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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
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How does stress affect eating? What are the reasons for this?

The German colloquialism ‘Kummerspeck’ meaning ‘fat of sorrow’ illustrates a widespread awareness of eating serving as a kind of self-help or behavioural coping function (1). Emotions can be defined in terms of valence and arousal, where research has shown emotions of a negative valence such as sadness to increase impulsive eating, eating to regulate the emotional state and consumption of junk food (2). High-arousal states such as fear and anger have been shown to decrease food intake (3). The literature on stress, a negative valence-high arousal emotion, is less straightforward. Stress as an emotion has proven illusive to definition, although in the literature and for the purpose of the current paper it is accepted as ‘an aversive 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 affect appetite, food intake, food choice and eating speed with differential effects in terms of individual weight and dieting status. The current paper will examine how stress affects individualised eating behaviours and the physiological and psychological explanations behind this. The general effect model when applied to food intake would predict stress as increasing eating in all exposed animals. The experimental paradigm for this model focuses on animal studies using a tail pinch or electric shock, and significant effects have been found across several species (5; 6;7). However, few human studies have been used and have shown inconsistent results (8; 9). It has been proposed that the dietary response to stress might be a stable individual difference, in that some people are consistently hyperphagic and others consistently hypophagic (10). This is a prediction of individual difference models which don’t limit themselves to physiological explanations, but instead focus on learning history, attitudes and biology as determining the effects of stress on eating. The individual difference models propose three main ways of identifying individuals predisposed to stress-induced eating which will be elaborated on in turn; normal weight individuals will decrease their eating while stressed, whereas eating by obese individuals is unaffected by stress (11), restrained eaters will increase their eating while stressed 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 threat will suppress hunger sensations in normal weight individuals, as a result of the ‘flight or fight’ response and its effect on the autonomic nervous system (14). Experimental manipulations support this (15; 16; 17), although the type of stress involved needs to be taken into account just as individual models recognise the population as a whole will not be uniformly affected by stress. Ego-threat is suggested to be mediated directly by levels of self-esteem, where only restrained eaters low in self esteem have been found to have disinhibited eating behaviours (18). Normal weight individuals would be expected to be more susceptible to physical fear manipulations, and indeed studies have shown physical fear suppresses appetite in normal weight individuals without having an effect on obese or restrained eaters (12; 15; 11). Conversely experimental manipulations of ego-threat do not affect the intake of normal weight individuals but significantly increase the intake of obese eaters (16; 19; 20; 17; 21, 22; 23, 24), although stress-induced eating in obese individuals is thought to be contingent on their status as a dieter (25) where they otherwise show no effect. Chronic dieting is increasingly thought to represent the same construct as restraint eating (26). Stress is expected to affect restrained eaters because it will disrupt the control that they normally try to exert over their eating (26). Several studies have shown a bilateral effect for restrained versus unrestrained eaters, with restrained eaters increasing their food intake (12; 27; 18). Two studies used restraint as a continuous variable to show interaction between levels of restraint and stress-induced eating, where food intake increased along with restraint levels (17; 28). These consistent findings are hindered in so far as they have focused entirely on women as a result of the interaction between restraint eating, bulimia nervosa and gender (29). The importance of including gender as a variable in emotional eating research has been focused upon in the paradigm of individual difference models. Literature has shown unstressed men to consume twice the amount of food as stressed men or either condition of women (13), although levels of restraint have not been taken into consideration using a male sample. In general the predisposition for women to be emotional eaters is tentative at best in the literature in regards to overall intake of food (30; 31; 32), which would be expected given that women are hard to 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 comfort foods (pizza, pasta, steak) in comparison with females’ snackrelated comfort foods (chocolate, ice-cream) (33), which may show an effect of stress-induced eating with an interaction between what individuals find familiar, palatable and anxiety alleviating. Early theories of stress-induced eating, such as the psychosomatic account, focus on stress-induced eating as purposive. Psychosomatic theory suggests obese individuals are unable to distinguish between internal hunger cues and feelings of anxiety as they have learned to associate them at an early age (34), and responding to these internal cues with eating behaviour is comforting. Similar to this comfort hypothesis, another explanation suggests that eating serves as a distraction from anxiety (12). An elaborative explanation, masking theory (25), believes individuals to put themselves in a position to misattribute distress to the overeating itself rather than the actual threat. These purposive theories of stressinduced eating behaviour have been criticised in that they imply that normal weight participants are unable to gain enough comfort or distraction to offset the activation of the autonomic response, and rather have inferred suppressed eating by normal weight individuals is a result of being more affected by physiological cues, that is appetite-suppressing catecholamines realised during emotional agitation (35). Chronic stress can lead to higher levels of neuroendocrine mediators such as cortisol (36). The effect of cortisol of eating behaviours is largely unknown, although some believe it to affect 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 to obesity, glucocorticoids lead to hyperphagia and weight gain and are necessary for the expression of their obesity (39). Similarly, cortisol reactivity is high in a subgroup of normal weight individuals, although results show these individuals to be restrained females (36). Cortisol may work as a marker for those susceptible to stress-induced eating and the long-terms effects of chronic stress on weight gain. In relation to normal weight individuals, an explanation of cortisol effects suggests eating to be suppressed during stress due to anorectic effects of CRH, and increased during recovery from stress due to appetite stimulating effects of residual cortisol (40) which may affect weight gain in the long-term. In keeping this in mind, it is important to realise that recognition of an underlying

