Relationship Between Stress, Eating and Obesity PDF

Nutrition 23 (2007) 887– 894 www.elsevier.com/locate/nut Review Relationship between stress,...

Nutrition 23 (2007) 887– 894 www.elsevier.com/locate/nut Review Relationship between stress, eating behavior, and obesity Susan J. Torres, M.Nutr.Diet.*, and Caryl A. Nowson, Ph.D. Centre for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, Burwood, Victoria, Australia Manuscript received March 3, 2007; accepted August 13, 2007. Abstract Stress is thought to influence human eating behavior and has been examined in animal and human studies. Our understanding of the stress-eating relation is confounded by limitations inherent in the study designs; however, we can make some tentative conclusions that support the notion that stress can influence eating patterns in humans. Stress appears to alter overall food intake in two ways, resulting in under- or overeating, which may be influenced by stressor severity. Chronic life stress seems to be associated with a greater preference for energy- and nutrient-dense foods, namely those that are high in sugar and fat. Evidence from longitudinal studies suggests that chronic life stress may be causally linked to weight gain, with a greater effect seen in men. Stress-induced eating may be one factor contributing to the development of obesity. Future studies that measure biological markers of stress will assist our understanding of the physiologic mechanism underlying the stress-eating relation and how stress might be linked to neurotransmitters and hormones that control appetite. © 2007 Elsevier Inc. All rights reserved. Keywords: Stress; Eating behavior; Sucrose; Fat; Rat; Weight gain; Obesity Introduction to seek out and consume energy-dense foods [9,10]. Obesity is a global epidemic and is increasing at an alarming rate, A complex array of internal and external factors influ- and can be attributed to a myriad of genetic and environ- ences appetite and consequently the amount and types of mental factors. If stress causes some individuals to food consumed by humans. Internal factors include physi- consume food in excess of requirements, then this may ologic mechanisms that regulate appetite, with hormones culminate in weight gain and obesity. such as neuropeptide-Y stimulating food intake and Our aim is to review the evidence from animal and human leptin reducing food intake. Many external factors can studies on the effect of acute and chronic stress on eating also influence food intake and include environmental factors behavior, and how stress-induced eating may contribute to the (e.g., economic, food availability) , social factors (e.g., development of obesity. First, we describe how stress can alter influence of others) , and the palatability of foods. It total food intake. Second, we discuss how stress can promote is a commonly held belief that stress can alter eating pat- consumption of nutrient-dense foods, specifically a preference terns. When an acute stress is experienced, such as a for sweet foods, which has been the recent focus of our re- threat to personal safety, there is an instant physiologic search work. Third, we present evidence to support the hy- response, the “flight or fight” response , which results pothesis that stress-induced eating may result in future weight in the suppression of appetite. Exposure to chronic gain and ultimately obesity. Fourth, we discuss how the phys- psychological stressors, e.g., job pressures, is one of many iologic responses to stress may interact with processes in- mental health disorders that contribute to the global burden volved in appetite regulation. of disease. For many, the typical response to these chronic stressful situations is not to avoid food but may be Stress response * Corresponding author. Tel.: ⫹61-3-9244-6668; fax: ⫹61-3-9244- Stress can be defined as “the generalized, non-specific 6017. response of the body to any factor that overwhelms, or E-mail address: [email protected] (S. J. Torres). threatens to overwhelm, the body’s compensatory abilities 0899-9007/07/$ – see front matter © 2007 Elsevier Inc. All rights reserved. doi:10.1016/j.nut.2007.08.008 888 S. J. Torres and C. A. Nowson / Nutrition 23 (2007) 887– 894 Stress can alter food consumption: effect of stressor severity Greeno and Wing outlined the individual-difference model, which suggests there are two ways in which stress may influence eating, resulting in eating or not eating. These opposing responses may be explained by the severity of stress that is encountered. Animal studies Animal studies provide a convenient way to measure the effect of stress on food intake. Rats can be subjected to different stressors in a controlled laboratory setting with close monitoring of food intake. In addition, there is evi- Fig. 1. Physiologic response to stress. ACTH, adrenocorticotropic hor- dence that animal models can provide valuable information mone; CRH, corticotropin-releasing hormone. about the interplay between stress and psychological/ emotional processes that drive humans to eat [22,23]. The severity of the stressor seems to influence food to maintain homeostasis”. The following stressors can intake in the rat model. Immobilization, a