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males were given nalmefene, a long-lasting opioid antagonist (39). Treatment with nalmefene decreased caloric intake by 22%, although the subjective ratings of hunger did not alter. The consumption of fat and protein, but not carbohydrate, decreased. Nalmefene did not influence the intake of particular macronutrients, but rather it influenced the intake of palatable foods, for example high-fat cheese such as Brie. The choice was between various savoury food items; chocolate and sweet foods were not on offer. In a similar study, naloxone differentially decreased the intake of high-fat/high-sugar foods (40).

Drewnowski et al. (41) examined the hypothesis that the influence of opiate antagonists on taste preferences and food consumption would be greater amongst binge eaters. Bingeing is typically associated with food cravings. They compared patients with a diagnosis of bulimia nervosa with a group without this history. Snack foods were presented and divided into four categories depending on whether they contained high or low levels of sugar or fat. The high-sugar/high-fat category contained chocolate bars and chocolate-containing cookies and candies. The infusion of naloxone, rather than saline, significantly reduced the total energy intake of binge eaters. The reduction in intake was most marked for the high-sugar/high-fat foods such as those containing chocolate. The obvious explanation is that such foods are highly palatable and that the pleasure associated with eating such foods is mediated via opioid mechanisms. Thus drugs such as naloxone, that block the action of endogenous opioids, reduce the pleasantness of high-sugar/high-fat foods such as chocolate.

In summary, a major theory is that the eating of palatable foods is associated with the release of endorphins. The blocking of the action of endorphins, with drugs such as naloxone or naltrexone, decreases the intake of chocolate.


Phenylethylamine is found in chocolate at levels that vary from 0.46.6 |ig/g of chocolate (42). Thus, a 50 g bar at the most contains about a third of a milligram. Naturally phenylethylamine is present in low concentrations in the brain; it has distinct binding sites, although it acts as a neuromodulator rather than as a neurotransmitter. If injected into the brain of animals it causes stereotyped behaviour, acting in a similar way to amphetamine. As phenylethylamine does not bind directly to dopamine sites, but its effects can be blocked by dopamine antagonists, it is assumed to release dopamine (43). At physiological doses, it potentiates the neurotransmitters dopamine and norepinephrine (44). Monoamine oxidase B preferentially oxidizes phenylethylamine, although this enzyme also oxidizes dopamine. Phenylethylamine is present in low concentrations in the brain (<10 ng/g) and has a rapid turnover (half-life is 510 min).

Two New York psychoanalysts associated passionate love with chocolate. They found that a group of 'love-addicted' women whom they were treating

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