Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior

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Abstract

To date, there are few known predictors of stress-induced eating. The purpose of this study was to identify whether physiological and psychological variables are related to eating after stress. Specifically, we hypothesized that high cortisol reactivity in response to stress may lead to eating after stress, given the relations between cortisol with both psychological stress and mechanisms affecting hunger. To test this, we exposed fifty-nine healthy pre-menopausal women to both a stress session and a control session on different days. High cortisol reactors consumed more calories on the stress day compared to low reactors, but ate similar amounts on the control day. In terms of taste preferences, high reactors ate significantly more sweet food across days. Increases in negative mood in response to the stressors were also significantly related to greater food consumption. These results suggest that psychophysiological response to stress may influence subsequent eating behavior. Over time, these alterations could impact both weight and health.

Introduction

Emotional arousal has been associated with both increased or decreased food intake and weight (Stone and Brownell, 1994, Willenbring et al., 1986), but little is known about the mechanisms that determine the direction of change. Understanding predictors of stress-induced eating is important, as stress can trigger relapses of both obesity (Rand and Stunkard, 1978) and bulimic episodes (Lingswiler et al., 1989). One's physical response to stress may help explain why some tend to eat while others lose their appetite after stress. The purpose of this study was to identify whether stress reactivity, both biological and psychological responses, distinguish stress over-eaters from under-eaters. Specifically, we hypothesized that high cortisol reactivity may lead to eating in response to stress, given the relations between cortisol with both stress and mechanisms affecting hunger.

Cortisol clearly plays an important role in energy regulation, increasing available energy through gluconeogenesis and lipolysis. In animals prone to obesity (either genetically or by brain lesions), glucocorticoids lead to hyperphagia and weight gain, and are necessary for the expression of their obesity (Bray, 1985). Adrenalectomy and glucocorticoid receptor antagonists prevent or reverse obesity (Okada et al., 1992), whereas administering corticosterone leads to increased appetite for sucrose (Bell et al., 2000), hyperphagia, and weight gain (Flatt, 1989).

In humans, stress-induced cortisol may also play a role in obesity. There are a few demonstrations that cortisol affects eating in humans. In cancer patients, prednisolone significantly increased appetite, compared to a control group (Willox et al., 1984). In healthy men, administering cortisol for four days led to slightly increased energy expenditure but dramatically increased food intake (Tataranni et al., 1996). Given these associations between exogenously administered cortisol, food intake, and obesity from animal and human studies, we predicted that endogenous cortisol release, stimulated by stress, may help explain stress-induced eating.

Macronutrient selection may also be altered by stress. Women tend to prefer high fat or sweet foods when moderately stressed (Grunberg and Straub, 1992, Klein et al., 1996). There is much evidence that adrenal steroids influence macronutrient selection, by increasing appetite for carbohydrates, primarily, and for fat, and regulating the timing of eating in rodents (McEwen et al., 1993, Tempel and Leibowitz, 1994). We wanted to test similar associations between cortisol and food intake in humans. We predicted that those who secreted more cortisol in response to stress would tend to eat more calories, as well as choose sweet or high fat food.

Section snippets

Study participants

Fifty nine healthy pre-menopausal women aged 30 to 45 years were recruited as part of a study on habituation to stress and body shape. We followed exclusion criteria to eliminate women with factors that would affect cortisol reactivity, such as oral contraceptive use and menopause. Other exclusion criteria were current smoking (and having smoked 10 or more cigarettes a day within the last two years), regular alcohol (more than seven drinks a week) or medication use, major depression, eating

Descriptive data

The sample was an average of 36 years old (SE=0.70, range=30 to 46). Forty four percent were single. They had an average of 16 years of education (SE=22, range 12 to 17 years). Their average annual household income was $35,537 (SE=$3334). The average BMI was 25.4 (SE=0.62, range 19 to 39.6). The average score on the EAT, summing across the three subscales, was 10.2, SD=7.7, which is similar to a comparison group of healthy female university students (mean=9.9, SD=9.2), and lower than bulimic

Discussion

Stress-induced cortisol reactivity was related to greater caloric intake after exposure to a novel laboratory stressor. Women who were high cortisol reactors to stress ate more food than low reactors while recovering from stress. On the rest day, however, high reactors tended to eat less and low reactors tended to eat more, eliminating the difference between groups. Further, the high reactors tended to consume more sweet foods than low reactors, across days. Cortisol reactivity may be a marker

Acknowledgements

We thank the John D. and Catherine T. MacArthur Foundation for their support of this study. Additional support came from the NIH/NCRR/GCRC Program Grant #RR00125. In addition, we thank Catherine McCrann, Jennifer Sauk, and Chris Schuck for their research assistance.

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