severe stressor, induce a stress response: physical stressors (trauma, sur- consistently reduced ordinary food (rat chow) intake in rats gery, intense heat or cold); chemical stressors (reduced when administered chronically [24 –27] and even acutely oxygen supply, acid-base imbalance); physiologic stressors. Moderate stressors (restraint, noise stress) adminis- (heavy exercise, hemorrhagic shock, pain); psychological or tered chronically have also been reported to reduce ordinary emotional stressors (anxiety, fear, sorrow); and social stres- food intake [26,28 –30]. This stress-induced inhibition of sors (personal conflicts, change in lifestyle). Stressors feeding behavior may have a physiological basis. As can be short term (acute stress) or occur on a daily basis corticotropin-releasing factor levels increase in response (chronic stress). Reactions to stressors have been suggested to stress, food intake decreases. Furthermore, this was confirmed by a study in rats that found corticotropin- to be of several types , and those of most importance are releasing factor inhibited the hyperphagia induced by the “active fight-or-flight” pattern (sympathetic adrenal med- neuropeptide-Y. ullary system) and the “passive” pattern (pituitary-adrenal cor- A mild stressor (tail pinch) increased intake of sweetened tical system involving the hypothalamic-pituitary-adrenal condensed milk in two studies [33,34] but did not alter [HPA] axis; Fig. 1). Activation of the sympathetic adrenal intake of chow , and another mild stressor (handling) in medullary system, with release of catecholamines (adrena- rats had no effect on chow intake. Therefore, mild line and noradrenaline), is typical during periods of acute stressors appear to have no effect on food intake when the stress. Hyperactivation of the HPA axis, with release of foods available have limited hedonic characteristics but may corticosteroids (cortisol), has been associated with individ- increase food consumption when the foods offered are uals who are chronically stressed. Furthermore, it has highly palatable. This is supported by studies in rats that been proposed that a hyperactive HPA axis may be pro- have demonstrated that exposure to a cafeteria diet (highly grammed during the prenatal period as a result of fetal palatable, high-fat diet) causes a greater increase in calorie growth retardation. Responses to acute or chronic stress intake and body weight when compared with rats offered can lead to physiologic changes that include slowed gastric ordinary chow [36,37]. emptying , elevation of blood pressure, increase in heart rate, mobilization of energy stores, and decrease in blood Human studies flow to non-essential organs, e.g., the digestive system, kidneys, and skin. Hormones released in response to Human studies have also found decreased and increased stress can specifically affect appetite. Noradrenaline eating in response to stress and this may also be related to and corticotropin-releasing hormone have been re- the severity of the stressor. A retrospective survey of United ported to suppress appetite during stress, whereas cortisol is States Marine’s food intake during combat provided an known to stimulate appetite during recovery from stress opportunity to examine the effect of a severely stressful. Anxiety, depression, uneasiness, anger, apathy, and situation on eating behavior. During the first day of alienation are emotions that commonly accompany chronic combat, 68% of marines reported eating less than usual. The stress. The responses to acute or chronic stress also main reason for eating less was lack of time, followed by include a number of modifying behaviors such as alcohol fear, which included being nervous, tense, and scared. In a consumption , smoking , and eating. prospective study, 158 male and female subjects completed  S. J. Torres and C. A. Nowson / Nutrition 23 (2007) 887– 894 889 84 daily records of stress. Subjects reported a decrease Animal studies and an increase in eating in response to stress; however, subjects were more likely to report eating less. Furthermore, Studies in rats, which have investigated the effect of the likelihood of eating less increased as the severity of the stress on absolute levels of sweet fluid/food intake, have stressor increased. The effects of self-reported stress on yielded mixed findings. Eleven published papers were ex- eating behavior were examined in 212 students. Ap- amined (reporting 14 separate studies) that used stressors of proximately equal numbers of subjects reported eating more varying duration and severity and a variety of sweet fluids (42%) and eating less (38%), but no information on the and foods (Table 1). Five studies reported an increase influence of stressor severity was reported. The effect of a [35,45– 47], three reported no change [45,48,49], and six major stressful event (school examination) on food con- reported a decrease in sweet fluid/food intake [50 –54]. An early study with rats provided convincing evidence sumption was investigated in 225 male and female high that stress may contribute to weight gain because chronic school students. Total energy intake was significantly tail pinch (mild stressor) in the