Phenomenon of hypocortisolism in individuals with obesity

Obesity has been associated with abnormalities of the hypothalamic-pituitary-adrenocortical (HPA)-axis. The aim of this study was to investigate patterns of cortisol stress reactivity and basal resting levels in individuals with obesity and healthy weight controls.

Forty-seven individuals with obesity (BMI: 33.60 ± 4.09 kg/m²) and 47 age- and gender-matched healthy weight controls (BMI: 22.58 ± 1.89 kg/m²) underwent the Trier Social Stress Test (TSST) and a resting condition. Based on the salivary cortisol measurement during the TSST, individuals with obesity and the healthy weight controls were categorized into high/low cortisol reactivity group.

Obese low cortisol reactors demonstrated significantly lower basal cortisol resting levels compared to obese high cortisol reactors and healthy weight high/low cortisol reactors (F _(1,90) = 7.780, p ≤ .001, η2 = .21). In individuals with obesity, we found an overlap between the high cortisol reactivity group and the high basal cortisol level group in the resting condition as well as between the low cortisol reactivity group and the low basal cortisol level group during the resting condition (x ²  = 7.671, df = 1, p ≤ .01, Cramér's V = .40). This overlap could not be observed in the healthy weight controls.

In conclusion, patterns of cortisol stress reactivity and basal resting levels were observed in the individuals with obesity but not in the healthy weight controls. The present data suggest that obesity may lead to the phenomenon of basal hypocortisolism.