Highly stressed and impoverished populations are more likely to be obese, and ultimately more likely to develop obesity-associated comorbidities. Preventing these adverse health outcomes relies on preventing the development of obesity early in the life span, since obesity, once established, tends to persist and prevention is more effective than treatment. Preventing obesity is highly urgent for low-income children, since obesity is common early on in this demographic and may contribute to substantial health disparities later in life. Current prevention programs have limited effectiveness, and novel targets for intervention are needed. The association between stress and eating behavior is one potential novel target. Our research program focuses on links between stress, eating behavior, and obesity in low-income children. Our preliminary findings suggest that, in early childhood, patterns of cortisol secretion reflecting chronic stress may promote eating in the absence of hunger, reduced satiety responsiveness, and tantrums over food;these eating behaviors, in turn, may lead to obesity. This early work has made clear, however, that the pathways linking stress to obesity via eating behavior are complex and multifactorial, and involve biologic and behavioral pathways. To date we have examined only a subset of eating behaviors that could mediate links between stress and obesity. Other mechanisms that may be affected by stress, such as high sensitivity to food as a reward or poor ability to delay gratification for food, have not been examined in this model. How such eating behaviors may cluster and develop over time, how different aspects of stress (i.e., chronic vs. immediate stressors) relate to these behaviors, and how genotypes may moderate such associations remains unknown. We propose to examine how these processes may be driven by stress, and ultimately lead to obesity in children. This application is submitted in response to RFA- HL-12-037: "Mechanistic Pathways Linking Psychosocial Stress and Behavior" with the goal of providing a deeper understanding of the psychological and bio-behavioral processes that connect psychosocial stress with eating behaviors and ultimately obesity.
The aims are:
Aim 1 : To examine the cross-sectional relationship of psychosocial stress (chronic and immediate stress) with obesity-promoting eating behaviors (including satiety responsiveness, reinforcing value of food, and the ability to delay gratification for food) and body mass index (BMI) z-score at age 7 years among low-income children.
Aim 2 : To test genetic moderators of stress-eating behavior links in our cohort of low-income children.
Aim 3 : To examine longitudinal associations of chronic stress and reactivity to stress early in life (age 3 years) with changes in obesity-promoting eating behaviors between ages 3 and 7 years. Improved understanding of the development of associations of psychosocial stress during early life with specific, well-phenotyped eating behaviors and excessive weight gain beginning in childhood may hold promise for novel obesity prevention efforts among low-income children, a demographic group at high risk.

Public Health Relevance

Psychosocial stress is linked with overeating and the development of obesity, but the mechanisms underlying these associations are not well-understood, particularly in children. Improved understanding of the development of associations of social-contextual and interpersonal stress with eating behavior and excessive weight gain beginning in childhood may hold promise for novel targets for obesity prevention. Given that psychosocial stress and obesity are both more common among low-income children, the work may also hold particular promise for addressing socioeconomic disparities in obesity prevalence.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Research Project (R01)
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Special Emphasis Panel (ZRG1-BBBP-J (50))
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Horlick, Mary
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University of Michigan Ann Arbor
Schools of Medicine
Ann Arbor
United States
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