presence of sweetened milk greater on the examination day when compared with the induced hyperphagia and led to weight gain. However, stress-free day (2225 versus 2074 kcal, 9.1 versus 8.5 MJ), when rats were subjected to chronic tail pinch and then respectively. In another study, the effect of a mild stressor given ordinary rat chow, the weight of stressed rats was less (stress-inducing film) on food consumption was assessed, than that of unstressed rats. This difference between and overall the male stress group consumed significantly these two studies may have been due to the type of foods less food compared with the male control group (99 versus offered to the rats: sweetened milk (very palatable) ver- 242 kcal, 406 versus 992 kJ), respectively. However, sus ordinary rat chow in the second study. The effect of there was no difference in food consumption between the acute restraint (moderate stressor) was investigated in female groups indicating that gender may influence eating rats prone to diet-induced obesity fed low-fat chow (low behavior after mild stress. energy) or medium-fat chow (high energy). Com- pared with unstressed controls, stressed rats fed low-fat chow gained less, whereas stressed rats fed high-fat chow Limitations and conclusions gained more. Therefore, in animal studies, severe stress appears to lead to decreased food intake and milder forms of stress have no Conclusions effect or lead to increased food intake. In humans, stress It is difficult to make strong conclusions about the effect appears to increase and decrease food intake, although it is of stress on absolute levels of sweet food/fluid intake in the difficult to determine if stressor severity has a role, because rat model. With regard to the effect of stress on subsequent there are few human studies. There are a number of limitations weight gain, this appears to be dependent on the nutrient inherent in these human studies and include the use of impre- composition of the available food, with greater weight gain cise methods to measure dietary intake [39,40]. Also, in the seen with high-energy diets. This has similarities to human laboratory study, prior eating was not controlled, which may studies such that individuals fed higher energy-density ad have influenced the amount of food consumed during the stress libitum diets increased their total energy intake. and control conditions. An alternative explanation for why energy intake is higher during periods of life stress may be Human studies: stress and nutrient density unrelated to the stress, but rather due to insufficient time to purchase and prepare foods and the increased use of conve- The effect of stress on the intake of fat and sugar has nience foods, which are typically energy dense. been investigated in humans. In a large cross-sectional study with 12 110 individuals, greater perceived stress was posi- tively associated with a higher-fat diet. Individuals in situations of greater perceived workload and perceived Stress, nutrient-dense foods, and weight gain stress reported increases in total energy and fat intake com- pared with periods of low workload and low perceived Obesity is a global epidemic that results from energy stress. The prevalence of obesity is greater in African imbalance, with energy intake exceeding energy expendi- Americans than in European Americans , and obesity ture over a long period. The causes of obesity are diverse has been positively associated with life stress in African- and complex and can be attributed to physiologic, environmen- American women. Furthermore, African Americans tal, and genetic factors. Specifically, weight gain and the appear to have a greater desire for intense sweet tastes and development of obesity have been attributed to lifestyle fac- greater perceived life stress compared with European Amer- tors, with the early work of Kaplan and Kaplan suggesting icans. This desire for intense sweet tastes may translate that one of the contributing factors to obesity may be due to into selection and consumption of energy- and nutrient- stress-induced eating, with a greater preference for nutrient- dense foods and may be a factor contributing to the greater dense foods, particularly those that are high in sugar and fat. prevalence of obesity in African Americans. 890 S. J. Torres and C. A. Nowson / Nutrition 23 (2007) 887– 894 Table 1 Intake of sweetened food/fluid in rats during stress Study Stressor Stressor Stressor Food/fluid No. No. Intake during stress Weight severity duration stressed unstressed versus unstressed condition Bertiere et al. Tail pinch Mild Acute Sweetened milk/ 12/12 12/12 Increased*/increased* sucrose solution Dess Tail shock Severe Acute Sucrose solution 11 11 Increased† Ely et al. Restraint Moderate Chronic Froot Loops 15 16 Increased Silvera et al. Restraint Moderate Chronic Froot Loops 9–12 9–12 Increased Ely et al. Restraint Moderate Acute Froot Loops 11 11 Unchanged Kant and Bauman Foot shock Moderate Chronic Sucrose pellets 12 12 Unchanged Matthews et al. Range Mild Chronic Sucrose solution 16 16 Unchanged Correction for body weight changes Baker et al. Range Mild Chronic Sucrose solution 9 10 Decreased No reported change in body weight