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<p>Polycystic ovary syndrome (PCOS) intersects with substance use through specific biological pathways, as demonstrated by this systematic review of 87 peer-reviewed studies from 2014 to 2024. The analysis reveals three clinically significant mechanisms: chronic alcohol consumption (&gt; 3 drinks/day) elevates serum testosterone through dual pathways—reducing hepatic SHBG production by 40–60% while directly stimulating ovarian theca cell androgen synthesis via oxidative stress. Nicotine exposure differentially impacts PCOS phenotypes, exacerbating adrenal hyperandrogenism in obese patients through nAChRα7-mediated 17α-hydroxylase upregulation while showing minimal metabolic effects in lean individuals. Cannabis use alters reproductive neuroendocrinology, with weekly consumption correlating to prolonged follicular phases and reduced ovulation rates through CB1 receptor-mediated suppression of LH surge amplitude. These substance-specific interactions compound core PCOS pathophysiology. Alcohol’s hepatic effects amplify existing hyperandrogenemia, nicotine’s adrenal stimulation creates an additional androgen source beyond ovarian dysfunction, and cannabis-induced gonadotropin disruption exacerbates anovulation. Clinically, the findings necessitate routine substance use screening in PCOS management and phenotype-specific interventions—particularly adrenal-focused approaches for nicotine users and GnRH pulse stabilization for cannabis consumers. The review identifies critical research gaps, including dose–response thresholds for substance effects and demographic disparities in study populations. Future investigations should prioritize longitudinal designs to establish temporal relationships and controlled interventions targeting identified mechanisms. These evidence-based insights refine clinical understanding of how specific substances modify PCOS trajectories, moving beyond generalized associations to delineate actionable biological pathways for therapeutic targeting.</p>

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Impact of substance abuse on polycystic ovarian syndrome

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年9月24日

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  • Lydia Oluwatoyin Ajayi,
  • Moyinoluwa Comfort Onaolapo,
  • Grace Bosede Akanbi,
  • Aduragbemi Hezekiah Ayodele,
  • Mariam Omotola Alabi,
  • Grace Oluwatomiwa Gbenga,
  • Oyedayo Phillips Akano,
  • Ayodeji Folorunsho Ajayi

摘要

Polycystic ovary syndrome (PCOS) intersects with substance use through specific biological pathways, as demonstrated by this systematic review of 87 peer-reviewed studies from 2014 to 2024. The analysis reveals three clinically significant mechanisms: chronic alcohol consumption (> 3 drinks/day) elevates serum testosterone through dual pathways—reducing hepatic SHBG production by 40–60% while directly stimulating ovarian theca cell androgen synthesis via oxidative stress. Nicotine exposure differentially impacts PCOS phenotypes, exacerbating adrenal hyperandrogenism in obese patients through nAChRα7-mediated 17α-hydroxylase upregulation while showing minimal metabolic effects in lean individuals. Cannabis use alters reproductive neuroendocrinology, with weekly consumption correlating to prolonged follicular phases and reduced ovulation rates through CB1 receptor-mediated suppression of LH surge amplitude. These substance-specific interactions compound core PCOS pathophysiology. Alcohol’s hepatic effects amplify existing hyperandrogenemia, nicotine’s adrenal stimulation creates an additional androgen source beyond ovarian dysfunction, and cannabis-induced gonadotropin disruption exacerbates anovulation. Clinically, the findings necessitate routine substance use screening in PCOS management and phenotype-specific interventions—particularly adrenal-focused approaches for nicotine users and GnRH pulse stabilization for cannabis consumers. The review identifies critical research gaps, including dose–response thresholds for substance effects and demographic disparities in study populations. Future investigations should prioritize longitudinal designs to establish temporal relationships and controlled interventions targeting identified mechanisms. These evidence-based insights refine clinical understanding of how specific substances modify PCOS trajectories, moving beyond generalized associations to delineate actionable biological pathways for therapeutic targeting.