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intake of standard rat food (25). The rate that rats will press a lever to stimulate electrodes placed in the lateral hypothalamus one of the brain's pleasure centres is enhanced by food deprivation (26).
As this food deprivation-induced increase in self-stimulation was blocked by naloxone, it was proposed that endogenous opiate activity promoted eating by enhancing the reward value of the food. The amount of b-endorphin occupying receptors in the rat hypothalamus has been reported to increase when chocolate milk and candy are eaten (24). Opioid antagonists are more effective in reducing food intake in obese animals than in those of a normal weight (27). Thus, there is increasing evidence that in rodents, endogenous opiates regulate food intake by modulating the extent to which pleasure is induced by palatable foods.
In humans, opioid antagonists decreased thinking about food, feelings of hunger (28, 29) and food intake (30). Naltrexone reduced the preference for sucrose (31). Spontaneous eating has been associated with an increased release of b-endorphin (32). There have been limited attempts to relate the effects of nutrients on the level of plasma b-endorphins. The eating of meat soup resulted in a rapid rise in b-endorphin in 15 min, that then fell and rose again after 60 min (33). In a similar study, 100 g of glucose resulted in a rise in b-endorphin after 150180 min (34).
The increase in b-endorphin may reflect either a pleasant sensory experience or alternatively a reaction to the metabolic consequences of eating. In rats, the anticipation of eating palatable food is associated with b-endorphin release (24), suggesting that psychological factors play a role. When the reactions to two chocolate drinks were compared in humans (35), plasma endorphins were more elevated with drinks sweetened with aspartame rather than sucrose. The authors suggested that b-endorphin release is more associated with glucose homeostasis than a pleasant taste.
Mandenoff et al. (36) proposed that with a monotonous diet, in a predictable environment, the endogenous opiate system is not necessary for the control of eating. However, with stress, fasting and the consumption of highly palatable foods it plays a role. In the rat, a stressor, such as pinching the tail, will induce a naloxone-reversible increase in eating (37). Mandenoff et al. (36) suggested that if a stress-induced release of endorphin is not enough to protect the animal, it is adaptive to eat and increase blood glucose levels. In this way further endorphin release can be stimulated. The authors pointed to the parallels between the stress-induced increase in rodent eating and the stressed humans who snack on palatable foods. As discussed above, there is a close association between negative mood and chocolate craving. The possibility that the binge eating of palatable foods may be modulated by the endogenous opiate systems has also been considered. Abnormally high levels of b-endorphin have been reported in both bulimic and obese women (38).
The suggestion that opiate mechanisms selectively influence the pleasure associated with palatable food was supported by a study in which healthy human
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