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The effect of stress on eating behaviours

The effect of stress on eating behaviours

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An essay for the 2011 Undergraduate Awards (Ireland) Competition by Lisa Graham. Originally submitted for BSc Psychology at Queen University Belfast, with lecturer Dr Katherine Appleton in the category of Medical Sciences
An essay for the 2011 Undergraduate Awards (Ireland) Competition by Lisa Graham. Originally submitted for BSc Psychology at Queen University Belfast, with lecturer Dr Katherine Appleton in the category of Medical Sciences

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Published by: Undergraduate Awards on Aug 31, 2012
Copyright:Attribution Non-commercial


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How does stress affect eating? What are the reasons forthis?
 The German colloquialism ‘Kummerspeck’ meaning ‘fat of sorrow’ illustrates a widespread awareness of eating serving asa kind of self-help or behavioural coping function (1). Emotionscan be defined in terms of valence and arousal, where researchhas shown emotions of a negative valence such as sadness toincrease impulsive eating, eating to regulate the emotionalstate and consumption of junk food (2). High-arousal statessuch as fear and anger have been shown to decrease foodintake (3). The literature on stress, a negative valence-higharousal emotion, is less straightforward. Stress as an emotionhas proven illusive to definition, although in the literature andfor the purpose of the current paper it is accepted as ‘anaversive state in which the wellbeing of the organism is in jeopardy and demands outstrip, or threaten to outstrip,resources to cope’ (4). Stress has been shown to affectappetite, food intake, food choice and eating speed withdifferential effects in terms of individual weight and dietingstatus. The current paper will examine how stress affectsindividualised eating behaviours and the physiological andpsychological explanations behind this. The general effect model when applied to food intake wouldpredict stress as increasing eating in all exposed animals. Theexperimental paradigm for this model focuses on animalstudies using a tail pinch or electric shock, and significanteffects have been found across several species (5; 6;7).However, few human studies have been used and have showninconsistent results (8; 9). It has been proposed that thedietary response to stress might be a stable individualdifference, in that some people are consistently hyperphagicand others consistently hypophagic (10). This is a prediction of individual difference models which don’t limit themselves tophysiological explanations, but instead focus on learninghistory, attitudes and biology as determining the effects of stress on eating. The individual difference models proposethree main ways of identifying individuals predisposed tostress-induced eating which will be elaborated on in turn;normal weight individuals will decrease their eating whilestressed, whereas eating by obese individuals is unaffected bystress (11), restrained eaters will increase their eating whilestressed while unrestrained eaters are unaffected by stress(12) and women are more likely to eat under stress than men(13).
Intuitively it has been proposed that stress from physical threatwill suppress hunger sensations in normal weight individuals,as a result of the ‘flight or fight’ response and its effect on theautonomic nervous system (14). Experimental manipulationssupport this (15; 16; 17), although the type of stress involvedneeds to be taken into account just as individual modelsrecognise the population as a whole will not be uniformlyaffected by stress. Ego-threat is suggested to be mediateddirectly by levels of self-esteem, where only restrained eaterslow in self esteem have been found to have disinhibited eatingbehaviours (18). Normal weight individuals would be expectedto be more susceptible to physical fear manipulations, andindeed studies have shown physical fear suppresses appetite innormal weight individuals without having an effect on obese orrestrained eaters (12; 15; 11). Conversely experimentalmanipulations of ego-threat do not affect the intake of normalweight individuals but significantly increase the intake of obeseeaters (16; 19; 20; 17; 21, 22; 23, 24), although stress-inducedeating in obese individuals is thought to be contingent on theirstatus as a dieter (25) where they otherwise show no effect.Chronic dieting is increasingly thought to represent the sameconstruct as restraint eating (26). Stress is expected to affectrestrained eaters because it will disrupt the control that theynormally try to exert over their eating (26). Several studieshave shown a bilateral effect for restrained versus unrestrainedeaters, with restrained eaters increasing their food intake (12;27; 18). Two studies used restraint as a continuous variable toshow interaction between levels of restraint and stress-inducedeating, where food intake increased along with restraint levels(17; 28). These consistent findings are hindered in so far asthey have focused entirely on women as a result of theinteraction between restraint eating, bulimia nervosa andgender (29). The importance of including gender as a variable in emotionaleating research has been focused upon in the paradigm of individual difference models.Literature has shown unstressed men to consume twice theamount of food as stressed men or either condition of women(13), although levels of restraint have not been taken intoconsideration using a male sample. In general thepredisposition for women to be emotional eaters is tentative atbest in the literature in regards to overall intake of food (30;31; 32), which would be expected given that women are hardto classify as a homogenous group in terms of restraint levels.Research has however shown greater preference than men for
high-fat, sweet foods (13) and males, similar to older people(33), have been shown to prefer more meal-related comfortfoods (pizza, pasta, steak) in comparison with females’ snack-related comfort foods (chocolate, ice-cream) (33), which mayshow an effect of stress-induced eating with an interactionbetween what individuals find familiar, palatable and anxietyalleviating.Early theories of stress-induced eating, such as thepsychosomatic account, focus on stress-induced eating aspurposive. Psychosomatic theory suggests obese individualsare unable to distinguish between internal hunger cues andfeelings of anxiety as they have learned to associate them atan early age (34), and responding to these internal cues witheating behaviour is comforting. Similar to this comforthypothesis, another explanation suggests that eating serves asa distraction from anxiety (12). An elaborative explanation,masking theory (25), believes individuals to put themselves ina position to misattribute distress to the overeating itself ratherthan the actual threat. These purposive theories of stress-induced eating behaviour have been criticised in that theyimply that normal weight participants are unable to gainenough comfort or distraction to offset the activation of theautonomic response, and rather have inferred suppressedeating by normal weight individuals is a result of being moreaffected by physiological cues, that is appetite-suppressingcatecholamines realised during emotional agitation (35).Chronic stress can lead to higher levels of neuroendocrinemediators such as cortisol (36). The effect of cortisol of eatingbehaviours is largely unknown, although some believe it toaffect motivation to eat rather than food intake directly,perhaps by modulating stress factors such as neuropeptide(37) which can increase appetite (38). In animals prone toobesity, glucocorticoids lead to hyperphagia and weight gainand are necessary for the expression of their obesity (39).Similarly, cortisol reactivity is high in a subgroup of normalweight individuals, although results show these individuals tobe restrained females (36). Cortisol may work as a marker forthose susceptible to stress-induced eating and the long-termseffects of chronic stress on weight gain. In relation to normalweight individuals, an explanation of cortisol effects suggestseating to be suppressed during stress due to anorectic effectsof CRH, and increased during recovery from stress due toappetite stimulating effects of residual cortisol (40) which mayaffect weight gain in the long-term. In keeping this in mind, it isimportant to realise that recognition of an underlying

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