Stress-associated testosterone suppression: central adaptation or hypogonadism?

Military and athlete studies suggest stress-related low testosterone is often reversible brain signaling, not testicular failure

Journal: The Journal of Clinical Endocrinology and Metabolism | Published: 2026-07-15 | Type: Journal Article, Review | PMID: 42044038 Authors: Friedl KE (U.S. Army Research Institute of Environmental Medicine), Nindl BC (University of Pittsburgh), Potter AW (U.S. Army Research Institute of Environmental Medicine) Funding/COI: Not listed. Notable given two of three authors are employed by the U.S. Army Research Institute of Environmental Medicine, an institution with direct institutional interest in normalizing hormonal changes seen in military personnel under operational stress.

Summary

This is a narrative review arguing that low testosterone measured in stressed populations, soldiers in combat, endurance athletes, people in negative energy balance, usually reflects the brain dialing down the hypothalamic-pituitary-gonadal (HPG) axis rather than the testes failing. The authors lean heavily on decades-old Korean War and Vietnam War field endocrinology studies alongside more modern human chorionic gonadotropin (hCG) stimulation data to make the case that this suppression is adaptive and reversible with energy and sleep recovery.

Claims

• Testosterone suppression under sustained stress is commonly centrally mediated (via suppressed GnRH/LH pulsatility), not due to intrinsic testicular failure
• hCG stimulation studies show preserved Leydig cell responsiveness in stressed states, meaning the testes can still make testosterone when directly stimulated, supporting a central rather than gonadal origin for low T
• Negative energy balance, sleep restriction, and uncontrollable psychological stress increase sex hormone-binding globulin (SHBG), which lowers free testosterone disproportionately to total testosterone
• Resistance-trained men with high mechanical loading do not show suppressed basal testosterone as long as energy availability is maintained, pointing to energy deficit rather than exercise type as the key driver
• Acute, controllable competitive stress can transiently raise testosterone through central activation, while sustained, uncontrollable stress suppresses it, an effect the authors say is appraisal-dependent and independent of SHBG
• Korean War-era 24-hour urinary 17-hydroxycorticosteroid data reportedly showed no progressive decline with prolonged combat exposure, which the authors use as evidence against global endocrine breakdown under sustained stress

Study Quality

This is a narrative review, not a systematic review or meta-analysis, despite covering territory (military endocrinology, exercise physiology, stress appraisal) where quantitative synthesis is possible. The methods section describes a PubMed/Web of Science search using topic terms but states no inclusion or exclusion criteria, no PRISMA-style flow, and no formal quality appraisal of the studies cited. "Priority was given to controlled human experiments" is the only stated selection rule, which leaves considerable room for the authors to select studies that fit the central-adaptation thesis.

A substantial part of the argument rests on Korean War and Vietnam War-era field studies from the 1950s-1970s, work that predates modern assay standards, used small and non-randomly selected military cohorts, and was not designed to isolate testosterone-specific mechanisms. The hCG stimulation data and SHBG/energy availability findings are more directly relevant and better supported by controlled human studies, but the review does not report effect sizes, confidence intervals, or sample sizes for any of the primary studies it leans on, making it impossible to judge how strong the underlying evidence actually is from the text alone.

Red Flags

• No funding or conflict-of-interest disclosure, despite two authors being employed by a U.S. Army research institute with an evident interest in reframing operationally-induced hormonal suppression as adaptive rather than harmful
• Narrative, not systematic, review with no stated inclusion/exclusion criteria or quality scoring of the cited literature
• Heavy reliance on 50+ year old combat cohort data with limited methodological detail available for scrutiny
• No sample sizes, effect sizes, or statistical detail given for any specific study cited in the abstract or summary
• The discussion of testosterone therapy trials for mood explicitly notes those trials were done in aging or chronically depressed populations, not stress-suppressed men, yet the review still uses them to caution against testosterone therapy in stress contexts, an extrapolation beyond what those trials actually tested

Strengths

• Synthesizes a genuinely wide range of contexts (combat, endurance sport, resistance training, competitive stress) under one mechanistic framework
• Correctly distinguishes total versus free testosterone and flags SHBG as a confound, a distinction often glossed over in lay coverage of "low T"
• Uses hCG stimulation studies, a legitimate functional test of Leydig cell capacity, to support the central-versus-gonadal distinction rather than relying on basal hormone levels alone
• Draws a clinically useful line between reversible functional suppression and pathological hypogonadism, which has real implications for who gets worked up for testicular disease versus counseled on energy and sleep

Verdict

The core mechanistic argument, that central HPG suppression and gonadal failure look similar on a basal blood panel but are physiologically distinct, is plausible and consistent with established reproductive endocrinology. But this is an unsystematic narrative review with no disclosed funding or COI from authors embedded in the institution most invested in the stress-is-adaptive framing, and it leans on decades-old military field data without giving readers the sample sizes or effect sizes needed to independently judge the strength of the evidence. Useful as a conceptual framework, not as proof that stress-related low testosterone should be routinely dismissed as benign.