Article

Leptin concentrations in response to acute stress predict subsequent intake of comfort foods

Department of Psychology, UCLA, Los Angeles, CA, USA.
Physiology & Behavior (Impact Factor: 3.03). 05/2012; 107(1):34-9. DOI: 10.1016/j.physbeh.2012.04.021
Source: PubMed

ABSTRACT Both animals and humans show a tendency toward eating more "comfort food" (high fat, sweet food) after acute stress. Such stress eating may be contributing to the obesity epidemic, and it is important to understand the underlying psychobiological mechanisms. Prior investigations have studied what makes individuals eat more after stress; this study investigates what might make individuals eat less. Leptin has been shown to increase following a laboratory stressor, and is known to regulate satiety. This study examined whether leptin reactivity accounts for individual differences in stress eating. To test this, we exposed forty women to standardized acute psychological laboratory stress (Trier Social Stress Test) while blood was sampled repeatedly for measurements of plasma leptin. We then measured food intake after the stressor. Increasing leptin during the stressor predicted lower intake of comfort food. These initial findings suggest that acute changes in leptin may be one of the factors modulating down the consumption of comfort food following stress.

Full-text

Available from: Eli Puterman, Feb 17, 2014
1 Follower
 · 
117 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Food insecurity is associated with deficits in child development and health, but little is known about how children's specific food-insecurity experiences play out through nutritional and non-nutritional pathways that may compromise well-being. This study used child self-reports of food insecurity to examine the types of food-insecurity experiences that were most prevalent and the relations between child food insecurity (CFI), child diet, and child physical activity (PA). A total of 3605 fourth- and fifth-grade children whose schools participated in the Network for a Healthy California-Children's PowerPlay! campaign completed 24-h diary-assisted recalls and surveys including items from the Child Food Security Assessment and questions about PA. Data were analyzed by using regression and logistic regression models. CFI was present in 60% of the children and included experiences of cognitive, emotional, and physical awareness of food insecurity. Greater levels of CFI were associated with higher consumption of energy, fat, sugar, and fiber and a diet lower in vegetables. For instance, a child at the highest level of CFI, on average, consumed ∼494 kJ/d (118 kcal), 8 g/d of sugar, and 4 g/d of fat more than a food-secure child. Higher CFI was associated with a marginally significant difference (P = 0.06) in minutes of PA (17 min/d less for children at the highest level of CFI vs. those who were food secure) and with significantly greater perceived barriers to PA. CFI is a troublingly frequent, multidomain experience that influences children's well-being through both nutritional (dietary) and non-nutritional (e.g., PA) pathways. CFI may lead to poor-quality diet and less PA and their developmental consequences. Practitioners should consider CFI when assessing child health and well-being and can do so by asking children directly about their CFI experiences. © 2015 American Society for Nutrition.
    Journal of Nutrition 03/2015; 145(3). DOI:10.3945/jn.114.194365 · 4.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The underlying cause of predisposition to obesity is complex but one marker is cortisol responsiveness. Selection of sheep for high (HR) or low (LR) cortisol responses to adrenocorticotropin shows that HR are more likely to become obese. Increased propensity to obesity is associated with reduced skeletal muscle thermogenesis. We sought to determine whether metabolic or behavioral responses to stress also contribute to altered propensity to obesity in LR and HR. Animals (n = 5–10/group) were exposed to 3 stressors and we measured food intake and thermogenesis (recorded with dataloggers implanted into muscle). Stressors were hypoglycaemia (0.125 units/kg insulin, IV), a barking dog and immune challenge (200 ng/kg lipopolysaccharide – LPS, IV). LR animals showed a greater catabolic state in response to both immune and psychosocial stressors. LPS reduced (P < 0.01) food intake in both groups but LR showed a greater (P < 0.05) reduction in food intake and a more substantial (P < 0.05) rise in muscle temperature. Introduction of the barking dog reduced (P < 0.05) food intake in LR only. These metabolic differences coincided with differences in cortisol responsiveness, where HR animals had increased (P < 0.05) cortisol in response to both immune and psychosocial stressors. We also assessed behavior in the following paradigms: 1, isolation in the open field test; 2, response to a human intruder; and 3, food competition. LR had greater (P < 0.05) activity, reduced fearfulness and displayed a proactive coping style of behavior. Thus we demonstrate that high cortisol responsiveness identifies animals with stress-induced metabolic and behavioral traits that may contribute to susceptibility to obesity.
    Psychoneuroendocrinology 09/2014; 47:166–177. DOI:10.1016/j.psyneuen.2014.05.015 · 5.59 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Significant comorbidities between obesity-related metabolic disease and stress-related psychological disorders suggest important functional interactions between energy balance and brain stress integration. Largely overlapping neural circuits control these systems, and this anatomical arrangement optimizes opportunities for mutual influence. Here we first review the current literature identifying effects of metabolic neuroendocrine signals on stress regulation, and vice versa. Next, the contributions of reward-driven food intake to these metabolic and stress interactions are discussed. Lastly, we consider the interrelationships between metabolism, stress, and reward in light of their important implications in the development of therapies for metabolism- or stress-related disease.
    Cell metabolism 03/2014; DOI:10.1016/j.cmet.2014.01.020 · 16.75 Impact Factor