Intensify Stress Relief

Abstract

Obesity is a heterogeneous construct that, despite multiple and diverse attempts, has been difficult to treat. One conceptualization gaining media and research attention in recent years is that foods, particularly hyperpalatable (e.g., high-fat, high sugar) ones, may possess addictive qualities. Stress is an important factor in the development of addiction and in addiction relapse, and may contribute to an increased risk for obesity and other metabolic diseases. Uncontrollable stress changes eating patterns and the salience and consumption of hyperpalatable foods; over time, this could lead to changes in allostatic load and trigger neurobiological adaptations that promote increasingly compulsively behavior. This association may be mediated by alterations in the hypothalamic-pituitary-adrenal (HPA) axis, glucose metabolism, insulin sensitivity, and other appetite-related hormones and hypothalamic neuropeptides. At a neurocircuitry level, chronic stress may affect the mesolimbic dopaminergic system and other brain regions involved in stress/motivation circuits. Together, these may synergistically potentiate reward sensitivity, food preference, and the wanting and seeking of hyperpalatable foods, as well as induce metabolic changes that promote weight and body fat mass. Individual differences in susceptibility to obesity and types of stressors may further moderate this process. Understanding the associations and interactions between stress, neurobiological adaptations, and obesity is important in the development of effective prevention and treatment strategies for obesity and related metabolic diseases.Keywords: Obesity, Food Addiction, Stress, HPA axis, Mesolimbic Dopaminergic SystemGo to:

Introduction

Defined as “abnormal or excessive fat accumulation that may impair health” 1, obesity is a condition that is increasingly common. In the United States, 35.7% of adults are obese (body mass index [BMI] ≥30 kg/m22. Globally, estimates from 2008 suggest that 1.4 billion adults globally were overweight (BMI ≥25 kg/m2), and that at least 200 million men and 300 million women were obese 1. Obesity represents an important risk factor for potentially life-threatening health problems including cardiovascular diseases, type II diabetes, osteoarthritis, and certain cancers 35.

There have been multiple and diverse attempts to provide mechanisms for individuals to lose weight and maintain a healthy body weight; however, most have failed to sustain lasting effects, with patients often regaining their lost weight within 5 years 68. The difficulty in treating and decreasing the prevalence of obesity may reflect the heterogeneity of obesity as a condition. One conceptualization supported by recent research in the addiction and nutrition fields is that foods, particularly highly palatable and energy-dense ones, may be “addictive” in ways similar to drugs of abuse 9; these findings have consequently led to the conceptualization of ‘foods as drugs’ 10. Stress has long been considered a critical risk factor in the development of addictive disorders and relapse to addictive behaviors 1112. However, few studies have reviewed links between stress and food intake, particularly of hyperpalable or “comfort” foods that may be consumed to reduce stress.Go to:

Stress and Eating Behavior

The term “stress” refers to processes involving perception, appraisal, and response to noxious events or stimuli 13. Stress experiences can be emotionally (e.g., interpersonal conflict, loss of loved ones, unemployment) or physiologically (e.g., food deprivation, illness, drug withdrawal states) challenging. In addition, regular and binge use of addictive substances may serve as pharmacological stressors. Acute stress activates adaptive responses, but prolonged stress leads to “wear-and-tear” (allostatic load) of the regulatory systems, resulting in biological alterations that weaken stress-related adaptive processes and increase disease susceptibility 14. Thus, mildly challenging stimuli limited in duration can be “good stress” or “eustress” and may increase motivation to achieve goal-direct outcomes and homeostasis – this can result in a sense of mastery and accomplishment, and can be perceived as positive and exciting 15. However, the more prolonged and more intense the stressful situation, the lower the sense of mastery and adaptability and thus the greater the stress response and risk for persistent homeostatic dysregulation 14. The perception and appraisal of stress relies on specific aspects of the presenting external or internal stimuli and may be moderated or mediated by personality traits, emotional state, and physiological responses that together contribute to the experience of distress.

Stress is a challenge to the natural homeostasis of an organism; in turn, the organism may react to stress by producing a physiological response to regain equilibrium lost by the impact of the stressor. One such homeostasis that is disrupted is that of feeding behavior. Physiological aspects of eating behaviors have been long studied, and information is often derived from animal models fed standard lab chow. However, experimental results have been inconsistent. Animals fed a single bland food diet have provided evidence both for acute stress-induced hyperphagia and hypophagia 1617. In humans, individual differences in food intake response are similarly noted – roughly 40% increase and 40% decrease their caloric intake when stressed, while approximately 20% of people do not change feeding behaviors during stressful periods 1820. These varying results may relate to the specific type of stressor manipulated, duration of stress provocation, and variations in the satiety and hunger levels at the start of the study. For example, mild stressors could induce hyperphagia, while more severe stressor, hypophagia 21. However, other individual differences warrant consideration.

The rather complex pattern of results may also be conflated by the lack of food choice. Understanding which foods are selected or avoided under stress is a crucial issue both due to the theoretical interpretation of the mechanisms involved and for the prediction of harmful effects of stress on health. In both human and animals, a shift toward choosing more pleasurable and palatable foods is observed irrespective of caloric intake changes associated with stress. The foods eaten during times of stress typically favor those of high fat and/or sugar content. For example, when rats were presented with a choice of highly palatable food such as lard or sugar, stress consistently increased intake of palatable food specifically 2224. Humans similarly turn to hyperpalatable comfort foods such as fast food, snacks, and calorie-dense foods 2527 even in the absence of hunger and lack of homeostatic need for calories 28; this effect may be exacerbated in overweight or obese individuals as compared to lean individuals 2029. Taken together, these findings suggest that stress may promote irregular eating patterns and strengthen networks towards hedonic overeating; these effects may be exacerbated in overweight and obese individuals. The factors underlying these and other behaviors that may contribute to obesity are slowly becoming understood.

The present article elucidates potential explanations for the stress-eating paradox, i.e. that stress can lead to both hyperphagia and hypophagia. We review overlaps in key elements of hormonal and brain stress neurocircuitry with that of appetite and motivation for food intake.Go to:

Acute and Chronic Stress Response: Role of the Hypothalamic-Pituitary-Adrenal Axis

The stress response, which maintains allostasis, is comprised of a cascade of adaptive responses and is manifested through two interacting stress pathways. First is the activation of the sympathetic adrenal medullary system, with release of catecholamines (adrenaline and noradrenaline) that is typical during periods of acute stress 30. The second key component is the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is a neuroendocrine system with inhibitory feedback loops involving hormone secretion from a remote target gland. Stress stimulates the release of corticotropin-releasing factor (CRF) from the paraventricular nucleus (PVN) of the hypothalamus which in turn stimulates the synthesis of adrenocorticotropic hormone (ACTH) from the anterior pituitary. ACTH subsequently triggers the production of glucocorticoids (GCs) such as cortisol or corticosterone in the adrenal cortex. In addition to these mechanisms of HPA axis activation, cytokines produced by immune cells or adipocytes can also stimulate the HPA axis, at the levels of the hypothalamus, anterior pituitary gland, and the adrenal cortex. The first evidence that cortisol levels may be related to obesity and metabolic disease was derived from clinical observations of Cushing’s syndrome; the pathological hypercortisolemia in Cushing’s syndrome is associated with upper body obesity, atherosclerosis, glucose intolerance, and hypertension. Conversely, adrenalectomy in Cushing’s syndrome patients reversed impaired glucose intolerance and obesity 31.