between groups Gronli et al. Range Mild Chronic Sucrose solution 20 20 Decreased No reported change in body weight between groups Papp et al. Range Mild Chronic Sucrose solution 8 8 Decreased No body weights recorded Wang Restraint Moderate Acute Mixed carbohydrate 60‡ Decreased diet Wang Restraint Moderate Chronic Mixed carbohydrate 60‡ Decreased No body weights diet recorded Willner et al. Range Mild Chronic Sucrose solution 10 10 Decreased No body weights recorded * Own control. † Intake measured after conclusion of stress. ‡ Total number. There have been few studies in humans that have published in this area, there is some evidence that chronic tested the effect of stress, induced in a laboratory setting, life stress is associated with a high-fat diet and a greater on the selection of foods. Men and women subjected to an preference for sweet foods. However, there are limitations acute stressor (preparation of a speech) consumed similar in the studies examined including the use of a less than amounts of high- and low-fat sweet foods after stress com- optimal method to measure stress levels and small pared with a control group. In a study with 59 pre- samples. Furthermore, we may not see an effect on a menopausal women, 45 min of stress (visuospatial puzzles, preference for nutrient-dense foods in laboratory studies serial subtraction of a prime number from a high number, because the stress induced in this artificial environment may and delivery of a videotaped speech) did not alter consumption not be sufficiently stressful to alter eating behavior. of a range of foods, including high- and low-fat sweet foods, compared with the non-stressed condition. They found Human studies: stress and weight gain that high cortisol reactors (defined as the increase from base- line to stress levels of salivary cortisol) consumed significantly In a large cross-sectional study in Finnish public sector more calories (220 versus 140 kcal, 902 versus 574 kJ) and workers, which included 37 161 women and 8649 men, more high-fat sweet foods on the stress day compared with low there was a weak association between work stress and body reactors, but consumed similar amounts on the control day. mass index (BMI; range 23–27 kg/m2). Stress-related There is evidence to suggest cortisol, a marker of HPA axis eating (defined as trying to make oneself feel better by activity, may affect the regulation of appetite via neuropeptide- eating or drinking in a stressful situation) was significantly Y and leptin. Increases in cortisol seem to be followed by associated with obesity, but only in women and not in men elevated secretion of neuropeptide-Y and blunting of the in-. There may be a gender-specific response to stress in hibitory arm of food intake, the leptin system. The overall which women are more likely to use food to deal with stress, effect may be an increase in food intake. whereas men are more likely to use other oral behaviors such as alcohol consumption or smoking as strat- Limitations and conclusions egies to cope with stress. When individuals respond to stress by eating more, an- If stress-induced eating is contributing to the develop- ecdotal evidence suggests the foods selected are typically ment of obesity, then it would be expected that obese indi- high in sugar and fat. Although there are few human studies viduals would consume more food in response to stress  S. J. Torres and C. A. Nowson / Nutrition 23 (2007) 887– 894 891 compared with lean individuals. The results from five stud- No correction for ies are summarized in Table 2. Two studies measured the body weight effect of life stress [65,66] and the remaining three studies Weight induced stress in a laboratory setting [67– 69]. Two of these studies reported an increase in food consumption in obese individuals [65,67]; however, only one of these corrected control condition for body weight. It would be expected that obese individ- pleasant days consumed on uals would consume larger amounts of food to maintain Intake versus Unchanged Unchanged Unchanged Unchanged Most food weight. Usual food consumption and perceived stress (pleas- Normal weight ant, neutral, or unpleasant) was recorded by normal-weight and overweight women over 4 mo. In overweight women, total food intake was not associated with the daily level of 14 80 32 42 37 stress, whereas normal-weight women ate the most on pleasant n days. Therefore, there is only one study that found food intake control condition increased with chronic stress in obese individuals. No association Intake versus In a longitudinal case-control study , children who Unchanged Decreased Increased Increased had shown an increment in relative weight of 15% between the ages of 7 and 10 y were selected and matched with a control group with the same relative weight at age 7 y. The Obese researchers found a significant relation between level of 23 80 32 41 37 n psychosocial stress and increased relative weight over this 3-y period. The “fetal origins hypothesis” argues that pre- During stress During stress During stress After stress natal growth retardation is associated with adult cardiovas- Timing of cular and metabolic disorders [71,72]. There is a growing eating 120 d