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. 2014 Aug:46:14-22.
doi: 10.1016/j.psyneuen.2014.04.003. Epub 2014 Apr 13.

Chronic stress increases vulnerability to diet-related abdominal fat, oxidative stress, and metabolic risk

Kirstin Aschbacher  1 , Sarah Kornfeld  2 , Martin Picard  3 , Eli Puterman  4 , Peter J Havel  5 , Kimber Stanhope  5 , Robert H Lustig  6 , Elissa Epel  7
Affiliations

Chronic stress increases vulnerability to diet-related abdominal fat, oxidative stress, and metabolic risk

Kirstin Aschbacher et al. Psychoneuroendocrinology. 2014 Aug.

Abstract

Background: In preclinical studies, the combination of chronic stress and a high sugar/fat diet is a more potent driver of visceral adiposity than diet alone, a process mediated by peripheral neuropeptide Y (NPY).

Methods: In a human model of chronic stress, we investigated whether the synergistic combination of highly palatable foods (HPF; high sugar/fat) and stress was associated with elevated metabolic risk. Using a case-control design, we compared 33 post-menopausal caregivers (the chronic stress group) to 28 age-matched low-stress control women on reported HPF consumption (modified Block Food Frequency Questionnaire), waistline circumference, truncal fat ultrasound, and insulin sensitivity using a 3-h oral glucose tolerance test. A fasting blood draw was assayed for plasma NPY and oxidative stress markers (8-hydroxyguanosine and F2-Isoprostanes).

Results: Among chronically stressed women only, greater HPF consumption was associated with greater abdominal adiposity, oxidative stress, and insulin resistance at baseline (all p's≤.01). Furthermore, plasma NPY was significantly elevated in chronically stressed women (p<.01), and the association of HPF with abdominal adiposity was stronger among women with high versus low NPY. There were no significant predictions of change over 1-year, likely due to high stability (little change) in the primary outcomes over this period.

Discussion: Chronic stress is associated with enhanced vulnerability to diet-related metabolic risk (abdominal adiposity, insulin resistance, and oxidative stress). Stress-induced peripheral NPY may play a mechanistic role.

Keywords: Abdominal adiposity; Metabolic syndrome; Obesity; Pre-diabetes; Psychological stress.

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Conflict of interest statement

Conflict of Interest Statements

No authors have conflicts of interest to declare.

Figures

Figure 1
Figure 1
Synergistic Effects of Chronic Stress and Highly Palatable Food on Waistline Circumference **p ≤.01, *p ≤.05. Note: For the sake of data visualization, p-values given here are derived from t-tests; however, Table 3 provides bootstrapped regression coefficients adjusted for the covariates, which provide the more appropriate, final statistical tests of synergistic (interaction) and main effects.
Figure 2
Figure 2
Synergistic Effects of Chronic Stress and Highly Palatable Food on Oxidative Stress and Insulin Sensitivity **p ≤.01, *p ≤.05. Note: For the sake of data visualization, p-values given here are derived from t-tests; however, Table 3 provides bootstrapped regression coefficients adjusted for the covariates, which provide the more appropriate, final statistical tests of synergistic (interaction) and main effects.
Figure 3
Figure 3
Peripheral Neuropeptide Y (NPY) is Elevated under Chronic Stress **p ≤.01. Mean + SEM depicted. An independent t-test using a critical alpha of .05 was conducted to obtain the p-value for the group comparison.
See this image and copyright information in PMC

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