Acute stress-related sympathetic arousal and GC release supports behavioral, automatic and endocrinological changes which promote energy mobilization including heighted cardiac output, blood pressure, gluconeogenesis, triglyceride levels, and redirection of blood flow to fuel the muscles, heart and the brain 32. Such responses are evolutionarily adaptive and serve to promote an immediate fight-or-flight reaction; activities requiring energy expenditure that may conflict with this response (e.g., food intake, digestion, and reproduction) are typically inhibited. Thus, part of the stereotypical acute stress response includes suppression of appetite and food intake 18. GCs terminates the acute effects of stress on CRF and ACTH via negative feedback signals to the hypothalamus 33; this serves to protect the organism from prolonged, detrimental cortisol exposure. The hypothalamus is also responsive to insulin concentration, which is secreted from the pancreas and is integral to glucose metabolism and glycogenolysis 34, as well as levels of other hormones such as leptin and ghrelin, which are involved with appetite inhibition and promotion respectively. Moreover, GCs alter the expression of a number of hypothalamic neuropeptides, such as CRF, orexigenic neuropeptide Y (NPY), agouti-related peptide, and proopiomelanocortin (POMC), all of which play a role in feeding behaviors 35. Together, these findings indicate the hypothalamus is a critical region in the stress-response circuit as well as in the regulation of feeding and energy balance.

Repeated and uncontrollable stress can over time dysregulate the HPA axis, which consequently affects energy homeostasis and eating behavior. Chronic activation of the HPA axis can alter glucose metabolism, promote insulin resistance and influence multiple appetite-related hormones and hypothalamic neuropeptides 36. Noradrenaline and CRF may suppress appetite during stress, whereas cortisol may stimulate appetite during recovery from stress 37. Prolonged stress-induced GC secretion can promote abdominal fat deposition; synergistically with insulin, this can decrease HPA axis activity 38. Moreover, those under chronic stress tend to eat more under acute stress conditions 39 and show heighted preference for and consumption of hyperpalatable, energy-dense foods high in sugar and fat 1840.Go to:

Potential Role of Insulin

Animal models have demonstrated that GCs act directly in a feed-forward manner that promotes food-associated drives and CRF and ACTH secretion. For example, adrenalectomized rats demonstrate reduced food intake, while GC administration increases food intake by stimulating the release of NPY and inhibiting CRF release 4142. However, these effects do not appear to increase feeding-motivated behaviors under all conditions. Adrenalectomy reduces chow intake, while subsequent corticosterone replacement normalizes it; however, high corticosterone levels neither stimulate nor reduce chow intake 43. When rats were made diabetic using streptozotocin (which kills pancreatic B-cells, and therefore reduces/eliminates insulin secretion), a marked, dose-dependent effect of corticosterone on intake of rat chow was noted 44. Together, these findings suggest that insulin secretion, also stimulated dose-dependently by GCs, partially blocks chow intake stimulated by corticosteroids.

Insulin is secreted in proportion to adiposity; it crosses the blood-brain barrier and serves to reduce food intake and body weight dose-dependently by acting on specific receptors in the hypothalamus. Insulin and corticosterone serve opposing roles in energy balance and storage; GCs inhibit energy storage while insulin promotes adiposity 44. For example, streptozotocin-diabetic rats displayed depletion of fat reserves, and this effect was prevented when given exogenous insulin treatment 45. Under conditions where there is a choice diet (chow and lard), corticosterone dose-dependently increases total calorie intake, whereas the proportion of calories derived from a certain food source is influenced by the prevailing insulin levels 44. In the presence of insulin, passive treatment of rats with high GCs reduces chow intake, body weight, and sympathetic activity but increases fat stores 38; under chronic stress, a relative increase in abdominal fat is also observed 46. Insulin contributes importantly to dampening ACTH and GC responses to stress; evidence that indicate plasma insulin levels are negatively correlated with PVN CRF mRNA expression support this notion 40. As such, the presence of insulin is important to consider when examining the relationship between stress, eating patterns, and energy storage.Go to:

Stress, Eating and the Reward System

Activation of the HPA is linked to activation of the mesolimbic dopaminergic system, a network strongly related to reward. Anatomically, stressors can stimulate increased CRF secretion which can in turn impinge on dopamine neurons in the ventral tagmental area (VTA) 47,48, which project not only to the nucleus accumbens (NAcc) but also to prefrontal and limbic regions – all of which are part of the brain reward system commonly implicated in substance abuse 949. Both food and drugs of abuse may exploit similar pathways in the brain including the dopaminergic and opioidergic systems 950. Increased drug taking and high-fat diets alter CRF, GC, and noradrenergic activity to increase sensitization of reward pathways (including within the VTA, NAcc, dorsal striatum, and the medial prefrontal cortex regions), which in turn influences preference for addictive substance and hyperpalatable foods and increases craving and intake 48. Adrenalectomy decreases dopamine release specifically in the shell of the NAcc in response to both drug injection and hypothalamic self-stimulation, and treatment with corticosterone restores both to normal 51. Moreover, dopamine transporters in the shell of the NAcc that are reduced by adrenalectomy are restored in a dose-dependent manner by corticosterone treatment 52. Although dopamine release is not equivalent to addictive properties, dopamine has been associated with reward sensitivity, conditioning and control with respect to both food and drugs of abuse. Increased dopamine release has been reported in response to food and food cues 53 – both of which are crucial aspects of food intake 54. Repeated stimulation of the dopaminergic reward pathways may trigger neurobiological adaptions that may promote progressively compulsive behavior 55. Further, administration of dopamine antagonists or lesions of the dopaminergic system may attenuate the responding for food and reduce the reward value of both high-sugar foods and drugs of abuse in rats 5658.

Exposure to acute stress during a positron emission tomography (PET) scan revealed that both stress and cortisol release enhanced dopamine release from the NAcc 59. Another study similarly found that individuals with greater cortisol reactivity released more dopamine in the ventral striatum, suggesting a strong interconnectictivity between the two 60. In parallel, peripheral homeostatic regulators of energy balance, such as leptin, ghrelin, insulin, and orexin (all of which are associated with the HPA axis), can also regulate behaviors that are non-homeostatic and modulate the rewarding properties of food 5461. These neuropeptides may be involved with food intake regulation by interacting with the dopaminergic system through cognate receptors on VTA dopamine neurons.

Importantly, this motivational circuit overlaps with limbic regions (e.g., the amygdala, anterior cingulate cortex, hippocampus, and insula) that underlie emotions, stress reactivity and learning and memory processes contributing to cognitive and behavioral responses critical to homeostasis 48. For example, limbic regions have been implicated in the coding of rewards, memories for highly emotional events, and reward-cue-based learning and feeding 62. In contrast, the prefrontal cortex (PFC) is involved in higher cognitive and executive control functions and the regulation of emotions, impulses, desires, and cravings 62. While during normal conditions cognition is dominated by reflective cognition, during stress PFC activity is dampened and limbic circuitry hyperactivated, thus promoting “automatic” behaviors that bias survival including being vigilant for food cues. Both acute and chronic stressors increase synaptic branching in the amygdala and anterior cingulate cortex while simultaneously reducing synaptic contacts with the hippocampus and prefrontal regions 63; this process further sculpts the chronic stress network towards limbic-biased stress responses. The stressed brain expresses both a strong drive to eat and an impaired capacity to inhibit eating – together creating a potent formula for obesity. These findings are consistent with behavioral and clinical research indicating that stress or negative affect decreases emotional and behavioral control and increases impulsivity, which may synergistically contribute to greater engagement in alcohol and substance abuse and eating 48.

