Libido and Stress describes the significant inverse relationship where chronic psychological or physiological stress acts as a potent suppressor of sexual desire and function. Sustained stress disrupts the delicate balance of the neuroendocrine system, leading to a measurable decline in the hormonal signals necessary for robust libido in both sexes. A comprehensive clinical evaluation must therefore consider the status of the HPA axis alongside the sex hormone profile.
Origin
This connection is deeply rooted in evolutionary biology, where stress signals, indicating a threat to survival, naturally prioritize energy away from non-essential functions like reproduction. The clinical recognition of stress as a major, reversible factor in sexual dysfunction is well-established in psychoneuroendocrinology.
Mechanism
Sustained activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis leads to chronically elevated cortisol levels. This hypercortisolemia suppresses the hypothalamic-pituitary-gonadal (HPG) axis, thereby inhibiting the pulsatile release of GnRH and subsequently reducing the production of sex hormones, including testosterone and estrogen. This endocrine cascade directly diminishes sexual motivation and compromises the physiological arousal response.
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