Cortisol, the primary stress hormone, can affect fertility through multiple pathways. Chronically elevated cortisol disrupts the hypothalamic-pituitary-gonadal (HPG) axis, leading to irregular ovulation, reduced sperm quality, and impaired implantation. Cortisol also suppresses GnRH, LH, and FSH secretion – key hormones for reproduction. However, the effect is highly individual and strongly modulated by lifestyle factors such as sleep, stress management, and diet. Direct genetic testing for cortisol-related genes (e.g., NR3C1, FKBP5) is not yet sufficiently validated to make clinically meaningful fertility predictions. Instead, blood or salivary cortisol (diurnal profile) and DHEA-S testing are more actionable. The evidence is based on endocrine physiology and observational studies, not on consumer DNA markers. Be cautious of overinterpreted 'stress gene' results – lifestyle usually has a greater impact.
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