Given that food and drugs of abuse appear to share similar mechanisms of action, engaging in one could potentially “cross-prime” for the other. Consistent with this notion, rats administered intra-accumbens opioid injections (versus saline) responded by overeating 64. Conversely, patients who underwent bariatric surgery and lost a significant amount of weight rapidly increased their alcohol use 65. Administration of naltrexone, an opioid antagonist, to rats following 17 weeks of hyperpalatable diet exposure did not modify the energy intake but suppressed hyperphagia of hyperpalatable food 66. As food is an inexpensive resource for providing reward with hyperpalatable foods offering short term pleasure and relief from discomfort, negative reinforcement and distress may motivate stress-related eating as a way to regulate stress responses.Go to:

Addictive Properties of Hyperpalatable Food

Food-intake research indicates there is significant overlap with substance addictions, with much to be learned from this relatively well-established field 67, including with regards to the role of stress and hyperpalatable food. Stress, particularly uncontrollable stress, is a potent negative reinforcer that promotes the acquisition of drugs of abuse 48. Pretreatment with corticosterone, thought to mimic the condition of chronic stress, exaggerates this effect 68. Conversely, adrenalectomy abolishes the effect of stress on drug acquisition 69.

Several studies have examined the consumption of high-fat, high-sugar diets and activity of the HPA axis. In animal models, palatable non-nutritious food dampens HPA axis activity. For example, rats stressed for 5 consecutive days following a 5-day diet with ad libitum access to chow, lard and sucrose (versus chow only) displayed attenuated ACTH responses. In the same study, stress also increased the consumption of hyperpalatable foods above and beyond that consumed by the unstressed group 22. Similarly, short-term exposure to a high-fat diet reduced anxiety on an elevated-plus maze 70. Early life stressors such as maternal separation in rats also appear to activate chronic stress responses. A palatable high-fat diet normalized the effects of prolonged maternal separation in rats, reversing increases in anxiety and depressive behaviors, increased corticosterone, increased hypothalamic CRF, and increased hippocampal GC receptor expression 71. Over time, rats fed a hyperpalatable diet developed greater mesenteric fat, which has been negatively correlated with CRF mRNA expression in the PVN 23. Taken together, these findings suggest that stress-related eating of hyperpalatable foods serves to provide a short-term gain but may be detrimental in the long-term, contributing to abdominal fat deposition and related metabolic derangements.

Chronic stressors alter brain function and may leave traces after their relief. After the actual stress event, ACTH and GCs activity in the HPA axis may be subnormal, resembling those observed in patients with post-traumatic stress disorder 72 and rats during opioid withdrawal 46. Hyperpalatable foods given to chronically stressed rats may negate chronic stress-induced inhibition of dopamine release that occurs in the shell of the NAcc. Although acute stress stimulates dopamine secretion in the NAcc, chronic stress inhibits dopamine secretion at this site and in others (such as the PFC) associated with reward pathways 73. Regular consumption of energy-dense food may be accompanied by concomitant changes in neuronal networks, carbohydrate and fat metabolism, insulin sensitivity, and appetite hormones that modify energy homeostasis closely interact to dynamically affect altering salience, food choice and selection, craving, and motivation for food intake 7475. Based on a diet-induced model of obesity, rats fed a high-sugar diet compared to those on an unrestricted diet showed decreased dopamine release in the NAcc following 26 hours of food deprivation 76. Furthermore, rats fed on hyperpalatable 77, high-sugar 58, and high-fat 78diets increased daily food intake over time, developed patterns of copious consumption, and displayed withdrawal symptoms when placed back on a normal chow diet. Such work has been expanded to human samples. For example, healthy adults placed under a nutritionally adequate but monotonous diet, compared to those on an unrestricted diet, showed greater activation of the hippocampus, insula, and caudate in response to cues of foods they favored 79. Repeated stimulation of the reward pathways through hyperpalatable food may lead to neurobiological adaptations that eventually increase the compulsive nature of overeating characterized by the frequent drive to initiate eating. Dampening of the HPA axis to stressors in rats eating hyperpalatable foods may account for the interplay between the negative effects of chronic stressors and the positive effects of hyperpalatable foods on inputs to brain regions associated with the reward system.Go to:

Factors Moderating the Relationship between Stress and Eating Behavior

Experiencing drive to eat, in the absence of true caloric need, is common but is subject to large individual differences. Discussed below are several common factors and types of stressor that may moderate the risk for stress-induced hyperphagia.Go to:

WEIGHT AND DIET-RELATED METABOLISM

Weight-related metabolic changes may alter allostatic load. Animal models have provided evidence that obesity is often characterized by a decreased amount of adipose signal or resistance at the receptor level 80. In a state of insufficient adipose signaling, which typically serves as a negative feedback by decreasing the hedonic value of food, food intake may be prolonged and termination of eating impaired. In addition to decreased sensitivity to negative feedback, peripheral tissue sensitivity of fat and skeletal muscle tissue may also have altered sensitivity to GCs 81. Increased weight, insulin resistance and high fat diets are associated with blunted GC responses to stress challenges and altered autonomic and peripheral catecholamine responses 82. This impaired “brake” system may in part explain the epidemic of non-homeostatic eating 83.

Individuals with high BMIs show a stronger association between chronic stress and weight gain than those with low BMIs who experience similar degrees of stress 20. Consistent with this notion, stress-related eating is significantly associated with obesity in women 84. Moreover, overweight and obese individuals appear sensitized to food cues, particularly after exposure to stress. A recent study found that among healthy lean participants, mean food craving and energy intake decreased in the absence of hunger in response to both rest and stress conditions 85. On the other hand, visceral overweight participants showed higher mean food craving and energy intake of hyperpalatable foods (e.g., desserts, snacks) in the absence of hunger when under stress versus rest, potentially as a mechanism to regulate and suppress stress 85. Obese (versus lean) individuals demonstrated significantly increased activation in brain reward regions including the striatum, insula, and thalamus during exposure to favorite food cue and stress 29. Moreover, the magnitude of insulin resistance positively correlated with the activation of the striatum and insula in response to both favorite food cue and stress conditions in obese but not lean individuals 29. Mild hypoglycemia, induced by a hyperinsulinemic clamp, potentiated activation of brain reward and limbic regions preferentially to hyperpalatable food cues, an effect that correlated with increased cortisol levels, while decreasing medial prefrontal activation, an effect that correlated with lowering glucose levels; these effects were moderated by BMI and were more pronounced among obese individuals 86. Chronic high levels of peripheral insulin and insulin resistance, as observed in many overweight and obese individuals 36, may impair insulin’s ability to suppress motivation pathways, resulting in heightened stress- and food-cue-related responses.Go to:

EMOTIONAL EATING

Chronic stress is often accompanied by anxiety, depression, anger, apathy, and alienation 87. Threatening and cognitively meaningful stimuli activate the emotional nervous system which, in part, determines behavioral output (e.g., fight-or-flight). Stress-induced elevations of GC secretion can intensify emotions and motivation 88. Given the rewarding properties of food, it is hypothesized that hyperpalatable foods may serve as “comfort food” that acts as a form of self-medication to dispel unwanted distress. Individuals in negative affective states have been shown to favor the consumption of hedonically rewarding foods high in sugar and/or fat, whereas intake during happy states favor less palatable dried fruits 89. Following laboratory exposure to ego threats, people exhibiting high negative affect or greater cortisol reactivity ate more food of high-sugar and high-fat content 28. Similarly, in naturalistic settings, people with high cortisol reactivity report greater snacking in response to daily stressors 90.Go to:

RESTRAINED EATING

Restrained eating refers to the voluntary cognitive control effort to restrict food intake typically for the purpose of weight loss or maintenance. Cognitive restraint has been related to food intake under stress, with highly restrained eaters increasing and unrestrained eaters decreasing their food intake during stressful conditions 91. This response differs from that of emotional eating – while restraint is associated with greater food intake after stressors, emotional eating is linked to increased intake after an ego-threat stressor 92. Restraint eating may exacerbate eating in response to food cues, stress and other stimuli, whereas emotional eating may serve to ameliorate negative self-focused emotions. People endorsing higher levels of dietary restraint often show little overall difference in calorie intake compared to people with low restraint, or in food intake when unobtrusively observed in laboratory 93 and naturalistic settings 94. Restraint may represent unsuccessful attempts at food restriction – eating less than one would during normal (low-stress) conditions, while tending to overeat during stress.

Several studies have found that high cognitive restraint is associated with increased cortisol concentrations 9596. Increased restraint may play an important role in promoting obesity and serve as a vulnerability marker for a reward system sensitized to palatable food. For example, rats exposed to either repeated stress or food restriction alone did not differ from controls in their total food intake, when ignoring food type. With restriction alone, rats increased their chow intake in response to negative energy balance. However, when restricted eating was combined with stress, rats displayed a greater cookie intake over chow, suggesting hedonic feeding and stress arousal reduction rather than feeding for metabolic need alone 97. In humans, a recent large-scale study reported that stress was related to various indices of increased drive to eat, including disinhibited eating, binge eating, and more frequent intake of hyperpalatable food (e.g., chips, hamburgers, and soda); additionally, greater stress exposure accounted for significantly higher rigid restraint 47. While flexible restraint may be effective in weight management and prevention of excessive consumption of palatable non-nutritious food, rigid restraint may lead to sensitization of such foods. People who maintain rigid rules around their food appear less attentive to the physiological cues of hunger and satiety, leading to overeating after a preload 98. It is hypothesized that people actively trying to restrain food intake may deplete the cognitive resources necessary to deal with stressors, thereby impairing their inhibitory control which in turn increases the likelihood of overeating. Lack of control over life events may lead to desperate and ineffective attempts to control eating such as by deprivation from a particular food followed by later binging. Moreover, chronic food restriction may augment the rewarding (i.e. threshold-lowering) effects of drugs of abuse 99.Go to:

SLEEP DEPRIVATION

Sleep deprivation is a common chronic stressor that may contribute to increased risk for obesity and metabolic diseases, including abdominal obesity, insulin resistance, hypertension, atherosclerosis, that may predispose individuals to cardiovascular disease and type II diabetes 100101. It is estimated that roughly 30% of all adults in the United States sleep less than 6h per night 102. Cross-sectional analyses have found a significant association between short sleep duration and increased prevalence of obesity or higher BMI in both adult and child samples 103. Two recent meta-analyses have found that short sleep duration (<5h per night for adults, <10h per night for children) significantly predicted obesity. Moreover, BMI was 0.35 kg/m2 lower for every additional hour of sleep 104105.

Sleep deprivation may dysregulate the HPA axis, although data have been inconsistent. In laboratory settings, insulin sensitivity was reduced in sleep-restricted individuals 106. Studies have demonstrated both increased 107108 and decreased 109 night-time and morning plasma cortisol levels. The Wisconsin Sleep Cohort Study reported that following one night of polysomnography in the laboratory, total sleep time from polysomnography was inversely associated with ghrelin levels while average habitual sleep duration was positively associated with leptin levels independent of BMI 110. In a similar vein, data from the Quebec Family Study of 740 adults sleeping 5-6h per night had leptin levels approximately 15-17% lower than predicted based on body fat alone 111. However, other studies have reported negative findings. For example, a sample of 173 obese, sedentary post-menopausal women aged 50-74 years found no cross-sectional associations between self-reported sleep duration and total leptin or ghrelin levels 112. Interestingly, although hunger ratings and average nocturnal sleep were not significantly associated, adolescents who slept 3h or more during the daytime reported greater caloric intake and food cravings, and this association was not confounded by nocturnal sleep duration 113. More research assessing the relationship between habitual insufficient sleep and food intake is needed.

Conclusion

Feeding is essential for life. The balance between energy storage and expenditure is critical for survival. It is therefore not surprising that neural networks that subserve feeding and stress responses form in early developmental stages 88. During human evolution, food was scarce and life-threatening stressors frequent; elevated GCs level and depressed insulin levels, except when feeding, therefore served adaptive purposes. However, in our current obesogenic environment where food is plentiful, palatable and easy accessible, the proliferation of stressors may drive non-homeostatic feeding – in other words, eating without metabolic need. Repeated bouts of minor daily stressors that keep the stress system in a chronically activated state may alter brain reward/motivation pathways involved in wanting and seeking hyperpalatable foods and induce metabolic changes that promote weight and body fat mass. Weight-related adaptions of the metabolic, neuroendocrine, and neuronal pathways can together potentiate food preference, craving and intake under conditions of stress. A sensitized feed-forward process may result in changes that promote elevated desires for and increased consumption of hyperpalatable foods. Individual differences in susceptibility to obesity and types of stress may further moderate this process.

While recent research has elucidated possible pathways for stress-related eating, there is considerable need for trying to better understand and prevent stress-related eating and non-homeostatic eating in general. Despite data suggesting potentially addictive properties of hyperpalatable foods, debate exists regarding the existence of food addiction 114116. For this and possibly other reasons, food addiction is generally overlooked in clinical settings. Large-scale prevention and treatment programs for food addiction (like those for substance addiction) are lacking with physicians, nurses, psychologists and other clinicians typically receiving little or no training in food addiction or its management. Identifying specific biomarkers and developing quantifiable measures to assess biobehavioral adaptations associated with stress and food addiction could be beneficial in developing public health intervention. Nonetheless, specific subgroups of individuals appear at elevated risk for food addiction. For example, binge-eating disorder shows a particularly close relationship with elevated odds of about 5 between food addiction and binge-eating disorder 117, and multiple other clinical characteristics (impaired impulse control, altered reward processing) linking binge-eating disorder and food addiction 118119. By integrating information across disciplines in order to promote the development of improved policy, prevention and treatment strategies, significant advances in halting and reversing the current obesity epidemic may be achieved 120.Go to:

ACKNOWLEDGEMENTS

This research was funded in part by NIH grants from NIAAA (RL1 AA017539), the Connecticut State Department of Mental Health and Addictions Services, and the Connecticut Mental Health Center. The funding agencies did not provide input or comment on the content of the manuscript, and the content of the manuscript reflects the contributions and thoughts of the authors and do not necessarily reflect the views of the funding agencies.Go to:

Footnotes

CONFLICT OF INTEREST

The authors report no conflicts of interest with respect to the content of this manuscript. Dr. Potenza has consulted for Lundbeck and Ironwood pharmaceuticals; has had financial interests in Somaxon pharmaceuticals; received research support from Mohegan Sun Casino, Psyadon pharmaceuticals, the National Center for Responsible Gambling, the National Institutes of Health (NIH), Veterans Administration; has participated in surveys, mailings, or telephone consultations related to drug addiction, impulse-control disorders, or other health topics; has consulted for gambling, legal and governmental entities on issues related to addictions or impulse-control disorders; has provided clinical care in the Connecticut Department of Mental Health and Addiction Services Problem Gambling Services Program; has performed grant reviews for the NIH and other agencies; has guest edited journal sections; has given academic lectures in grand rounds, Continuing Medical Education events, and other clinical or scientific venues; and has generated books or book chapters for publishers of mental health texts. Yvonne Yau reports no disclosures.Go to:

References

1. World Health Organization [2012 Jan 29];Obesity and overweight. 2012 Available from:http://www.who.int/mediacentre/factsheets/fs311/en/2. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of Obesity in the United States. National Center for Health Statistics, U.S. Department of Health and Human Services; 2012. [Google Scholar]3. Joranby L, Pineda KF, Gold MS. Addiction to food and brain reward systems. Sexual Addiction & Compulsivity. 2005;12(2-3):201–17. [Google Scholar]4. Mokdad AH, Ford ES, Bowman BA, Dietz WH, Vinicor F, Bales VS, et al. Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA : the journal of the American Medical Association. 2003;289(1):76–9. Epub 2002/12/31. [PubMed] [Google Scholar]5. Must A, Spadano J, Coakley EH, Field AE, Colditz G, Dietz WH. The disease burden associated with overweight and obesity. JAMA : the journal of the American Medical Association. 1999;282(16):1523–9.Epub 1999/11/05. [PubMed] [Google Scholar]6. Astrup A, Meinert Larsen DT, Harper A. Atkins and other low-carbohydrate diets: hoax or an effective tool for weight loss? Lancet. 2004;364(9437):897–9. [PubMed] [Google Scholar]7. Geloneze B, Mancini MC, Coutinho W. Obesity: Knowledge, care, and commitment, but not yet cure. Obesidade. 2009;53(2):117–9. [PubMed] [Google Scholar]8. Maciejewski ML, Livingston EH, Smith VA, Kavee AL, Kahwati LC, Henderson WG, et al. Survival among high-risk patients after bariatric surgery. Journal of the American Medical Association. 2011;305(23):2419–26. [PubMed] [Google Scholar]9. Volkow ND, Wang GJ, Fowler JS, Tomasi D, Baler R. Food and Drug Reward: Overlapping Circuits in Human Obesity and Addiction. In: Carter CS, Dalley JW, editors. Brain Imaging in Behavioral Neuroscience. Springer; Berlin Heidelberg: 2012. pp. 1–24. [PubMed] [Google Scholar]10. Davis C, Carter JC. Compulsive overeating as an addiction disorder. A review of theory and evidence. Appetite. 2009;53(1):1–8. [PubMed] [Google Scholar]11. Kreek MJ, Nielsen DA, Butelman ER, LaForge KS. Genetic influences on impulsivity, risk taking, stress responsivity and vulnerability to drug abuse and addiction. Nature Neuroscience. 2005;8(11):1450–7.[PubMed] [Google Scholar]12. Koob GF. A Role for Brain Stress Systems in Addiction. Neuron. 2008;59(1):11–34. [PMC free article][PubMed] [Google Scholar]13. Fink G. Stress: Definition and history. Stress Science: Neuroendocrinology. 2010:3–9.[Google Scholar]14. McEwen BS. Protection and Damage from Acute and Chronic Stress: Allostasis and Allostatic Overload and Relevance to the Pathophysiology of Psychiatric Disorders. Annals of the New York Academy of Sciences. 2004;1032(1):1–7. [PubMed] [Google Scholar]15. Seyle H. The Stress of Life. McGraw-Hill; New York: 1976. [Google Scholar]16. Levine AS, Morley JE. Stress-induced eating in rats. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 1981;241(1):R72–R6. [PubMed] [Google Scholar]17. Morley JE, Levine AS, Rowland NE. Stress induced eating. Life Sciences. 1983;32(19):2169–82.[PubMed] [Google Scholar]18. Torres SJ, Nowson CA. Relationship between stress, eating behavior, and obesity. Nutrition. 2007;23(11–12):887–94. [PubMed] [Google Scholar]19. Pasquali R. The hypothalamic–pituitary–adrenal axis and sex hormones in chronic stress and obesity: pathophysiological and clinical aspects. Annals of the New York Academy of Sciences. 2012;1264(1):20–35. [PMC free article] [PubMed] [Google Scholar]20. Block JP, He Y, Zaslavsky AM, Ding L, Ayanian JZ. Psychosocial Stress and Change in Weight Among US Adults. American Journal of Epidemiology. 2009;170(2):181–92. [PMC free article] [PubMed] [Google Scholar]21. Robbins TW, Fray PJ. Stress-induced eating: fact, fiction or misunderstanding? Appetite. 1980;1(2):103–33. [Google Scholar]22. Pecoraro N, Reyes F, Gomez F, Bhargava A, Dallman MF. Chronic Stress Promotes Palatable Feeding, which Reduces Signs of Stress: Feedforward and Feedback Effects of Chronic Stress. Endocrinology. 2004;145(8):3754–62. [PubMed] [Google Scholar]23. Dallman MF, Pecoraro N, Akana SF, la Fleur SE, Gomez F, Houshyar H, et al. Chronic stress and obesity: A new view of “comfort food”. Proceedings of the National Academy of Sciences. 2003;100(20):11696–701. [PMC free article] [PubMed] [Google Scholar]24. La Fleur SE, Houshyar H, Roy M, Dallman MF. Choice of lard, but not total lard calories, damps adrenocorticotropin responses to restraint. Endocrinology. 2005;146(5):2193–9. [PubMed] [Google Scholar]25. Zellner DA, Loaiza S, Gonzalez Z, Pita J, Morales J, Pecora D, et al. Food selection changes under stress. Physiology & behavior. 2006;87(4):789–93. [PubMed] [Google Scholar]26. Epel E, Lapidus R, McEwen B, Brownell K. Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior. Psychoneuroendocrinology. 2001;26(1):37–49.[PubMed] [Google Scholar]27. Oliver G, Wardle J, Gibson EL. Stress and food choice: A laboratory study. Psychosomatic medicine. 2000;62(6):853–65. [PubMed] [Google Scholar]28. Rutters F, Nieuwenhuizen AG, Lemmens SG, Born JM, Westerterp-Plantenga MS. Acute stress-related changes in eating in the absence of hunger. Obesity. 2009;17(1):72–7. Epub 2008/11/11. [PubMed] [Google Scholar]29. Jastreboff AM, Sinha R, Lacadie C, Small DM, Sherwin RS, Potenza MN. Neural Correlates of Stress- and Food- Cue-Induced Food Craving In Obesity: Association with insulin levels. Diabetes care. 2013Epub 2012/10/17. [PMC free article] [PubMed] [Google Scholar]30. Schommer NC, Hellhammer DH, Kirschbaum C. Dissociation between reactivity of the hypothalamus-pituitary-adrenal axis and the sympathetic-adrenal-medullary system to repeated psychosocial stress. Psychosomatic medicine. 