What is the Origin of Male Obesity-Secondary Hypogonadism (MOSH)?

This diagnostic categorization emerged from the convergence of the global obesity epidemic and a deeper, mechanistic understanding of the endocrine interplay between adipose tissue and sex hormone regulation. It is a modern term recognizing obesity not merely as a state of excess weight but as an active, potent endocrine-disrupting condition.

What is the Mechanism of Male Obesity-Secondary Hypogonadism (MOSH)?

Adipose tissue, particularly the metabolically active visceral fat, expresses high levels of the aromatase enzyme, which converts circulating androgens, including testosterone, into estrogens. These elevated estrogen levels then provide exaggerated negative feedback to the pituitary gland, suppressing the release of Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH). This suppression ultimately reduces testicular testosterone production, completing the secondary hypogonadal loop.

Male Obesity-Secondary Hypogonadism (MOSH) ∞ Area

Male Obesity-Secondary Hypogonadism (MOSH)

Meaning

Male Obesity-Secondary Hypogonadism, or MOSH, is a distinct clinical entity where excessive visceral adiposity leads to the functional suppression of the hypothalamic-pituitary-gonadal axis, resulting in low serum testosterone levels. This is classified as a form of secondary hypogonadism where the primary driver of the hormonal deficiency is the chronic metabolic stress and systemic inflammation associated with obesity. The condition manifests with classic symptoms of low testosterone, including fatigue and decreased libido.