body of evidence from animal and human studies that sug- gests prenatal growth retardation may program a persis- tently hyperactive HPA axis in the fetus that continues into Self-reported food intake childhood and even the adult years , and this may influence eating behavior. Furthermore, this programming may be gender specific, with prenatal growth retardation M&M candy influencing adrenocortical responses to stress in boys and Food/fluid Chocolate Ice cream Peanuts basal adrenocortical activity in girls. Cortisol secretion, a marker of HPA axis activity, is also known to be elevated in obese individuals. Three studies in adults have in- vestigated the effect of stress on future weight gain. Ele- duration Stressor Chronic Chronic Acute Acute Acute vated levels of stress at baseline predicted a weight gain of 10 kg over a period of 6 y in men but not in women. The Whitehall II study, a large prospective study in men and (pleasant, neutral, unpleasant) women, found that work stress increased the likelihood of Intelligence test, performance linked to threat of shock Stress-induced eating in obese versus normal weight subjects weight gain over 5 y in those with a higher BMI, but was Impressing strange man Threat of electric shock Self-reported life stress likely to predict weight loss in lean individuals, and this observed bidirectional effect of work stress and BMI was Life stress (college seen only in men and not in women. The effect of examination) stressful life events over a 6-mo period on change in BMI was studied in men and women who were classified as high Stressor (respond to stress by eating more) or low (respond to stress by eating less) emotional eaters. Only male, high emo- tional eaters who reported more than three stressful life Rosenfeld and Stevenson events had an increase in weight within 6 mo. These three studies collectively suggest that higher levels of stress in- Reznick and Balch Slochower et al. crease the likelihood of weight gain, with a greater effect seen in men than in women. Recently, “night eating syn- Ruderman drome,” which is characterized by morning anorexia and night-time hyperphagia , has been associated with dis- Pine Table 2 turbances in the HPA axis and positively associated Study with BMI. 892 S. J. Torres and C. A. Nowson / Nutrition 23 (2007) 887– 894 Obesity is associated with comorbidities such as coro- nary heart disease, type 2 diabetes, hypertension, and dys- lipidemia, and the additional presence of abdominal obesity (central location of body fat) confers an even greater risk for coronary heart disease and type 2 diabetes. Stress reactions have been linked with the development of abdom- inal obesity. It has been proposed that repeated activation of the HPA axis by stress, with the elevation of cortisol that follows, leads to activation of adipose tissue lipoprotein lipase and then accumulation of abdominal fat mass. Stress-induced cortisol secretion has been found to be greater among men and women with abdominal obesity, but is it not clear if the obesity is responsible for the higher levels of cortisol with stress or if the higher level of cortisol is driving the obesity. Limitations and conclusions We can conclude from cross-sectional studies that stress Fig. 2. Predominant response pathways to acute and chronic stresses. is positively associated with body weight, although these findings need to be interpreted cautiously because it is based behavior in a laboratory setting, which allows close moni- on self-reported weight and height, which can cause bias toring of food intake. Laboratory studies are limited to the. In humans subjected to laboratory or life stress, only testing of acute stressors, rather than chronic stressors, the one study of five reported, which measured the effect of life latter possibly having a greater effect on eating behavior. stress, actually demonstrated a significant increase in food Longitudinal studies can investigate the effect of chronic consumption in obese individuals. We may not see an effect life stress on eating behavior; however, accurate dietary data in laboratory studies that induce acute stress because indi- can be difficult to collect over long periods. viduals may not be sufficiently stressed in this artificial Despite the limitations discussed, we can make some environment when compared with stress that is experienced broad conclusions that support the idea that stress can in- in the real world. Furthermore, laboratory studies can only fluence food intake. The studies examined revealed that measure the effect of acute stress rather than chronic stress, stress can lead to decreased and increased eating, which which may have a greater effect on eating behavior. We can may be related to stressor severity, such that in animals a also conclude from longitudinal studies that there appears to severe stress results in a lower intake and in humans the be an association between chronic life stress and future response is variable. There is some evidence to suggest that weight gain, with a greater effect seen in men compared elevated stress levels are associated with a greater desire for with women, although the reason for this difference is not hedonic, highly palatable