دانلود مقاله ISI انگلیسی شماره 39026
عنوان فارسی مقاله

واکنش پذیری محرک و تنظیم مصرف غذا

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
39026 2002 12 صفحه PDF سفارش دهید محاسبه نشده
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عنوان انگلیسی
Cue reactivity and regulation of food intake
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Eating Behaviors, Volume 3, Issue 1, Spring 2002, Pages 61–72

کلمات کلیدی
پرخوری - غذا خوردن مهار - تهویه - واکنش پذیری محرک
پیش نمایش مقاله
پیش نمایش مقاله واکنش پذیری محرک و تنظیم مصرف غذا

چکیده انگلیسی

Abstract A robust finding in eating research is the so-called counterregulation in restrained eaters. This means that while normal subjects eat less during a taste test, after they consumed a preload, restrained eaters consume more. An explanation is that food exposure causes stronger physiological preparatory reactivity in the restrained eaters. This reactivity is experienced as craving and leads to an increased food intake. To test this theory, 46 high and low restrained eaters were exposed to food or soap, while physiological measurements were made. Afterwards, the subjects performed a taste test, during which food intake was secretly measured. Unrestrained eaters showed an increase in heart rate, gastric activity, and saliva during food exposure; however, restrained eaters did not. Gastric activity significantly correlated with food intake. Group or exposure type did not influence food intake. It can be concluded that unrestrained eaters prepared for food intake, whereas the restrained eaters did not. A possible explanation is that restrained eaters used cognitive suppression to block physiological responding, thereby controlling their food intake.

مقدمه انگلیسی

Introduction A large group of people is struggling with their food intake, trying to restrict it, but often fail to do so. Herman and Mack (1975) performed an elegant experiment, using the so-called preload paradigm, in which this phenomenon is shown. In that experiment, unrestrained eaters showed normal regulation of their eating behavior; after they ate a preload (milkshake), they ate less ice cream during a subsequent taste test than when they ate no preload. Restrained eaters, however, defined as subjects who want to restrict their food intake, consumed less during a taste test when they did not eat a preload, but they consumed more during the taste test when they did eat a preload. This illogical behavior is called counterregulation and Herman and Mack's experiment initiated a large body of research. Restrained eaters repeatedly showed abnormal regulation of food intake (for an overview, see Boon, 1998). How can this eating pattern of restrained eaters be explained? A widespread cognitive explanation stems from the boundary model (Herman & Polivy, 1984). In this model, biological boundaries determine when a person feels hungry or satiated and thereby when a person starts and stops eating. Restrained eaters have another self-imposed boundary, marking their maximum desired consumption, the so-called diet boundary. As long as this boundary is not broken, the restrained eater succeeds in restricting food intake. When this diet boundary is broken, for example, after eating the preload, restrained eaters have disinhibitory thoughts, like “I've already blown my diet, I might as well continue to eat,” and start overeating. However, restrained eaters also showed abnormal regulation after exposure to the sight, smell, or thought of food, without actually eating it Fedoroff et al., 1997 and Jansen & Van den Hout, 1991. These findings cannot be explained with the disinhibitive thoughts of the boundary model; the “preload” was not consumed, and, thus, no diet rule was broken. Furthermore, no evidence of disinhibitive thoughts was found when restrained eaters were instructed to think aloud during the preload condition (Jansen, Merckelbach, Oosterlaan, Tuiten, & van den Hout, 1988). An alternative explanation for the counterregulation phenomenon stems from the cue reactivity theory. This theory states that when a person regularly has eating binges, and these binges are reliable preceded by certain cues (e.g., the sight, smell and taste of the food, environment, cognitions, and emotions), these cues become predictors of the start of a binge. Exposure to these cues induces conditioned physiological reactivity, which can prepare the person for the intake of food. In normal subjects, physiological responses to food cues are widely documented and called cephalic phase responses Mattes, 1997 and Nederkoorn et al., 2000. Binge eaters are expected to show even larger cephalic phase responses because the enormous amount of food intake during a binge threatens the homeostatic balances of the body, and anticipation is more important compared to normal food intake. In addition, more intense unconditioned stimulus, in this case the food intake, strengthens the conditioning. The cue reactivity is experienced as craving for the food and triggers an eating binge Jansen, 1994, Jansen, 1998 and Wardle, 1990. The theory originates in the addiction field, where increased psychophysiological reactivity and craving are found when the substance abuser is exposed to drug/alcohol cues Glautier & Remington, 1995 and Robbins et al., 1997, and studies suggest that craving for a substance is a classical conditioned response (Drummond, Tiffany, Glautier, & Remington, 1995). At least a part of the restrained eaters shows an eating pattern of dieting and overeating, which resembles the eating pattern of subjects with eating binges. Applied to the preload paradigm, the cue reactivity model of binge eating states that exposure to a preload, either by seeing and smelling or actually eating it, will elicit conditioned physiological responses and craving in the restrained eater. This, in turn, leads to increased food intake and counterregulation. From the model, it also follows that, when not exposed to the preload or other binge cues, the restrained eater is able to control food intake and eats less. In sum, the cue reactivity model predicts that: (1) restrained eaters show more physiological reactivity when exposed to binge cues than unrestrained eaters. (2) Cue reactivity is experienced as craving and (3) the increased reactivity and craving during the exposure lead to increases in the food intake of the restrained eaters during the taste test afterwards. Furthermore, the cognitive theory on overeating predicts that (4) a preload (or exposure to “forbidden” food) elicits disinhibitive thoughts in restrained eaters, which lead to an increased food intake during the taste test. The present experiment was designed to test these four hypotheses. Restrained and unrestrained women participated in an adjusted “preload” experiment, in which half of them was exposed to the sight and smell of food, without consuming it, and the other half was exposed to control stimuli. During the exposure, physiological reactivity was measured. Before and after the exposure, the subjects rated several subjective states, like craving for food. Afterwards, the participants performed a taste test and food intake was measured. At the end, the subjects rated retrospectively the frequency of disinhibitory thoughts during the exposure period.

