Elsevier

Biological Psychiatry

Volume 73, Issue 9, 1 May 2013, Pages 827-835
Biological Psychiatry

Review
Stress as a Common Risk Factor for Obesity and Addiction

https://doi.org/10.1016/j.biopsych.2013.01.032Get rights and content

Stress is associated with obesity, and the neurobiology of stress overlaps significantly with that of appetite and energy regulation. This review will discuss stress, allostasis, the neurobiology of stress and its overlap with neural regulation of appetite, and energy homeostasis. Stress is a key risk factor in the development of addiction and in addiction relapse. High levels of stress changes eating patterns and augments consumption of highly palatable (HP) foods, which in turn increases incentive salience of HP foods and allostatic load. The neurobiological mechanisms by which stress affects reward pathways to potentiate motivation and consumption of HP foods as well as addictive drugs is discussed. With enhanced incentive salience of HP foods and overconsumption of these foods, there are adaptations in stress and reward circuits that promote stress-related and HP food-related motivation as well as concomitant metabolic adaptations, including alterations in glucose metabolism, insulin sensitivity, and other hormones related to energy homeostasis. These metabolic changes in turn might also affect dopaminergic activity to influence food motivation and intake of HP foods. An integrative heuristic model is proposed, wherein repeated high levels of stress alter the biology of stress and appetite/energy regulation, with both components directly affecting neural mechanisms contributing to stress-induced and food cue-induced HP food motivation and engagement in overeating of such foods to enhance risk of weight gain and obesity. Future directions in research are identified to increase understanding of the mechanisms by which stress might increase risk of weight gain and obesity.

Section snippets

Obesity and Addiction: The Integral Role of Stress

Addiction to alcohol and drugs continues to be a significant public health problem with devastating medical, social, and societal consequences (1). Stress is a critical risk factor affecting both the development of addictive disorders and relapse to addictive behaviors, hence jeopardizing the course and recovery from these illnesses (2). Obesity is a global epidemic, and the United States is at the forefront of the pandemic with two thirds of its population classified as overweight or obese

Stress and Allostasis

Most simply, “stress” is the process by which any highly challenging, uncontrollable, and overwhelming emotional or physiological event or series of events result in adaptive or maladaptive processes required to regain homeostasis and/or stability 2, 6. Examples of emotional stressors include interpersonal conflict, loss of a meaningful relationship, unemployment, death of a close family member, or loss of a child. Some common physiological stressors include hunger or food deprivation, insomnia

Stress, Chronic Adversity, and Increased Vulnerability to Obesity

Considerable evidence from population-based and clinical studies indicates a significant and positive association of high uncontrollable stressful events and chronic stress states with adiposity, BMI, and weight gain 8, 9, 10, 11, similar to the effects of repeated and chronic stress on increasing addiction vulnerability (2). This relationship also seems to be strongest among individuals who are overweight and those who binge eat 8, 9, 12. With a comprehensive interview assessment of cumulative

Stress and Eating Behaviors

Acute stress significantly alters eating 9, 10, 13. Although some studies show decreases in food intake under acute stress, acute stress can also increase intake, especially when highly palatable (HP), calorie-dense foods are available 9, 13, 14, 15, 16. For example, by self-report alone, 42% of students reported increased food intake with perceived stress, and 73% of the participants reported increase in snacking during stress (17). One third to half of animal or human laboratory studies show

The Overlapping Neurobiology of Stress and Energy Homeostasis

The physiological responses to acute stress are manifested through two interacting stress pathways. The first is the hypothalamic-pituitary-adrenal (HPA) axis, in which corticotropin-releasing factor (CRF) is released from the paraventricular nucleus of the hypothalamus, stimulating secretion of adrenocorticotrophin hormone (ACTH) from the anterior pituitary, which subsequently stimulates the secretion of glucocorticoids (GC) (cortisol or corticosterone) from the adrenal glands. The second is

Stress Effects on Food Reward, Motivation, and Intake

The hypothalamic stress circuits are under the regulation of extrahypothalamic cortico-limbic pathways modulated by CRF, NPY, and noradrenergic pathways. The stress response is initiated via the amygdala, and stress regulation occurs via GC negative feedback to the hippocampus and medial prefrontal cortical (PFC) regions (6). The extrahypothalamic projections of CRF are involved in subjective and behavioral responses to stress, whereas release of orexigenic NPY during stress and increased NPY

Food Cues, Food Reward, Motivation, and Intake

Highly palatable food cues are ubiquitous in the current obesogenic environment. Exposure to these HP food cues might increase food intake and contribute to weight gain (48). Such foods are rewarding, stimulate the brain reward pathways, and—via learning/conditioning mechanisms—increase the likelihood of HP food seeking and consumption 55, 56, 57. Animals and humans can become conditioned to seek out and consume these HP foods, particularly in the context of stimuli or “cues” associated with HP

Weight and Diet-Related Metabolic and Stress Adaptations: Influences on Food Craving and Intake

Increasing levels of weight above healthy lean levels and overeating of HP foods result in changes in glucose metabolism, insulin sensitivity and hormones regulating appetite and energy homesostasis 56, 57, 84. As indicated in the previous sections, these metabolic factors not only influence neural reward regions to impact motivation but also affect hypothalamic circuits, interacting with the overlapping stress and energy regulation circuitry. Thus, it is not surprising that increased weight,

Summary and Proposed Model

The converging lines of evidence presented suggest that ubiquitous HP food cues and high levels of stress might alter eating behaviors and affect brain reward/motivation pathways involved in wanting and seeking HP foods. Such behavioral responses might further promote changes in weight and body fat mass. Growing evidence supports weight-related bio-behavioral adaptations in interacting metabolic, neuroendocrine, and neural (cortico-limbic-striatal) pathways, to potentiate food craving and

Future Directions

Although there is growing scientific attention to the complex interactions between stress, energy balance, and appetite regulation and food reward and motivation and their effects on the obesity epidemic, there are significant gaps in our understanding of these relationships. A number of key questions remain unanswered. For example, it is not known how stress-related neuroendocrine changes in cortisol, ghrelin, insulin, and leptin influence HP food motivation and intake. If chronic stress

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