This term describes the clinically significant link between chronically elevated levels of the glucocorticoid hormone cortisol and the preferential accumulation of visceral adipose tissue, commonly known as belly fat. Sustained stress response activation drives this metabolic dysregulation, leading to a specific pattern of central adiposity. This type of fat deposition is metabolically active and poses a higher risk for cardiometabolic disease and insulin resistance than subcutaneous fat. Clinical management requires simultaneous stress and metabolic intervention.
Origin
The connection between stress and central fat distribution has been recognized clinically for decades, notably in Cushing’s syndrome, a condition of extreme cortisol excess. The common usage of the term reflects a growing public and clinical awareness of how chronic psychological and physiological stress impacts body composition. It integrates endocrinology with metabolic health and is a key area of preventative medicine.
Mechanism
High cortisol levels increase lipolysis, releasing fatty acids into the bloodstream, while simultaneously promoting the differentiation of pre-adipocytes into mature fat cells, particularly those expressing a high density of glucocorticoid receptors in the abdominal region. Cortisol also counteracts insulin action, driving insulin resistance, which further favors fat storage and inhibits fat mobilization in other areas. This dual action shifts the body’s energy partitioning toward central fat accumulation.
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