Mindfulness Intervention for Stress Eating to Reduce Cortisol and Abdominal Fat among Overweight and Obese Women: An Exploratory Randomized Controlled Study
Abstract
Psychological distress and elevated cortisol secretion promote abdominal fat, a feature of the Metabolic Syndrome. Effects of stress reduction interventions on abdominal fat are unknown. Forty-seven overweight/obese women (mean BMI = 3 1 . 2) were randomly assigned to a 4-month intervention or waitlist group to explore effects of a mindfulness program for stress eating. We assessed mindfulness, psychological distress, eating behavior, weight, cortisol awakening response (CAR), and abdominal fat (by dual-energy X-ray absorptiometry) pre- and posttreatment. Treatment participants improved in mindfulness, anxiety, and external-based eating compared to control participants. Groups did not differ on average CAR, weight, or abdominal fat over time. However, obese treatment participants showed significant reductions in CAR and maintained body weight, while obese control participants had stable CAR and gained weight. Improvements in mindfulness, chronic stress, and CAR were associated with reductions in abdominal fat. This proof of concept study suggests that mindfulness training shows promise for improving eating patterns and the CAR, which may reduce abdominal fat over time.
1. Introduction
Many of the adverse health effects of excess weight are associated with abdominal obesity independent of total weight. Visceral obesity, in particular, produces inflammatory molecules which promote insulin resistance and the Metabolic Syndrome [1]. Thus, abdominal adiposity is an important target for reducing risk of type 2 diabetes and cardiovascular disease (CVD) [2].
One modifiable risk factor that may contribute to abdominal adiposity is chronic psychological stress. Low socioeconomic status and job stress, two indicators of chronic stress, are associated with greater abdominal adiposity in cross-sectional and prospective studies [3–5]. Stress can impact abdominal adiposity through repeated activation of the hypothalamic-pituitary-adrenal (HPA) axis, resulting in hypersecretion of cortisol. Cortisol binds to glucocorticoid receptors (GR) on fat cells activating lipoprotein lipase, an enzyme that converts circulating triglycerides into free fatty acids in adipocytes [6]. Increases in cortisol in combination with increased levels of insulin mobilize amino acids and fatty acids from peripheral to abdominal regions for immediate use by the liver for gluconeogenesis and ketones for energy use by the brain [7, 8]. A greater density of GR’s are found on visceral compared to peripheral fat cells partly explaining why fat stores are redistributed to intra-abdominal regions in the presence of elevated cortisol [9–11].