# From Genes to Lives: Integrating the Complexities of Primary Ovarian Insufficiency

## TL;DR

This review explores the genetic and environmental factors behind primary ovarian insufficiency, a condition affecting fertility and aging in women.

## Contribution

The paper integrates genetic, epigenetic, and environmental factors to explain the multifactorial causes of primary ovarian insufficiency.

## Key findings

- Genetic pathways related to DNA repair and meiosis are linked to primary ovarian insufficiency.
- Environmental toxins and lifestyle factors contribute to premature ovarian aging.
- Racial and ethnic disparities exist in POI prevalence and research representation.

## Abstract

Primary ovarian insufficiency (POI) affects up to 3% of reproductive-aged women and is a critical yet underrecognized contributor to infertility and systemic accelerated aging. While most cases remain idiopathic, advances in genomics increasingly reveal a genetic basis, implicating pathways that govern DNA repair, meiosis, chromosomal stability, and folliculogenesis. This review synthesizes the multifactorial etiology of POI, integrating genetic contributions with emerging evidence on epigenetic dysregulation, mitochondrial dysfunction, and environmental influences such as toxins and lifestyle factors. These mechanisms converge on core cellular processes, driving premature follicular depletion and shortening reproductive lifespan. We also highlight racial and ethnic disparities in POI prevalence and research representation, alongside the profound psychosocial burden experienced by affected individuals. Addressing these challenges through integrative strategies that unite mechanistic insight with equity is essential, not only for improving POI care but also for advancing precision approaches to ovarian aging and safeguarding reproductive health across the lifespan.