foods that are energy dense. This clear. When examining the relation between life stress and may contribute to excess energy intakes and weight gain, future weight gain, it is important to consider both sides of which is supported by longitudinal studies that suggest there the energy balance equation: energy intake and energy ex- is an association between chronic life stress and future penditure. In all the studies cited, energy intake or energy weight gain. expenditure was not measured, so it is not known if the Stress appears to have an effect on eating behavior in weight gain reported was due to increased energy intake or humans, and the responses that predominate during acute decreased physical activity levels. With regard to the rela- and chronic stress are summarized in Figure 2. Responses to tion between stress and physical activity levels, two studies acute stress are associated with physiologic changes that reported no association [84,85], and one study demonstrated might be expected to reduce food intake in the short term, that physical activity levels decreased from baseline to a e.g., slowed gastric emptying and shunting of blood from stress period. It may be the case that chronic life stress the gastrointestinal tract to muscles. In other situations is contributing to this observed weight gain, and data on chronic stress elicits a more passive response driven by the dietary intake and physical activity levels need to be col- HPA axis, with increases in cortisol that may entice people lected to determine which is the major factor. to consume hedonic, energy-dense foods and potentially lead to unwanted weight gain and obesity. Cortisol may also contribute to the accumulation of abdominal fat mass. It is Conclusions important to clarify the underlying physiologic mechanism whereby stress leads to overconsumption of food. Most of Our understanding of the stress-eating relation is con- the studies examined in this review have quantified stress founded by limitations inherent in the study designs. Many using only subjective measurements. Some physiologic studies have measured the effect of acute stress on eating measurement of stress could be incorporated into future  S. J. Torres and C. A. Nowson / Nutrition 23 (2007) 887– 894 893 studies to measure levels of cortisol and catecholamines. model of stress induced binge eating. Int J Eat Disord 2003;34: Animal studies could identify any links between stress hor- 183–97. Michajlovskij N, Lichardus R, Kvetnansky JP. Effect of acute and mones and neurotransmitters involved in appetite regula- repeated immobilization stress on food and water intake, urine output tion, which would assist in our understanding of the mech- and vasopressin changes in rats. Endocrinol Exp 1988;22:143–57. anism and possibly lead to preventative treatments. Monteiro F, Abraham ME, Sahakari SD, Mascarenhas JF. Effect of immobilization stress on food intake, body weight and weights of various organs in rats. Ind J Physiol Pharmac 1989;33:186 –90. Marti O, Marti J, Armario A. Effects of chronic stress on food intake References in rats: influence of stressor intensity and duration of daily exposure. Physiol Behav 1994;55:747–53. Levine AS, Billington CJ. Why do we eat? A neural systems ap- Valles A, Marti O, Garcia A, Armario A. Single exposure to stressors proach. Annu Rev Nutr 1997;17:597– 619. causes long-lasting, stress-dependent reduction of food intake in rats. Blundell JE, Goodson S, Halford JCG. Regulation of appetite: role of Am J Physiol Regul Integr Comp Physiol 2000;279:R1138 – 44. leptin in signalling systems for drive and satiety. Int J Obes 2001;25: Alario P, Gamallo A, Beato MJ, Trancho G. Body weight gain, food S29 –34. intake and adrenal development in chronic noise stressed rats. Physiol Popkin BM, Duffey K, Gordon-Larsen P. Environmental influences Behav 1987;40:29 –32. on food choice, physical activity and energy balance. Physiol Behav Krebs H, Macht M, Weyers P, Weijers H-G, Janke W. Effects of 2005;86:603–13. stressful noise on eating and non-eating behavior in rats. Appetite Pliner P, Mann N. Influence of social norms and palatability on 1996;26:193–202. amount consumed and food choice. Appetite 2004;42:227–37. Harris RBS, Zhou J, Youngblood BD, Rybkin II, Smagin GN, Ryan Wardle J, Gibson EL. Impact of stress on diet: process and implica- DH. Effect of repeated stress on body weight and body composition tions. In: Stansfield S, Marmot M, editors. Stress and the heart. of rats fed low- and high-fat diets. Am J Physiol Regul Integr Comp Psychosocial pathways to coronary heart disease. London: BMJ Pub- Physiol 1998;44:R1928 –38. lishing Group; 2002:124 – 49. Arborelius L, Owens MJ, Plotsky PM, Nemeroff CB. The role of Sherwood L. Human physiology from cells to systems. 