Pleasure and alcohol: manipulating pleasantness and the acute effects of alcohol on food intake
Introduction
Alcohol has pharmacological effects on the nervous system altering a number of neurochemical systems. Alcohol has no capacity to be stored, and so takes precedence in the oxidative hierarchy, potentially suppressing the oxidation of dietary fat [1]. It appears that alcohol is the least satiating macronutrient with energy from alcohol increasing total energy intake without compensation in the short term. Also in the short term, alcohol stimulates food intake and at certain doses has been associated with increased subjective feelings of hunger [2]. All these factors may independently or synergistically influence the effects of alcohol on energy intake.
Recent studies indicate a potential role of alcohol consumption in the development of obesity, demonstrating a positive relationship between BMI and alcohol intake [3], [4]. Other data suggest a role of alcohol in the development specifically of abdominal adiposity [5]. Short term laboratory based investigations consistently suggest that consumers fail to compensate for alcohol preloads. For example, alcohol consumed before a meal fails to reduce subsequent food intake [6], [7] and alcohol promotes greater food intake when alcohol is consumed relative to no-alcohol [2], [8], [9], [10], [11], [12], [13]. So, it appears that alcohol is not only additive to total energy intake, but may also, in moderate doses, have a stimulatory effect on food intake in the short term.
Whilst the precise mechanisms underlying the stimulatory effects of alcohol on appetite remain unclear, one possibility is that the pharmacological effects of alcohol may directly affect the appetite system by modulating the orosensory reward from food. Several strands of evidence suggest that perceived palatability of food plays an important role in food intake and food choice. Meal size tends to rise as palatability increases [14], [15], [16], [17]. de Castro et al. [18] reported that higher levels of palatability were related to larger meals in a 7-day food diary study with French participants. In a further study [19] with North Americans, meals rated as highly palatable were 44% larger than those rated lower in palatability.
Yeomans and Wright [20] have considered the role of endogenous opioid peptides in the determination of orosensory reward mechanisms during feeding. The opioid antagonist nalmefene had the most profound effects on foods that are typically highly flavoured and rated as highly palatable (pakora, gouda). Also, nalmefene reduced intake of a buffet style lunch by 20%, with a proportional reduction in intake of foods in relation to their perceived palatability.
Acute ethanol administration in vivo increases release of endorphin and enkephalin from the pituitary gland, the hypothalamus and other distinct brain regions of rodents [21]. Endogenous opioid release via administration of alcohol may be involved in the reinforcing effects of alcohol, the hedonic response to alcohol and possibly involved in orosensory reward components of eating [22]. Endogenous opioid release stimulated by alcohol may modulate food-induced opioid release contributing to increased pleasantness of foods, leading to overconsumption. Furthermore, many of the physiological and pharmacological effects of alcohol have been attributed to its effects on the GABA system [23]. GABA also is implicated in the control of feeding. Drugs that promote GABAnergic activity, such as the benzodiazepines [24] and baclofen [25] reliably increase food intake in rodents. Benzodiazepines also increase food intake in humans [26]. Short term stimulation of food intake by alcohol closely resembles the stimulation of food intake following stimulation of GABAnergic activity by the benzodiazepines. GABA may therefore be involved in the short term stimulation of food intake by alcohol. Both the GABA and opioid systems are likely to constitute key neurophysiological substrates involved in the enhancement of food intake by alcohol. Alcohol may promote the intake of food by enhancing the pleasure derived from food, and by disrupting the normal development of sensory specific satiety, which reduces pleasantness of a food or drink as it is consumed. Sensory specific satiety is defined as the decline in pleasantness of an eaten food in comparison to uneaten food items and operates to limit intake of a specific food whilst facilitating intake of other, still pleasant, uneaten foods [27].
The present investigation was designed to examine the role of pleasure in the enhancement of food intake by alcohol, specifically, the effect of alcohol on the development of sensory specific satiety and on perceived palatability of foods. This was achieved by comparing intake of two similar, but distinctly flavoured food items at lunch following a preload with and without a moderate dose of alcohol. Pleasantness ratings of bland and tasty foods were measured to examine both the effects of alcohol on sensory specific satiety and the perceived pleasantness of bland, sweet, and savoury foods. Thus, the main objective of the present study was to test the hypothesis that alcohol promotes the intake of food by increasing the palatability and intake of specific types of foods.
Section snippets
Participants
Twelve male participants aged 18–50 were recruited from the staff and student population at the University of Liverpool via recruitment posters. Participants were screened prior to recruitment to ensure that they were suitable for inclusion in the investigation. Participants were required to be of normal weight (BMI<27 kg/m2), they were unrestrained eaters with a score of 2.5 or less on the restraint subscale of the Dutch Eating Behavior Questionnaire (DEBQ: [28]), they consumed less than 21
Energy intake
Intake at lunch was significantly higher following the alcohol preloads in comparison to the no-alcohol preloads (Fig. 1). ANOVA revealed a significant main effect of alcohol [F(1,11)=10.88, p<0.01]. The taste manipulation had no significant effect on food intake. Pairwise comparisons indicated that participants consumed more energy from food following alcohol in both taste conditions (plain=2053±663 kJ, flavoured=1989±570 kJ) in comparison to the no-alcohol preloads (plain=1548±356 kJ,
Discussion
Administration of a moderate dose of alcohol (3 units/24 g) increased energy intake at lunch by 20%. No compensation for the extra energy received in the alcohol containing preloads was observed. Thus alcohol containing preloads stimulated food intake and energy received in the form of alcohol was additive to total energy intake by enhancing total energy intake by 33%. Alcohol did not differentially enhance intake of specific food items. Moreover, alcohol did not increase the pleasantness of
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