Aprajita Shukla , Sneha Verma , Ramakant , Ambuj Mishra , Kesar Farzana
Article Info: Received: 19 Mar 2025; Received in revised form: 16 Apr 2025; Accepted: 23 Apr 2025; Available online: 02 May 2025
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DOI: 10.22161/ijfaf.9.2.2
Journal : International Journal Of Forest, Animal And Fisheries Research(IJFAF)
Polycystic ovary syndrome (PCOS) is a prevalent endocrinopathy with a complex etiology involving metabolic, reproductive, and psychological components. Dehydroepiandrosterone (DHEA), an adrenal androgen and stress biomarker, has been implicated in PCOS pathophysiology, yet its role remains controversial. To critically examine the contribution of DHEA to the development and clinical progression of PCOS, emphasizing its hormonal, metabolic, and neuroendocrine implications. This review synthesizes evidence from clinical, biochemical, and experimental studies evaluating DHEA levels and regulatory pathways in women with PCOS, including analyses of phenotypic variation, adrenal versus ovarian androgen production, and stress-axis dysregulation. Elevated DHEA and its sulfated form (DHEAS) are observed in a subset of women with PCOS, particularly those exhibiting hyperandrogenism. However, findings across studies remain inconsistent due to heterogeneity in diagnostic criteria, age-related hormonal variability, and methodological differences. DHEA has been shown to influence ovarian function, metabolic status, and neuropsychological symptoms, suggesting a multifactorial role in PCOS pathogenesis. DHEA contributes to the complex hormonal milieu of PCOS and may serve as both a biomarker and a mechanistic factor in its pathophysiology. Standardized measurement protocols and stratified phenotypic analyses are essential for elucidating its diagnostic and therapeutic relevance.