The progressive, involuntary reduction in the body’s capacity for constructive metabolic processes, specifically those related to tissue building and repair. This physiological shift is a characteristic feature of aging, leading to a net catabolic state over time. Clinically, it manifests as sarcopenia, decreased bone density, and impaired wound healing due to reduced protein synthesis and hormonal signaling. This decline represents a fundamental shift in homeostatic balance, favoring breakdown over regeneration.
Origin
The concept originates from endocrinology and gerontology, combining the biological process of ‘aging’ with the metabolic state of ‘anabolism’ and its ‘decline’. It describes a natural, though clinically manageable, trajectory of human physiological function. This term highlights the shift in hormonal and cellular efficiency that underlies physical frailty in later life.
Mechanism
The decline is primarily driven by a reduced responsiveness to anabolic hormones, such as growth hormone, insulin-like growth factor 1 (IGF-1), and testosterone, a phenomenon known as anabolic resistance. Additionally, chronic low-grade inflammation, or inflammaging, contributes to the catabolic environment by upregulating protein degradation pathways. Mitochondrial dysfunction further limits the energy available for cellular repair and synthesis, compounding the systemic deficit in building capacity.
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