physiological hypothesis does not mean normal weight individuals cannot be affected beyond a noticeable threshold by functional or purposeful mechanisms. Purpositive theories refer to the temporary anxiolytic effects of stress-induced eating, whereas more functional theories will study longer-term eating behaviours. An example of a functional theory of stress-induced eating is the ‘internalexternal’ hypothesis (11) which suggests that a labelling of a set of physiological hunger cues is a learned phenomenon that obese individuals have missed out on, meaning they do not eat in response to internal hunger cues as normal individuals would but rather rely on external cues. Slochower (22) has attempted to reconcile the externality formulation with the psychosomatic hypothesis, and suggests that stress-induced eating in obese and restrained individuals results in a shift in responsiveness to external cues, predominantly sensory-level food cues (35). Heatherton and Baumeister (41) support this theory with their study on ego-threat, where they posit a stressed individual will shift higher-level thinking about one’s self towards lower-level thinking to the immerse themselves in the external cues of the immediate situation, in line with the distraction (12) and masking (25) hypotheses. The studies on external cues would suggest that manipulating the palatability of a salient food would lead to heightened intake in restrained eaters, although research has shown that this is not the case and even foods of low-palatability were consumed significantly more in the stressed than the unstressed condition (42). In support of this functional hypothesis, researchers have called for taste to be disregarded as an external cue (43), and indeed reports have shown that bulimics eat unpalatable foods when binges are triggered by distress (44). However, support for purpositive hypotheses cannot be discounted where stimulus binding effects such as the taste of the cookies in the Polivy et al (42) study resulted in higher happiness ratings as the participants were consuming them, even if distress was not alleviated. This is directly related to palatability and perhaps the comfort hypothesis (34). Several naturalistic studies of stress effects have observed intake of fat and carbohydrate tends to be specifically increased in both genders (45; 46; 47; 48), and particularly in restrained eaters where normal intake of high-fat foods may be significantly inhibited (49). This would give evidence for hedonic mechanisms explaining stress-induced eating through immediate affective reactions elicited by palatable foods (50), a more plausible explanation when compared to that of the

postprandial improvements in mood (51), such as the serotonin hypothesis (52). The ecological validity of the serotonin hypothesis has been questioned in that the small proportions of protein contained in most meals may deteriorate the increase of tryptophan levels at the blood-brain barrier and the subsequent increase in serotonin (53). Another physiological mechanism is the reduction in activity of the hypothalamo-pituitary-adrenal axis which dampens stress responses as a result of high fat or carbohydrate intake (54). The postingestive effects that occur with both these physiological responses involve too long a delay to explain stress-induced eating, although there is inconclusive evidence where palatability could serve as an indicator for energy-dense foods for during stress when energy requirements are high and eating is a low priority (26). Evidence for this may come in some degree from animal studies showing increased eating speed in a stressful environment (55; 56) where the opportunity to eat is capitalised on. Regardless, these results lead to the proposal that stress might modify responsiveness to more palatable foods meaning total food intake is an indirect resultant of stress (Drewnowski, 1992). In conclusion, evidence on stress as an effective mediator of eating behaviours is of crucial importance to the escalating obesity pandemic and the increase in eating disorders. The population can be affected as a whole, with normal weight, unrestrained individuals suppressing their appetite in response to stress as restrained eaters increase intake, in particular of high-fat/high-carbohydrate foods. Immediate affective processes in response to palatability have shown most evidence for motivating this stress-induced behaviour, where the research paradigm appears to be moving away from purely physiological explanations towards more integrated theories involving purposeful action. Interestingly, it is thought that a subgroup of 30% of the global population compose the hypophagic population, where the remainder are somewhere on the spectrum of restrained eaters (Stone & Brownell, 1994); reasonable when real life data show a high prevalence of obesity compared to eating disorders. References (1) Macht, M., & Simons, G. (2000). Emotions and eating in everyday life. Appetite, 35, 65-71 (2) Ekman, P. (1992). An argument for basic emotions.

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