2003;65(3):450–60. Epub 2003/05/24. [PubMed] [Google Scholar]31. Nieuwenhuizen AG, Rutters F. The hypothalamic-pituitary-adrenal-axis in the regulation of energy balance. Physiology & behavior. 2008;94(2):169–77. Epub 2008/02/16. [PubMed] [Google Scholar]32. Majzoub JA. Corticotropin-releasing hormone physiology. European Journal of Endocrinology. 2006;155(suppl 1):S71–S6. [Google Scholar]33. Herman JP, Cullinan WE. Neurocircuitry of stress: central control of the hypothalamo–pituitary–adrenocortical axis. Trends in Neurosciences. 1997;20(2):78–84. [PubMed] [Google Scholar]34. Schwartz MW, Figlewicz DP, Baskin DG, Woods SC, Porte D., Jr Insulin in the brain: a hormonal regulator of energy balance. Endocrine reviews. 1992;13(3):387–414. Epub 1992/08/11. [PubMed] [Google Scholar]35. Maniam J, Morris MJ. The link between stress and feeding behaviour. Neuropharmacology. 2012;63(1):97–110. [PubMed] [Google Scholar]36. Adam TC, Epel ES. Stress, eating and the reward system. Physiology & behavior. 2007;91(4):449–58.Epub 2007/06/05. [PubMed] [Google Scholar]37. Takeda E, Terao J, Nakaya Y, Miyamoto K, Baba Y, Chuman H, et al. Stress control and human nutrition. The journal of medical investigation : JMI. 2004;51(3-4):139–45. Epub 2004/10/06. [PubMed] [Google Scholar]38. Dallman MF, Pecoraro NC, la Fleur SE. Chronic stress and comfort foods: self-medication and abdominal obesity. Brain, Behavior, and Immunity. 2005;19(4):275–80. [PubMed] [Google Scholar]39. Gibson EL. Emotional influences on food choice: sensory, physiological and psychological pathways. Physiology & behavior. 2006;89(1):53–61. Epub 2006/03/21. [PubMed] [Google Scholar]40. Warne JP. Shaping the stress response: Interplay of palatable food choices, glucocorticoids, insulin and abdominal obesity. Molecular and Cellular Endocrinology. 2009;300(1–2):137–46. [PubMed] [Google Scholar]41. Bell ME, Bhatnagar S, Liang J, Soriano L, Nagy TR, Dallman MF. Voluntary sucrose ingestion, like corticosterone replacement, prevents the metabolic deficits of adrenalectomy. Journal of Neuroendocrinology. 2000;12(5):461–70. [PubMed] [Google Scholar]42. Bhatnagar S, Bell ME, Liang J, Soriano L, Nagy TR, Dallman MF. Corticosterone facilitates saccharin intake in adrenalectomized rats: Does corticosterone increase stimulus salience? Journal of Neuroendocrinology. 2000;12(5):453–60. [PubMed] [Google Scholar]43. Devenport L, Thomas T, Knehans A, Sundstrom A. Acute, chronic, and interactive effects of type I and II corticosteroid receptor stimulation on feeding and weight gain. Physiology & behavior. 1990;47(6):1221–8. [PubMed] [Google Scholar]44. la Fleur SE, Akana SF, Manalo SL, Dallman MF. Interaction between corticosterone and insulin in obesity: regulation of lard intake and fat stores. Endocrinology. 2004;145(5):2174–85. [PubMed] [Google Scholar]45. Warne JP, Horneman HF, Wick EC, Bhargava A, Pecoraro NC, Ginsberg AB, et al. Comparison of superior mesenteric versus jugular venous infusions of insulin in streptozotocin-diabetic rats on the choice of caloric intake, body weight, and fat stores. Endocrinology. 2006;147(11):5443–51. Epub 2006/07/29. [PubMed] [Google Scholar]46. Houshyar H, Manalo S, Dallman MF. Time-dependent alterations in mRNA expression of brain neuropeptides regulating energy balance and hypothalamo-pituitary-adrenal activity after withdrawal from intermittent morphine treatment. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2004;24(42):9414–24. Epub 2004/10/22. [PubMed] [Google Scholar]47. Groesz LM, McCoy S, Carl J, Saslow L, Stewart J, Adler N, et al. What is eating you? Stress and the drive to eat. Appetite. 2012;58(2):717–21. Epub 2011/12/15. [PMC free article] [PubMed] [Google Scholar]48. Sinha R. Chronic stress, drug use, and vulnerability to addiction. Annals of the New York Academy of Sciences. 2008;1141(1):105–30. [PMC free article] [PubMed] [Google Scholar]49. Clark AM. Reward processing: a global brain phenomenon? J Neurophysiol. 2012;109(1):1–4. Epub 2012/07/21. [PMC free article] [PubMed] [Google Scholar]50. Koob GF, Volkow ND. Neurocircuitry of addiction. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2010;35(1):217–38. Epub 2009/08/28. [PMC free article] [PubMed] [Google Scholar]51. Barr AM, Brotto LA, Phillips AG. Chronic corticosterone enhances the rewarding effect of hypothalamic self-stimulation in rats. Brain research. 2000;875(1-2):196–201. Epub 2000/09/01. [PubMed] [Google Scholar]52. Sarnyai Z, McKittrick CR, McEwen BS, Kreek MJ. Selective regulation of dopamine transporter binding in the shell of the nucleus accumbens by adrenalectomy and corticosterone-replacement. Synapse (New York, NY) 1998;30(3):334–7. Epub 1998/10/17. [PubMed] [Google Scholar]53. Di Chiara G, Imperato A. Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proc Natl Acad Sci U S A. 1988;85(14):5274–8. Epub 1988/07/01. [PMC free article] [PubMed] [Google Scholar]54. Volkow ND, Wang G-J, Baler RD. Reward, dopamine and the control of food intake: implications for obesity. Trends in cognitive sciences. 2011;15(1):37–46. [PMC free article] [PubMed] [Google Scholar]55. Everitt BJ, Belin D, Economidou D, Pelloux Y, Dalley JW, Robbins TW. Review. Neural mechanisms underlying the vulnerability to develop compulsive drug-seeking habits and addiction. Philosophical transactions of the Royal Society of London Series B, Biological sciences. 2008;363(1507):3125–35. Epub 2008/07/22. [PMC free article] [PubMed] [Google Scholar]56. Wise RA, Rompre PP. Brain dopamine and reward. Annual review of psychology. 1989;40:191–225.Epub 1989/01/01. [PubMed] [Google Scholar]57. Colantuoni C, Rada P, McCarthy J, Patten C, Avena NM, Chadeayne A, et al. Evidence that intermittent, excessive sugar intake causes endogenous opioid dependence. Obesity Research. 2002;10(6):478–88. [PubMed] [Google Scholar]58. Avena NM, Hoebel BG. A diet promoting sugar dependency causes behavioral cross-sensitization to a low dose of amphetamine. Neuroscience. 2003;122(1):17–20. [PubMed] [Google Scholar]59. Wand GS, Oswald LM, McCaul ME, Wong DF, Johnson E, Zhou Y, et al. Association of amphetamine-induced striatal dopamine release and cortisol responses to psychological stress. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2007;32(11):2310–20. Epub 2007/03/08. [PubMed] [Google Scholar]60. Pruessner JC, Champagne F, Meaney MJ, Dagher A. Dopamine release in response to a psychological stress in humans and its relationship to early life maternal care: a positron emission tomography study using [11C]raclopride. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2004;24(11):2825–31. Epub 2004/03/19. [PubMed] [Google Scholar]61. Yau Y, Yip S, Potenza MN. Understanding “Behavioral Addictions”: Insights from Research. In: Fiellin DA, Miller SC, Saitz R, editors. Principles of Addiction Medicine. 5th ed. Lippincott Williams & Wilkins; Philadelphia, PA: in press. [Google Scholar]62. Berthoud HR. The neurobiology of food intake in an obesogenic environment. The Proceedings of the Nutrition Society. 2012;71(4):478–87. Epub 2012/07/18. [PMC free article] [PubMed] [Google Scholar]63. Vyas A, Mitra R, Shankaranarayana Rao BS, Chattarji S. Chronic stress induces contrasting patterns of dendritic remodeling in hippocampal and amygdaloid neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2002;22(15):6810–8. Epub 2002/08/02. [PubMed] [Google Scholar]64. Kelley AE, Bakshi VP, Fleming S, Holahan MR. A pharmacological analysis of the substrates underlying conditioned feeding induced by repeated opioid stimulation of the nucleus accumbens. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2000;23(4):455–67. Epub 2000/09/16. [PubMed] [Google Scholar]65. King WC, Chen JY, Mitchell JE, Kalarchian MA, Steffen KJ, Engel SG, et al. Prevalence of alcohol use disorders before and after bariatric surgery. JAMA : the journal of the American Medical Association. 2012;307(23):2516–25. Epub 2012/06/20. [PMC free article] [PubMed] [Google Scholar]66. Apfelbaum M, Mandenoff A. Naltrexone suppresses hyperphagia induced in the rat by a highly palatable diet. Pharmacology Biochemistry and Behavior. 1981;15(1):89–91. [PubMed] [Google Scholar]67. Gearhardt AN, Grilo CM, DiLeone RJ, Brownell KD, Potenza MN. Can food be addictive? Public health and policy implications. Addiction. 2011;106(7):1208–12. [PMC free article] [PubMed] [Google Scholar]68. Mantsch JR, Saphier D, Goeders NE. Corticosterone facilitates the acquisition of cocaine self-administration in rats: opposite effects of the type II glucocorticoid receptor agonist dexamethasone. The Journal of pharmacology and experimental therapeutics. 1998;287(1):72–80. Epub 1998/10/09. [PubMed] [Google Scholar]69. Goeders NE, Guerin GF. Effects of surgical and pharmacological adrenalectomy on the initiation and maintenance of intravenous cocaine self-administration in rats. Brain research. 1996;722(1–2):145–52.[PubMed] [Google Scholar]70. Prasad A, Prasad C. Short-term consumption of a diet rich in fat decreases anxiety response in adult male rats. Physiology & behavior. 1996;60(3):1039–42. [PubMed] [Google Scholar]71. Maniam J, Morris MJ. Palatable cafeteria diet ameliorates anxiety and depression-like symptoms following an adverse early environment. Psychoneuroendocrinology. 2010;35(5):717–28. [PubMed] [Google Scholar]72. Aardal-Eriksson E, Eriksson TE, Thorell L-H. Salivary cortisol, posttraumatic stress symptoms, and general health in the acute phase and during 9-month follow-up. Biological psychiatry. 2001;50(12):986–93. [PubMed] [Google Scholar]73. Nanni G, Scheggi S, Leggio B, Grappi S, Masi F, Rauggi R, et al. Acquisition of an appetitive behavior prevents development of stress-induced neurochemical modifications in rat nucleus accumbens. Journal of Neuroscience Research. 2003;73(4):573–80. [PubMed] [Google Scholar]74. Alsiö J, Olszewski PK, Norbäck AH, Gunnarsson ZEA, Levine AS, Pickering C, et al. Dopamine D1 receptor gene expression decreases in the nucleus accumbens upon long-term exposure to palatable food and differs depending on diet-induced obesity phenotype in rats. Neuroscience. 2010;171(3):779–87.[PubMed] [Google Scholar]75. Gearhardt A, Davis C, Kuschner R, Brownell K. The addiction potential of hyperpalatable foods. Current drug abuse reviews. 2011;4(3):140. [PubMed] [Google Scholar]76. Avena NM, Bocarsly ME, Rada P, Kim A, Hoebel BG. After daily bingeing on a sucrose solution, food deprivation induces anxiety and accumbens dopamine/acetylcholine imbalance. Physiology & behavior. 2008;94(3):309–15. Epub 2008/03/08. [PMC free article] [PubMed] [Google Scholar]77. Johnson PM, Kenny PJ. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci. 2010;13(5):635–41. [PMC free article] [PubMed] [Google Scholar]78. Lutter M, Nestler EJ. Homeostatic and hedonic signals interact in the regulation of food intake. Journal of Nutrition. 2009;139(3):629–32. [PMC free article] [PubMed] [Google Scholar]79. Pelchat ML, Johnson A, Chan R, Valdez J, Ragland JD. Images of desire: food-craving activation during fMRI. NeuroImage. 2004;23(4):1486–93. [PubMed] [Google Scholar]80. Ikeda H, West DB, Pustek JJ, Figlewicz DP, Greenwood MRC, Porte D, Jr, et al. Intraventricular insulin reduces food intake and body weight of lean but not obese zucker rats. Appetite. 1986;7(4):381–6.[PubMed] [Google Scholar]81. Reynolds RM, Chapman KE, Seckl JR, Walker BR, McKeigue PM, Lithell HO. Skeletal muscle glucocorticoid receptor density and insulin resistance. JAMA : the journal of the American Medical Association. 2002;287(19):2505–6. Epub 2002/05/22. [PubMed] [Google Scholar]82. Tyrka AR, Walters OC, Price LH, Anderson GM, Carpenter LL. Altered response to neuroendocrine challenge linked to indices of the metabolic syndrome in healthy adults. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2012;44(7):543–9. Epub 2012/05/03. [PMC free article] [PubMed] [Google Scholar]83. Figlewicz DP, Sipols AJ, Bennett J, Evans SB, Kaiyala K, Benoit SC. Intraventricular insulin and leptin reverse place preference conditioned with high-fat diet in rats. Behavioral Neuroscience. 2004;118(3):479–87. [PubMed] [Google Scholar]84. Laitinen J, Ek E, Sovio U. Stress-related eating and drinking behavior and body mass index and predictors of this behavior. Prev Med. 2002;34(1):29–39. Epub 2001/12/26. [PubMed] [Google Scholar]85. Lemmens SG, Rutters F, Born JM, Westerterp-Plantenga MS. Stress augments food ‘wanting’ and energy intake in visceral overweight subjects in the absence of hunger. Physiology & behavior. 2011;103(2):157–63. Epub 2011/01/19. [PubMed] [Google Scholar]86. Page KA, Seo D, Belfort-DeAguiar R, Lacadie C, Dzuira J, Naik S, et al. Circulating glucose levels modulate neural control of desire for high-calorie foods in humans. J Clin Invest. 2011;121(10):4161–9.[PMC free article] [PubMed] [Google Scholar]87. Cohen JI. Stress and mental health: a biobehavioral perspective. Issues in mental health nursing. 2000;21(2):185–202. Epub 2000/06/06. [PubMed] [Google Scholar]88. Dallman MF. Stress-induced obesity and the emotional nervous system. Trends in Endocrinology & Metabolism. 2010;21(3):159–65. [PMC free article] [PubMed] [Google Scholar]89. Garg N, Wansink B, Inman JJ. The influence of incidental affect on consumers’ food intake. Journal of Marketing. 