ReviewFrontiers in endocrinology2026
Adaptive changes in adrenal steroid metabolism under extreme physical and psychological stress: a narrative review.
Review in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
3 authors.
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Abstract
Background: Chronic exposure to sleep deprivation, insufficient recovery, inadequate energy availability, extreme environmental conditions, repetitive high-intensity exercise, and psychological threat can alter hypothalamic-pituitary-adrenal (HPA) axis function. Acute activation of the HPA axis is adaptive, whereas prolonged or repetitive activation may contribute to allostatic load, altered daily glucocorticoid exposure, and changes associated with psychological and metabolic maladaptation. Methods: This narrative review synthesizes evidence on adrenal steroid metabolism under extreme physical and psychological stress, with emphasis on glucocorticoids, mineralocorticoids, and adrenocorticotropic hormone (ACTH)-responsive adrenal androgens, including dehydroepiandrosterone sulfate (DHEA-S) and androstenedione. PubMed and Google Scholar were searched through 22 May 2026. Recent human and military studies were prioritized, and earlier seminal work was included when it provided a mechanistic or historical context not captured by recent literature. Summary of evidence: The review describes how acute stress responses may support substrate mobilization and performance, whereas chronic exposure may flatten circadian patterns, alter ultradian glucocorticoid pulsatility, suppress downstream reproductive and metabolic axes, and produce heterogeneous effects on DHEA-S, aldosterone, and neurosteroid pathways. The strongest clinical and military evidence concerns sleep/circadian disruption, energy deficit, and prolonged military training; evidence for direct nutrient-mediated prevention of HPA-axis maladaptation remains preliminary or indirect. Conclusion: Addressing energy deficit, sleep deprivation and circadian disruption, inadequate recovery, dehydration/heat strain, and clinically relevant nutrient deficiencies may reduce the stressor load that contributes to functional hypercortisolism. Nutritional interventions should focus on correcting deficiencies, maintaining energy, supporting musculoskeletal function, and reducing stress, rather than serving as direct hormonal therapy. Future studies should use standardized steroid sampling, report sex-specific outcomes, and account for energy intake, expenditure, sleep, baseline fitness, and environmental exposures.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.