• editor.aipublications@gmail.com
  • Track Your Paper
  • Contact Us
  • ISSN: 2456-8791

International Journal Of Forest, Animal And Fisheries Research(IJFAF)

Role of Dehydroepiandrosterone (DHEA) in the Pathophysiology and Clinical Manifestations of Polycystic Ovary Syndrome (PCOS)

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

Download | Downloads : 8 | Total View : 1284

DOI: 10.22161/ijfaf.9.2.2

Journal : International Journal Of Forest, Animal And Fisheries Research(IJFAF)

Share

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.

Polycystic ovary syndrome, DHEA, hyperandrogenism, HPA axis, metabolic dysfunction, adrenal androgens

[1] Escobar-Morreale HF. Polycystic ovary syndrome: definition, aetiology, diagnosis and treatment. Nat Rev Endocrinol. 2018;14(5):270. doi:10.1038/nrendo.2018.24
[2] Stein IF, Leventhal ML. Amenorrhea associated with bilateral polycystic ovaries. Am J Obstet Gynecol. 1935;29(2):181–191.
[3] Bharathi RV, Swetha S, Rani N, et al. An epidemiological survey: Effect of predisposing factors for PCOS in Indian urban and rural population. Middle East Fertil Soc J. 2017;22(4):313–316.
[4] Futterweit W. Polycystic ovary syndrome: clinical perspectives and management. Obstet Gynecol Surv. 1999;54(6):403–413. doi:10.1097/00006254-199906000-00024
[5] Palomba S, Santagni S, Falbo A, La Sala GB. Complications and challenges associated with polycystic ovary syndrome: current perspectives. Int J Womens Health. 2015;7:745. doi:10.2147/IJWH.S70314
[6] Dokras A, Clifton S, Futterweit W, Wild R. Increased risk for abnormal depression scores in women with PCOS: a systematic review and meta-analysis. Obstet Gynecol. 2011;117(1):145–152. doi:10.1097/AOG.0b013e318202b0a4
[7] Rosenfield RL, Ehrmann DA. The pathogenesis of PCOS: the hypothesis of functional ovarian hyperandrogenism revisited. Endocr Rev. 2016;37(5):467–520. doi:10.1210/er.2015-1104
[8] Cooney LG, Lee I, Sammel MD, Dokras A. High prevalence of moderate and severe depressive and anxiety symptoms in PCOS: a systematic review and meta-analysis. Hum Reprod. 2017;32(5):1075–1091. doi:10.1093/humrep/dex044
[9] Chaudhari AP, Mazumdar K, Mehta PD. Anxiety, depression, and quality of life in women with PCOS. Indian J Psychol Med. 2018;40(3):239–246. doi:10.4103/IJPSYM.IJPSYM_561_17
[10] Spritzer MP, Barone CR, de Oliveira FB. Hirsutism in PCOS: pathophysiology and management. Curr Pharm Des. 2016;22(36):5603–5613. doi:10.2174/1381612822666160720151243
[11] Lennartsson AK. Effects of psychosocial stress on DHEA and DHEA-S levels—acute and long-term effects. [Thesis]. 2013.
[12] Manji HK, Drevets WC, Charney DS. The cellular neurobiology of depression. Nat Med. 2001;7(5):541. doi:10.1038/87865
[13] Li Y, Yu Q, Ma L, et al. Dehydroepiandrosterone stimulates inflammation and impairs ovarian functions of PCOS. J Cell Physiol. 2019;234(5):7435–7447. doi:10.1002/jcp.27501
[14] Benjamin JJ, Valsan C, Kumar A, et al. Meta-analysis of association between IL-6-174 G/C polymorphism and female infertility-related disorders. J Reprod Immunol. 2020;140:103134. doi:10.1016/j.jri.2020.103134
[15] Benjamin JJ, Koshy T, N M. Cortisol and PCOS: a meta-analysis of case-control studies. Gynecol Endocrinol. 2021:1–7. doi:10.1080/09513590.2021.1908254
[16] WHO. Polycystic ovary syndrome: fact sheet. Available at: https://www.who.int/news-room/fact-sheets/detail/polycystic-ovary-syndrome
[17] Li X, Wu W, Zhang C, et al. [Online article] Sciencedirect. Available at: https://www.sciencedirect.com/science/article/abs/pii/S0025712522001341
[18] Teede H, Misso M, Costello M, et al. PCOS guideline: evidence-based guideline for the assessment and management of polycystic ovary syndrome. J Clin Endocrinol Metab. 2021;106(3):e1071. doi:10.1210/clinem/dgaa1455
[19] Sciencedirect. Dehydroepiandrosterone profile. Available at: https://www.sciencedirect.com/topics/psychology/dehydroepiandrosterone