Cortisol and Abdominal Obesity

Interesting observation taken from:

The molecular neurobiology of depressionVaishnav Krishnan and Eric J. Nestler


Published in final edited form as:

Nature. 2008 October 16; 455(7215): 894–902. doi:10.1038/nature07455.

Abstract
Unravelling the pathophysiology of depression is a unique challenge. Not only are depressive syndromes heterogeneous and their aetiologies diverse, but symptoms such as guilt and suicidality are impossible to reproduce in animal models. Nevertheless, other symptoms have been accurately modelled, and these, together with clinical data, are providing insight into the neurobiology of depression. Recent studies combining behavioural, molecular and electrophysiological techniques reveal that certain aspects of depression result from maladaptive stress-induced neuroplastic changes in specific neural circuits. They also show that understanding the mechanisms of resilience to stress offers a crucial new dimension for the development of fundamentally novel antidepressant treatments.

Here's the interesting bit related to obesity:

Several metabolic abnormalities that are often associated with depression, such as insulin resistance and abdominal obesity, can be at least partly explained by an increase in glucocorticoids. Hypercortisolaemia in depression is manifested at several levels, including impaired glucocorticoid-receptor-mediated negative feedback, adrenal hyper-responsiveness to circulating adreno-corticotropic hormone (ACTH) and hypersecretion of cortico tropinreleasing factor, the hypothalamic activator of ACTH release from the pituitary. In line with these findings, glucocorticoid and corticotropin-releasing factor receptor antagonists are currently being tested in clinical trials.