The Contribution of cocoa additive to cigarette smoking addiction

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Page 154 of 207 RIVM report 650270002 Phenylethylamine phenylethylamine in neural processes underlying reward or reinforcement. Evidence for reinforcing properties of phenylethylamine in the drug self-administration and place preference paradigms have been investigated (38). The reinforcement properties of phenylethylamine compared to amphetamine or cocaine were investigated in dogs. The relative potencies of these compounds in maintaining self-administration behaviour during the 4-hr session was damphetamine greater than cocaine greater than or equal to phenylethylamine. It was concluded that phenylethylamine can function as a reinforcer or may play a physiological role in the reinforcement process (39). Furthermore, it was shown that in MAOI-B treated squirrel monkeys, phenylethylamine (0.3 – 1.0 mg/kg) affected the discriminative-stimulus and reinforcing-stimulus compared with amphetamine (0.3 mg/kg) (40). Effects of smoking cessation No data available. Critical assessment Phenylethylamine has reinforcing properties qualitatively comparable to amphetamine. Whether phenylethylamine in cigarette plays a role in the reinforcing effect of cigarette smoking is unknown. Conclusion Phenylethylamine has reinforcing properties. COMMERCIAL USE No data available. BENEFICIAL EFFECTS In depressed subjects treated with an MAOI, phenylethylamine markedly improves mood (because phenylethylamine is rapidly metabolized by MAO, phenylethylamine alone produces no noticeable effects). The addition of 10 to 30 mg/day of phenylethylamine to current treatment with amitryptiline plus phenelzine terminated the episode of depression in 2 of the 3 inpatients with major depressive disorder who had not achieved any significant recovery with tricyclic antidepressants, MAOI, or their combination (16). Critical assessment Phenylethylamine could be used to treat depression disorder in human. Whether phenylethylamine in cigarette plays a role to the possible anti-depressive effect of cigarette smoking is unknown. Conclusion Phenylethylamine has anti-depressive properties. SUMMARY AND FINAL CONCLUSION Phenylethylamine is a natural tobacco component and is also added to tobacco as a component of cocoa powder, which is used as a flavouring agent. The estimated
RIVM report 650270002 Page 155 of 207 Phenylethylamine phenylethylamine amount in dried tobacco plant is 70 – 485 µg/g dry weight. The average amount of phenylethylamine in cocoa varies between 0.22 – 22 µg/g. The estimated natural phenylethylamine amount from tobacco plant in cigarette is at least 2200 times higher than phenylethylamine from added cocoa. Therefore, it is debatable whether phenylethylamine should be considered as an additive to tobacco. The daily potential intake of phenylethylamine (12.1 mg/25 cigarettes/day) from cigarettes (from tobacco plant and added cocoa) is higher than phenylethylamine intake from other sources such as chocolate, sausage and cheese (0.5 – 4 mg/day). Assuming similar bioavailability and no loss by combustion, the plasma concentration reached after ingestion of phenylethylamine from chocolate sources or other food sources is expected to be lower than after exposure from cigarettes. Also the different route of application via smoking as compared with other sources should be taken into account. Therefore, the systemic and the local effect of smoking related exposure to phenylethylamine might be a point of concern. Since nothing is known about the pyrolysis/combustion products of phenylethylamine, this may also be a point of concern. Phenylethylamine is classified as a neuromodulator of dopaminergic and possibly serotonergic and noradrenergic synapses. At the molecular physiological level, phenylethylamine potentiates transmission by postsynaptic and possibly presynaptic action. Phenylethylamine produced a bronchoconstriction of isolated perfused lungs of guinea-pig. No data are available on phenylethylamine inhalation effects in human. Therefore, it is unknown whether the phenylethylamine dose in cigarette will exert bronchoconstrictory effects. Phenylethylamine exerts both positive inotropic and vasoconstrictory effects in dogs. Phenylethylamine tended to produce an initial tachycardia followed by a bradycardia in dogs. Phenylethylamine has amphetamine-like effects in rats including symphatomimetic effects, increasing nonspecific motoractivity, exploratory behavior, stereotypic behavior, electrophysiological alerting, reinforcement of complex behavior and anorectic effects. It is suggested that endogenous phenylethylamine may contribute to the antidepressant, stimulant, or euphoriant effects of several drugs. Phenylethylamine exerts its CNS effect at high doses or when the MAO is inhibited. Based on the current CNS data, it is unknown whether the phenylethylamine dose in cigarette is enough to exert any CNS effect. In vitro studies have shown that phenylethylamine is rapidly absorbed by the pulmonary endothelial tissue and is also rapidly inactivated by pulmonary MAO. Phenylethylamine is distributed throughout the body. Phenylethylamine crosses the blood-brain barrier easily and its concentration in the brain after peripheral injection peaks within 5 minutes and returns to normal level within 30 min. The turnover of endogenous phenylethylamine in the brain is high with a half-life of 0.4 min. Phenylethylamine is metabolized by MAO, primarily by type-B (and to a small extent MAO-A), and aldehyde dehydrogenase to phenylacetic acid, which is the major metabolite of phenylethylamine in the brain. There are no in vivo pharmacokinetic data available on respiratory intake of phenylethylamine. Based on the in-vitro kinetic data of phenylethylamine, the pulmonary MAO will reduce the phenylethylamine intake through cigarette smoking.
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