Abstract
Background Depression and stress promote obesity. This study addressed the impact of daily stressors and a history of major depressive disorder (MDD) on obesity-related metabolic responses to high-fat meals. Methods This double-blind, randomized, crossover study included serial assessments of resting energy expenditure (REE), fat and carbohydrate oxidation, triglycerides, cortisol, insulin, and glucose before and after two high-fat meals. During two separate 9.5-hour admissions, 58 healthy women (38 breast cancer survivors and 20 demographically similar control subjects), mean age 53.1 years, received either a high saturated fat meal or a high oleic sunflower oil meal. Prior day stressors were assessed by the Daily Inventory of Stressful Events. Results Greater numbers of stressors were associated with lower postmeal REE (p = .008), lower fat oxidation (p = .04), and higher insulin (p = .01), with nonsignificant effects for cortisol and glucose. Women with prior MDD had higher cortisol (p = .008) and higher fat oxidation (p = .004), without significant effects for REE, insulin, and glucose. Women with a depression history who also had more stressors had a higher peak triglyceride response than other participants (p = .01). The only difference between meals was higher postprandial glucose following sunflower oil compared with saturated fat (p = .03). Conclusions The cumulative 6-hour difference between one prior day stressor and no stressors translates into 435 kJ, a difference that could add almost 11 pounds per year. These findings illustrate how stress and depression alter metabolic responses to high-fat meals in ways that promote obesity.
| Original language | English (US) |
|---|---|
| Article number | 12226 |
| Pages (from-to) | 653-660 |
| Number of pages | 8 |
| Journal | Biological Psychiatry |
| Volume | 77 |
| Issue number | 7 |
| DOIs | |
| State | Published - Apr 1 2015 |
Keywords
- Cortisol
- Daily stressors
- Depression
- Insulin
- Resting energy expenditure
- Triglycerides
ASJC Scopus subject areas
- Biological Psychiatry
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