One human behavioural trait related to food consumption is the seeking out of foods and beverages made with chocolate. In addition to the methylxanthines present in cocoa products (theobromine, caffeine), also present is the constituent beta-phenylethylamine or 2-phenylethylamine (2PEA).
Phenylethylamines comprise a variety of chemicals sharing the chemical backbone in 2PEA, including the weight-loss drugs sibutramine, fenfluramine and phentermine (?fen-phen?); the endogenously produced nerve chemicals dopamine and adrenaline; and amphetamine. An ostensibly plausible hypothesis is that 2PEA exhibits appetite-suppressing/thermogenic effects, given that several anti-obesity drugs share the same chemical skeleton.
One study examined the effects of chocolate consumption upon brain activity (via PET scanning) under conditions when the subjects were hungry and when they experienced aversion (eating chocolate beyond satiety).1 Although a 2PEA-free chocolate control was not implemented, the study did suggest that the sensory-reinforcing (taste and smell) experience of chocolate consumption was involved in the early stage of eating.
This is reinforced by earlier work where college-age female and male self-admitted chocolate cravers were assigned, in random order, to one of six different treatments. When they experienced a chocolate craving, they were instructed to consume: 1) a milk chocolate bar; 2) an isocaloric white chocolate bar, having only trace amounts of 2PEA and methylxanthines; 3) capsules containing the same cocoa powder and amount present in the milk chocolate bar; 4) placebo capsules; 5) a white chocolate bar plus cocoa powder capsules; or 6) no treatment.2 The objective was to assess the impact of each treatment on subjective chocolate cravings.
Given the limitations of the study (eg, unblinding of subjects to chocolate bars, the absence of an artificially sweetened placebo bar), the results showed the milk chocolate bar produced the greatest acute craving attenuation, with the white chocolate bar and white chocolate bar plus cocoa powder exhibiting intermediate efficacy. The cocoa powder capsules fared no better than placebo or no treatment.
Recent studies suggest the existence of receptors for 2PEA in humans, implicating a biological role.3 However, there do not appear to be any systematic investigations exploring the influence of 2PEA upon overall food intake or body weight, leaving unanswered the question of its pharmacodynamics in relation to appetite.
Additionally, 2PEA is asserted to not be capable of being efficiently transported into the brain.4 Additional investigations into the chemistry of chocolate have revealed the presence of lipid molecules that alter the turnover of chemicals produced in the brain. These molecules bind to some of the same receptors to which the principle bioactive in hemp (Cannabis sativa) binds.5 Whether they could modulate food intake (up or down), given their low concentrations and questionable oral bioavailability,6 remains a topic well suited for discussion, accompanied by a serving of dark chocolate.
Anthony Almada, MSc, is president and chief scientific officer of IMAGINutrition Inc.
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All correspondence will be forwarded to the author.
1. Small DM, et al. Changes in brain activity related to eating chocolate: pleasure to aversion. Brain 2001; 124:1720-33.
2. Borowsky B, et al. Trace amines: Identification of a family of mammalian G protein-coupled receptors. PNAS 2001; 98:8966-71.
3. Michener W and Rozin P. Pharmacological vs sensory factors in the satiation of chocolate craving. Physiol Behav 1994; 56:419-22.
4. Shimazu S and Miklya I. Pharmacological studies with endogenous enhancer substances: ?-phenylethylamine, tryptamine and their synthetic derivatives. Prog Neuro-Psychopharmacol Biol Psychiatry 2004; 28:421-7.
5. Di Tomaso E, et al. Endocannabinoids in chocolate. Nature 1996; 382:677-8.
6. Di Marzo V, et al. Trick or treat from food endocannabinoids? Nature 1998; 396:636-7.