نتیجه گیری انگلیسی

3. Results Unrestrained and restrained eaters did not differ in age. Restrained eaters, however, had significantly higher BMI and scored higher on the RS and the EDE-Q. Mean age, BMI, and scores on the RS and EDE-Q are revealed in Table 1. The first hypothesis of the cue reactivity theory was that: Hypothesis 1. Restrained eaters show more reactivity to food exposure, compared to control exposure, than unrestrained eaters. Several physiological effects were found. A significant main effect of group on heart rate emerged. The unrestrained eaters showed a higher heart rate than restrained eaters [F(1,43)=15.9, P<.001]. A marginal significant effect of condition was found; overall, the subjects showed a higher heart rate during food exposure than during control exposure [F(1,43)=4.0, P=.052]. There was also a significant interaction effect [F(1,43)=4.1, P<.05]; the heart rate of the unrestrained eaters was higher during food exposure, whereas there was no effect on the heart rate of the restrained subjects (see Fig. 1a). Gastric activity also showed a significant interaction [F(1,43)=8.4, P<.01]. Restrained eaters had a larger increase in gastric power during control exposure than during food exposure, whereas unrestrained eaters showed the opposite pattern (see Fig. 1b). Mean and standard error of heart rate (a), salivation (b), and gastric activity ... Fig. 1. Mean and standard error of heart rate (a), salivation (b), and gastric activity (c) during control and food exposure, compared to the baseline, of restrained and unrestrained eaters. Figure options The same pattern was found for swallowing, restrained eaters swallowed more often during the control exposure than during food exposure; unrestrained eaters swallowed more during food exposure [F(1,43)=5.0, P<.05] (see Fig. 1c). Restrained eaters had a higher skin temperature than unrestrained eaters, irrespective of exposure type [F(1,43)=5.9, P<.05]. No effects were found on blood pressure (systolic, diastolic, or mean blood pressure) and skin conductance level. The second hypothesis of the cue reactivity theory states that: Hypothesis 2. The physiological reactivity was experienced as craving. Both groups reported an increase in craving after food exposure compared to exposure to the control stimuli [F(1,43)=12.3, P<.001]. However, there was no significant correlation between any physiological measurement and craving (Fig. 2). Mean and standard error of the increase in reported craving after food and ... Fig. 2. Mean and standard error of the increase in reported craving after food and control exposure of restrained and unrestrained eaters. Figure options The third hypothesis from the cue reactivity theory states that: Hypothesis 3. An increase in cue reactivity and craving during the exposure is related to an increase in food intake during the taste test. However, the type of exposure (control or food) did not influence food intake, in neither group. No significant difference in food intake between the groups was found. There was also no correlation between craving and food intake. Yet, there was a significant correlation between gastric activity during exposure and food intake during the taste test (r=.39, P<.01). No other correlation between a physiological measurement and food intake was found. Mean kilocalories consumed during the taste test are revealed in Table 2. Table 2. Mean and standard error of kilocalories consumed during the taste test, by the restrained and unrestrained eaters, after control or food exposure Restrained eaters (kcal) Unrestrained eaters (kcal) Control exposure 324 (82) 408 (72) Food exposure 227 (44) 300 (50) Table options The fourth hypothesis, derived from the cognitive theory, states that: Hypothesis 4. During food exposure, restrained eaters have more disinhibitive cognitions, leading to an increased food intake during the taste test. Retrospectively, restrained eaters indeed reported more disinhibitive cognitions than unrestrained eaters [F(1,43)=10.2, P<.005]; however, the cognitions were reported as frequently in the food, as well as in the control condition. No significant interaction effect was found, and there were no significant correlations between the reported cognitions and craving for food, as well as food intake. Exploratively, the subjective ratings of emotion (anger, fear, and relaxation) before and after the exposure were analyzed. There was a significant interaction effect on anger [F(1,43)=4.4, P<.05]; restrained eaters reported more anger after control exposure and less after food exposure. Unrestrained eaters reported less anger after control exposure than after food exposure. There were no significant effects of group or exposure on ratings of other subjective states (hunger and nausea). There were also no significant correlations between physiological measurements and subjective ratings.

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