2007;71(1):194–206. [Google Scholar]90. Newman E, O’Connor DB, Conner M. Daily hassles and eating behaviour: The role of cortisol reactivity status. Psychoneuroendocrinology. 2007;32(2):125–32. [PubMed] [Google Scholar]91. Wardle J, Steptoe A, Oliver G, Lipsey Z. Stress, dietary restraint and food intake. Journal of Psychosomatic Research. 2000;48(2):195–202. [PubMed] [Google Scholar]92. Wallis DJ, Hetherington MM. Stress and eating: the effects of ego-threat and cognitive demand on food intake in restrained and emotional eaters. Appetite. 2004;43(1):39–46. Epub 2004/07/21. [PubMed] [Google Scholar]93. Stice E, Sysko R, Roberto CA, Allison S. Are dietary restraint scales valid measures of dietary restriction? Additional objective behavioral and biological data suggest not. Appetite. 2010;54(2):331–9.[PMC free article] [PubMed] [Google Scholar]94. Stice E, Fisher M, Lowe MR. Are Dietary Restraint Scales Valid Measures of Acute Dietary Restriction? Unobtrusive Observational Data Suggest Not. Psychological Assessment. 2004;16(1):51–9.[PubMed] [Google Scholar]95. Anderson DA, Shapiro JR, Lundgren JD, Spataro LE, Frye CA. Self-reported dietary restraint is associated with elevated levels of salivary cortisol. Appetite. 2002;38(1):13–7. [PubMed] [Google Scholar]96. McLean JA, Barr SI, Prior JC. Cognitive dietary restraint is associated with higher urinary cortisol excretion in healthy premenopausal women. The American Journal of Clinical Nutrition. 2001;73(1):7–12.[PubMed] [Google Scholar]97. Boggiano MM, Chandler PC. Binge eating in rats produced by combining dieting with stress. Current protocols in neuroscience / editorial board, Jacqueline N Crawley [et al] 2006 Chapter 9:Unit9 23A. Epub 2008/04/23. [PubMed] [Google Scholar]98. Heatherton TF, Polivy J, Herman CP. Restraint and internal responsiveness: effects of placebo manipulations of hunger state on eating. Journal of abnormal psychology. 1989;98(1):89–92. Epub 1989/02/01. [PubMed] [Google Scholar]99. Carr KD. Augmentation of drug reward by chronic food restriction: Behavioral evidence and underlying mechanisms. Physiology & behavior. 2002;76(3):353–64. [PubMed] [Google Scholar]100. Knutson KL, Van Cauter E. Associations between sleep loss and increased risk of obesity and diabetes. Ann N Y Acad Sci. 2008;1129:287–304. Epub 2008/07/02. [PMC free article] [PubMed] [Google Scholar]101. Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome. The Lancet. 365(9468):1415–28.[PubMed] [Google Scholar]102. National Center for Health Statistics QuickStats: percentage of adults who reported an average of ≤6 h of sleep per 24-hour period, by sex and age group – United States, 1985 and 2004. Morbidity and Mortality Weekly Report. 2005:933. [Google Scholar]103. Patel SR, Hu FB. Short sleep duration and weight gain: A systematic review. Obesity. 2008;16(3):643–53. [PMC free article] [PubMed] [Google Scholar]104. Chen X, Beydoun MA, Wang Y. Is sleep duration associated with childhood obesity? A systematic review and meta-analysis. Obesity. 2008;16(2):265–74. [PubMed] [Google Scholar]105. Cappuccio FP, Taggart FM, Kandala NB, Currie A, Peile E, Stranges S, et al. Meta-analysis of short sleep duration and obesity in children and adults. Sleep. 2008;31(5):619–26. [PMC free article] [PubMed] [Google Scholar]106. Spiegal LA. Comments on the psychoanalytic psychology of adolescence. Psychoanalytic Study of the Child. 1958;13:296–308. [PubMed] [Google Scholar]107. Schussler P, Uhr M, Ising M, Weikel JC, Schmid DA, Held K, et al. Nocturnal ghrelin, ACTH, GH and cortisol secretion after sleep deprivation in humans. Psychoneuroendocrinology. 2006;31(8):915–23.Epub 2006/07/04. [PubMed] [Google Scholar]108. Spiegel K, Leproult R, L’Hermite-Baleriaux M, Copinschi G, Penev PD, Van Cauter E. Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. The Journal of clinical endocrinology and metabolism. 2004;89(11):5762–71.Epub 2004/11/09. [PubMed] [Google Scholar]109. Wu H, Zhao Z, Stone WS, Huang L, Zhuang J, He B, et al. Effects of sleep restriction periods on serum cortisol levels in healthy men. Brain research bulletin. 2008;77(5):241–5. Epub 2008/09/02. [PubMed] [Google Scholar]110. Taheri S, Lin L, Austin D, Young T, Mignot E. Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index (BMI). Sleep. 2004;27(SUPPL.):A146–A7. ABSTR. [PMC free article] [PubMed] [Google Scholar]111. Chaput J-P, Després J-P, Bouchard C, Tremblay A. Short Sleep Duration is Associated with Reduced Leptin Levels and Increased Adiposity: Results from the Québec Family Study. Obesity. 2007;15(1):253–61. [PubMed] [Google Scholar]112. Littman AJ, Vitiello MV, Foster-Schubert K, Ulrich CM, Tworoger SS, Potter JD, et al. Sleep, ghrelin, leptin and changes in body weight during a 1-year moderate-intensity physical activity intervention. International journal of obesity (2005) 2007;31(3):466–75. Epub 2006/08/16. [PubMed] [Google Scholar]113. Landis AM, Parker KP, Dunbar SB. Sleep, hunger, satiety, food cravings, and caloric intake in adolescents. Journal of Nursing Scholarship. 2009;41(2):115–23. [PubMed] [Google Scholar]114. Ziauddeen H, Farooqi IS, Fletcher PC. Food addiction: is there a baby in the bathwater? Nat Rev Neurosci. 2012;13(7):514. [PubMed] [Google Scholar]115. Ziauddeen H, Farooqi IS, Fletcher PC. Obesity and the brain: how convincing is the addiction model? Nat Rev Neurosci. 2012;13(4):279–86. [PubMed] [Google Scholar]116. Avena NM, Gearhardt AN, Gold MS, Wang G-J, Potenza MN. Tossing the baby out with the bathwater after a brief rinse? The potential downside of dismissing food addiction based on limited data. Nat Rev Neurosci. 2012;13(7):514. [PubMed] [Google Scholar]117. Gearhardt AN, White MA, Masheb RM, Morgan PT, Crosby RD, Grilo CM. An examination of the food addiction construct in obese patients with binge eating disorder. International Journal of Eating Disorders. 2012;45(5):657–63. [PMC free article] [PubMed] [Google Scholar]118. Gearhardt A, White M, Potenza M. Binge eating disorder and food addiction. Curr Drug Abuse Rev. 2011;4(3):201–7. [PMC free article] [PubMed] [Google Scholar]119. Balodis IM, Kober H, Worhunsky PD, White MA, Stevens MC, Pearlson GD, et al. Monetary reward processing in obese individuals with and without binge eating disorder. Biological psychiatry. 2013[PMC free article] [PubMed] [Google Scholar]120. Potenza MN. Obesity, Food and Addiction: Emerging Neuroscience and Clinical and Public Health Implications. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. under review. [PMC free article] [PubMed] [Google Scholar]

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