4th ed. Cal- corticotropin-releasing factor in depression and anxiety disorders. ifornia: Brooks/Cole; 2001. J Endocrinol 1999;160:1–12. Charmandari E, Tsigos C, Chrousos G. Endocrinology of the stress Heinrichs SC, Cole BJ, Merlo Pich E, Menzaghi F, Koob GF, Hauger response. Annu Rev Physiol 2005;67:259 – 84. RL. Endogenous corticotropin-releasing factor modulates feeding in- World Health Organisation. The world health report: 2001: mental duced by neuropeptide Y or a tail-pinch stressor. Peptides 1992;13: health: new understanding, new hope. Geneva, Switzerland: World 879 – 84. Health Organisation; 2001. Rowland NE, Antelman SM. Stress-induced hyperphagia and obesity Schiffman SS, Graham BG, Sattely-Miller EA, Peterson-Dancy M. in rats: a possible model for understanding human obesity. Science Elevated and sustained desire for sweet taste in African-Americans: a 1976;191:310 –2. potential factor in the development of obesity. Nutrition 2000;16: Wallach MB, Dawber M, McMahon M, Rogers C. A new anorexigen 886 –93. assay: stress-induced hyperphagia in rats. Pharmacol Biochem Behav Oliver G, Wardle J, Gibson L. Stress and food choice: a laboratory 1977;6:529 –31. study. Psychosom Med 2000;62:853– 65. Bertiere MC, Mame Sy T, Baigts F, Mandenoff A, Apfelbaum M. World Health Organisation. Obesity: preventing and managing the Stress and sucrose hyperphagia: role of endogenous opiates. Pharma- global epidemic. Technical report series 894. Geneva, Switzerland: col Biochem Behav 1984;20:675–9. World Health Organisation; 2000. Rozen R, Brigant L, Apfelbaum M. Effects of cycles of food restric- Folkow B. Physiological aspects of the “defence” and “defeat” reac- tion followed by ad libitum refeeding on body composition and tions. Acta Physiol Scand Suppl 1997;640:34 –7. energy expenditure in obese rats. Am J Clin Nutr 1994;59:560 –5. Cohen JI. Stress and mental health: a biobehavioral perspective. Hansen MJ, Schioth HB, Morris MJ. Feeding responses to a mela- Issues Ment Health Nurs 2000;21:185–202. nocortin agonist and antagonist in obesity induced by a palatable Bjorntorp P, Holm G, Rosmond R, Folkow B. Hypertension and the high-fat diet. Brain Res 2005;1039:137– 45. metabolic syndrome: closely related central origin? Blood Press Popper R, Smits G, Meiselman HL, Hirsch E. Eating in combat: a 2000;9:71– 82. survey of U.S. Marines. Mil Med 1989;154:619 –23. Welberg LAM, Seckl JR. Prenatal stress, glucocorticoids and the Stone AA, Brownell K. The stress-eating paradox: multiple daily programming of the brain. J Neuroendocrinol 2001;13:113–28. measurements in adult males and females. Psychol Health 1994;9: Bhatia V, Tandon RK. Stress and the gastrointestinal tract. J Gastro- 425–36. enterol Hepatol 2005;20:332–9. Oliver G, Wardle J. Perceived effects of stress on food choice. Halford JC. Pharmacology of appetite suppression: implication for Physiol Behav 1999;66:511–5. the treatment of obesity. Curr Drug Targets 2001;2:353–70. Michaud C, Kahn JP, Musse N, Burlet C, Nicolas JP, Mejean L. Takeda E, Terao J, Nakaya Y, Miyamoto K, Baba Y, Chuman H, et Relationships between a critical life event and eating behaviour in al. Stress control and human nutrition. J Med Invest 2004;51:139 – 45. high-school students. Stress Med 1990;6:57– 64. Mehlum L. Alcohol and stress in Norwegian United Nations peace- Grunberg NE, Straub RO. The role of gender and taste class in the keepers. Mil Med 1999;164:720 – 4. effects of stress on eating. Health Psychol 1992;11:97–100. Conway TL, Vickers RR, Ward HW, Rahe RH. Occupational stress Prentice AM, Jebb SA. Fast foods, energy density and obesity: a and variation in cigarette, coffee, alcohol consumption. J Health Soc possible mechanistic link. Obes Rev 2003;4:187–94. Behav 1981;22:155– 65. Kaplan HI, Kaplan HS. The psychosomatic concept of obesity. J Nerv Greeno CG, Wing RR. Stress-induced eating. Psychol Bull 1994;115: Ment Dis 1957;125:181–201. 444 – 64. Ely DR, Dapper V, Marasca J, Correa JB, Gamaro GD, Xavier MH, Geary N. A new model of binge eating. Int J Eat Disord 2003;34: et al. Effect of restraint stress on feeding behavior of rats. Physiol 198 –9. Behav 1997;61:395– 8. Hagan MM, Chandler PC, Wauford PK, Rybak RJ, Oswald KD. The Silvera PP, Xavier MH, Souza FH, Manoli LP, Rosat RM, Ferreira role of palatable food and hunger as trigger factors in an animal MB, et al. Interaction between repeated restraint stress and concom- 894 S. J. Torres and C. A. Nowson / Nutrition 23 (2007) 887– 894 itant midazolam administration on sweet food ingestion in rats. Braz Pine C. Anxiety and eating behavior in obese and nonobese American J Med Biol Res 2000;33:1343–50. Indians and White Americans. J Pers Soc Psychol 1985;49:774 – 80. Dess NK. Divergent responses to saccharin vs. sucrose availability Reznick H, Balch P. The effects of anxiety and response cost manip- after stress in rats. Physiol Behav 1992;52:115–25. ulations on the eating behavior of obese and normal-weight subjects. Matthews K, Forbes N, Reid IC. Sucrose consumption as an hedonic Addict Behav 1977;2:219 –25. measure following chronic unpredictable mild stress. Physiol Behav Ruderman AJ. Obesity, anxiety, and food consumption. Addict Behav 1995;57:241– 8. 1983;8:235– 42. Kant GJ, Bauman R. Effects of chronic stress and time of day on Mellbin T, Vuille JC. Rapidly developing overweight in school chil- preference for sucrose. Physiol Behav 1993;54:499 –502. dren as an indicator of psychosocial stress. Acta Paediatr Scand Wang SWJ. Effects of restraint stress and serotonin on macronutrient 1989;78:568 –75. selection: a rat model of stress-induced anorexia. Eat Weight Disord Barker DJ. Fetal origins of coronary heart disease. BMJ 1995;311: 2002;7:23–31. 