A clinical state characterized by insufficient levels of hormones that promote tissue growth and repair, such as testosterone, DHEA, and growth hormone. This endocrine imbalance directly impedes the body’s capacity for anabolism, leading to a net catabolic state. Patients often present with symptoms including reduced muscle mass, decreased bone mineral density, and persistent fatigue. Identifying these specific hormonal deficits is crucial for developing targeted therapeutic interventions.
Origin
The concept stems from endocrinology, combining ‘anabolic’ (from Greek anabolē, meaning “a building up”) and ‘hormone’ (from Greek hormáein, meaning “to set in motion”), paired with the clinical term ‘deficiencies’. This framework emerged from observing the physiological decline associated with age-related or pathological reductions in these key signaling molecules.
Mechanism
The deficiency operates by reducing the hormonal signaling that typically binds to nuclear or membrane receptors, thereby failing to stimulate protein synthesis and cellular proliferation. Specifically, low circulating levels of these anabolic agents diminish the downstream activation of mTOR and IGF-1 pathways, impairing muscle protein turnover and connective tissue repair. This fundamental biochemical failure contributes significantly to sarcopenia and overall physiological frailty.
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