequently — the structural basis for the liver-injury distinction between oral alkylated and injectable testosterone compounds.
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Clinical
In 545 AAS-positive men compared with 5,450 matched controls, AAS use was strongly associated with psychiatric morbidity, including higher incidence of anxiolytic, antipsychotic, antidepressant, and psychostimulant treatment, particularly in the years following a doping sanction. AAS use disorder is a recognized clinical entity involving dependence and withdrawal.
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Clinical
Estimated a global lifetime prevalence of AAS use of 3.3% (95% CI 2.8–3.8), with significantly higher prevalence among males (6.4%) than females (1.6%). Established nonmedical AAS use as a widespread public-health problem rather than a phenomenon limited to elite athletes.
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Adjacent compounds
The evidence status of compounds used off-label around testosterone therapy and AAS use — clomiphene, hCG, anastrozole, SARMs, and post-cycle therapy. None of these are presented as protocols.
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Clinical
Clomiphene citrate increased total testosterone and other hormone concentrations and improved clinical symptoms of hypogonadism, with few reported side effects and no serious adverse events. Clomiphene is not FDA-approved for male hypogonadism and is used off-label; it works by blocking estrogen feedback at the hypothalamus and pituitary.
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Clinical
hCG can re-establish or maintain spermatogenesis in hypogonadal men by replacing LH-driven intratesticular testosterone production, and can serve as an alternative or adjunct to testosterone replacement in men seeking to preserve fertility. Exogenous testosterone suppresses intratesticular testosterone and spermatogenesis; hCG addresses this axis directly.
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Clinical
In 88 hypogonadal men aged 60 and older, daily anastrozole normalized androgen production and modestly decreased estradiol production, but did not improve body composition or strength. Aromatase inhibitors are not FDA-approved for male hypogonadism and are used off-label.
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Preclinical
SARMs act as androgen-receptor agonists or antagonists with tissue-selective effects and have been studied across multiple potential indications, but had no FDA-approved indications and faced uncertain efficacy and regulatory endpoints. No SARM is FDA-approved as of this review.
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Unverified
The FDA warns that SARMs are not FDA-approved, cannot legally be marketed in the U.S. as dietary supplements or drugs, and have been associated with serious or life-threatening problems including heart attack, stroke, psychosis, liver injury and acute liver failure, infertility, and testicular shrinkage.
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Unverified
Clomiphene citrate is the most commonly used off-label pharmacological approach in anabolic steroid-induced hypogonadism and can improve gonadotropin and testosterone levels, but evidence specific to post-cycle therapy following AAS use is limited, clinical recovery is variable, and safety and long-term efficacy remain incompletely defined. No controlled clinical trials of post-cycle therapy as a protocol were identified; the evidence base consists of narrative reviews and retrospective series.
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What this index is not
This page is a bibliography of published research and regulatory documents. It contains no dosing schedules, no amounts, no injection frequencies, no cycle lengths, and no instructions for use of any compound. Nothing here is medical advice, diagnosis, or a recommendation to administer any substance. Several compounds referenced — clomiphene, hCG, anastrozole, SARMs, and post-cycle therapy regimens — are not FDA-approved for the purposes described and are used off-label. Consult a licensed physician before making any health decision.
Cellaire Labs publishes research and educational reference material only. Nothing here is medical advice, and nothing here is a recommendation to administer any substance to a human or animal.