The complex, bidirectional physiological relationship where chronic psychological or physiological stress acts as a potent endocrine modulator, promoting the accumulation of adipose tissue, particularly in the visceral depot. This clinical phenomenon is mediated by sustained activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system. Understanding this connection is critical for effective weight management strategies that extend beyond simple caloric balance.
Origin
The understanding of this link began with the early endocrinology research on the stress hormone cortisol in the mid-20th century. The formalization of chronic stress as a primary driver of central adiposity and metabolic syndrome emerged from clinical and epidemiological studies in the late 20th century.
Mechanism
Chronic stress leads to sustained hypercortisolemia, which increases appetite, promotes preferential fat storage in the abdominal area, and induces insulin resistance in peripheral tissues. Concurrently, the elevated sympathetic tone increases circulating catecholamines, which, while initially catabolic, can lead to a compensatory increase in caloric intake and a shift toward energy conservation over time. This hormonal cascade favors energy storage and metabolic dysregulation.
We use cookies to personalize content and marketing, and to analyze our traffic. This helps us maintain the quality of our free resources. manage your preferences below.
Detailed Cookie Preferences
This helps support our free resources through personalized marketing efforts and promotions.
Analytics cookies help us understand how visitors interact with our website, improving user experience and website performance.
Personalization cookies enable us to customize the content and features of our site based on your interactions, offering a more tailored experience.