171– 4. Baker SL, Zentner AC, Konkle ATM, Santa-Maria Barbagallo L, Barker DJ. The fetal origins of type 2 diabetes mellitus. Ann Intern Bielajew C. Behavioral and physiological effects of chronic mild Med 1999;130:322– 4. stress in female rats. Physiol Behav 2006;87:314 –22. Jones A, Godfrey KM, Wood P, Osmond C, Goulden P, Phillips DI. Gronli J, Murison R, Eldbjorg F, Bjorvatn B, Sorensen E, Portas CM, Fetal growth and the adrenocortical response to psychological stress. et al. Effects of chronic mild stress on sexual behavior, locomotor J Clin Endocrinol Metab 2006;91:1868 –71. activity and consumption of sucrose and saccharine solutions. Physiol Bjorntorp P, Rosmond R. Obesity and cortisol. Nutrition 2000;16: Behav 2005;2005:571–7. 924 –36. Papp M, Willner P, Muscat R. An animal model of anhedonia: Korkeila M, Kaprio J, Rissanen A, Koskenvuo M, Sorenson TIA. attenuation of sucrose consumption and place preference conditioning Predictors of major weight gain in adults Finns: stress, life satisfac- by chronic unpredictable mild stress. Psychopharmacology 1991;104: tion and personality traits. Int J Obes 1998;22:949 –57. 255–9. Kivimaki M, Head J, Ferrie JE, Shipley MJ, Brunner E, Vahtera J, Willner P, Towell A, Sampson D, Sophokleous S, Muscat R. Reduc- et al. Work stress, weight gain and weight loss: evidence for bidirec- tion of sucrose preference by chronic unpredictable mild stress, and tional effects of job strain on body mass index in the Whitehall II its restoration by a tricyclic antidepressant. Psychopharmacology study. Int J Obes (Lond) 2006;30:982–7. 1987;93:358 – 64. Van Strien T, Rookus MA, Bergers GPA, Frijters JER, Defares PB. Levine AS, Morley JE. Stress-induced eating in rats. Am J Physiol Life events, emotional eating and change in body mass index. Int J 1981;241:R72– 6. Obes 1986;10:29 –35. Michel C, Levin BE, Dunn-Meynell AA. Stress facilitates body Stunkard AJ, Grace WJ, Wolff HG. The night-eating syndrome; a weight gain in genetically predisposed rats on medium-fat diet. Am J pattern of food intake among certain obese patients. Am J Med Physiol Regul Integr Comp Physiol 2003;285:R791–9. 1955;19:78 – 86. Ng DM, Jeffery RW. Relationships between perceived stress and Birketvedt GS, Sundsfjord J, Florholmen JR. Hypothalamic-pituitary- health behaviors in a sample of working adults. Health Psychol adrenal axis in the night eating syndrome. Am J Physiol Endocrinol 2003;22:638 – 42. Metab 2002;282:E366 –9. McCann BS, Warnick GR, Knopp RH. Changes in plasma lipids and dietary intake accompanying shifts if perceived workload and stress. Colles SL, Dixon JB, O’Brien PE. Night eating syndrome and noc- Psychosom Med 1990;52:97–108. turnal snacking: association with obesity, binge eating and psycho- Folsom AR, Burke GL, Byers CL, Hutchison RG, Heiss G, Flack JM, logical distress. Int J Obes (Lond) 2007: doi:10.1038/sj.ijo.0803664. et al. Implications of obesity for cardiovascular disease in blacks: the Rippe JM, Crossley S, Ringer R. Obesity as a chronic disease: CARDIA and ARIC studies. Am J Clin Nutr 1991;53:1604S-11. modern medical and lifestyle management. J Am Diet Assoc 1998; Walcott-McQuigg JA. The relationship between stress and weight- 98:S9 –15. control behavior in African-American women. J Natl Med Assoc Rosmond R, Dallman MF, Bjorntorp P. Stress-related cortisol secre- 1995;87:427–32. tion in men: relationships with abdominal obesity and endocrine, Epel E, Lapidus R, McEwen B, Brownell K. Stress may add bite to metabolic and hemodynamic abnormalities. J Clin Endocrinol Metab appetite in women: a laboratory study of stress-induced cortisol and 1998;6:1853–9. eating behavior. Psychoneuroendocrinology 2001;26:37– 49. Epel ES, McEwen B, Seeman T, Matthews K, Castellazzo G, Bjorntorp P. Do stress reactions cause abdominal obesity and comor- Brownell KD, et al. Stress and body shape: stress-induced cortisol bidities? Obes Rev 2001;2:73– 86. secretion is consistently greater among women with central fat. Psy- Kouvonen A, Kivimaki M, Cox SJ, Cox T, Vahtera J. Relationship chosom Med 2000;62:623–32. between work stress and body mass index among 45,810 female and Anton SD, Miller PM. Do negative emotions predict alcohol con- male employees. Psychosom Med 2005;67:577– 83. sumption, saturated fat intake, and physical activity in older adults. Laitinen J, Ek E, Sovio U. Stress-related eating and drinking behavior Behav Modif 2005;29:677– 88. and body mass index and predictors of this behavior. Prev Med Jones DH, Harel Y, Levinson RM. Living arrangements, knowledge 2002;34:29 –39. of health risks, and stress as determinants of health-risk behavior Slochower J, Kaplan SP, Mann L. The effects of life stress and weight among college students. J Am Coll Nutr 1992;41:43– 8. on mood and eating. Appetite 1981;2:115–25. Steptoe A, Wardle J, Pollard TM, Canaan L, Davies GJ. Stress, social Rosenfield SN, Stevenson JS. Perception of daily stress and oral support and health-related behavior: a study of smoking, alcohol coping behaviors in normal, overweight, and recovering alcoholic consumption and physical exercise. J Psychosom Res 1996;41: women. Res Nurs Health 1988;11:165–74. 171– 80.