The Somatopause Cascade refers to the progressive, age-related decline in the pulsatile secretion of Growth Hormone (GH) and its downstream mediator, Insulin-like Growth Factor 1 (IGF-1), leading to a systemic state of anabolic deficiency. This cascade is a significant component of biological aging, resulting in reduced lean body mass, altered body composition, decreased bone mineral density, and compromised cellular repair capacity. The reduction in these somatotropic signals is a hallmark of this physiological change.
Origin
This clinical term is rooted in endocrinology, combining “somato” (body) and “pause” (cessation), mirroring the terminology of other age-related hormonal declines like menopause and andropause. The “cascade” descriptor emphasizes the downstream effects that the primary reduction in GH secretion has on the entire body, mediated largely through the decline in hepatic IGF-1 production.
Mechanism
The cascade is initiated by age-related changes in the hypothalamic regulation of the pituitary, specifically a reduction in the release of Growth Hormone-Releasing Hormone (GHRH) and an increase in the inhibitory hormone somatostatin. This altered neuroendocrine signaling leads to a diminished amplitude of the nocturnal GH pulses. Consequently, the liver produces less IGF-1, resulting in a systemic decrease in anabolic signaling and a shift toward a more catabolic physiological state.
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