The Contribution of cocoa additive to cigarette smoking addiction

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Page 60 of 207 RIVM report 650270002 Serotonin human. Nicotine binds to nicotinic receptors in the brain, augmenting the release of numerous neurotransmitters, including serotonin. Cigarette smoke has other psychoactive properties apart from nicotinic receptor stimulation. For example, it inhibits monoamine oxidase (the enzyme responsible for breaking serotonin) in the brain. Serotonin plays a role in de reward mechanism of smoking and the antidepressive effect of smoking (51, 52) Epidemiological studies on humans have shown that tobacco smoking is being prevalent in patients with depressive disorder (31). The craving qualities of chocolate have been thoroughly reviewed and the conclusion seems to be that the pharmacological active compounds (including serotonin) in cocoa do not contribute to chocolate craving (52). Effects of smoking cessation Serotonin reuptake inhibitors (SSRIs) and 5-HT antagonist was shown to be effective in diminishing the smoking withdrawal negative effects. It was shown in rats that sertraline (SSRI) can counteract the hyperphagia and rapid weight gain associated with nicotine withdrawal, and might therefore be a useful adjunct to smoking cessation (53). In another study it was shown that ondansetron, a selective 5-HT3receptor antagonist, may attenuate the aversion effect associated with nicotine withdrawal, and may be useful for the treatment of nicotine dependence (54). Critical assessment The serotoninergic system in the brain is affected by tobacco smoking and this system plays a role in the tobacco dependency and smoking cessation. From literature on chocolate craving, it seems that exogenous serotonin does not contribute to chocolate craving quality. Considering the large endogenous serotonin pool (estimated 10 mg), it seems unlikely that the low serotonin dose from cigarette smoke (estimated 15 µg/day) will affect the serotonin level in the body. Conclusion Serotonin released in the brain through nicotine stimulation plays a role in the nicotine dependency. It seems unlikely that serotonin from cigarette smoke could play a significant role in the addiction process due to the large endogenous serotonin pool. However, the longterm effects of serotonin and its interaction effects with other agents in the cigarette smoke on the pulmonary system and in the tobacco addiction process is not known and need to be studied. COMMERCIAL USE Serotonin itself is used in the treatment of myoclonus. Tryptophan is a precursor of serotonin. Because CNS depletion of serotonin is considered to be involved in depression, tryptophan has been used in its treatment. Although it has been given alone, evidence of effectiveness is scant and tryptophan has generally been used as adjunctive therapy in depression. Pyridoxine and ascorbic acid are involved in the metabolism of tryptophan to serotonin and have sometimes been given concomitantly. In the treatment of depression the usual dose of tryptophan is 1 g given three times daily, but some patients may require up to 6 g daily in divided doses. Lower doses may be required in the elderly especially those with renal or hepatic impairment. (55).
RIVM report 650270002 Page 61 of 207 Serotonin BENEFICIAL EFFECTS Serotonin itself can be used as a drug in the treatment of myoclonus (48). Critical assessment Not relevant. Conclusion Not relevant. SUMMARY AND FINAL CONCLUSION Serotonin contains the characteristic heterocyclic indole structure, accounting for the aromatic properties (electrophilic substitution). In addition the chemical; the presence of the ring bound hydroxyl group accounts for its polar character. An additional characterising chemical feature is the presence of the aliphatic amino-group. A source of serotonin in tobacco is cocoa powder, which is used as a flavouring agent. Little is known about the profile of pyrolysis/combustion products of serotonin. The daily intake via cigarettes smoke (estimated to be 15 µg/day) is low compared to the oral intake via chocolate, cocoa drinks and banana (estimated 19 – 15000 µg/day), and to the endogeneous pool of serotonin (10 mg). Serotonin binds to a large family of serotonin receptors (5-HT1-7 subtypes). Serotonin stimulates and inhibits nerves and smooth muscles in the cardiovascular, respiratory and gastrointestinal systems. Some contradictory results were obtained about the bronchoconstrictory effect of serotonin in humans in respiratory studies. The main conclusion seems to be that serotonin has a negligible effect on the bronchi. It has a pulmonary hypertension effect on the pulmonary system. Depending on the serotonin level, it exerts complex effects on the cardiovascular system, including hypotension or hypertension, vasodilatation or vasoconstriction, and/or bradycardia or tachycardia. It also has complex effects on the CNS and is involved in the nicotine dependency. Serotonin is an endogenous compound. It is widely distributed in the body and about 90 % is stored in the enterochromaffin cells of the gastrointestinal tract; the remainder is present in platelets and in CNS. Serotonin is metabolized by monoamine oxidase; it is extensively removed from the plasma (70%) by the pulmonary microvascular endothelium during a single passage through the lungs. The turnover of serotonin is 1h in the brain to 17 h in the gastrointestinal tract. Pharmacokinetics on exogenous serotonin through the respiratory and the intestinal tract are not available. The toxicity data on serotonin that are available in the literature are mostly related to increased endogenous serotonin or its metabolites level in the body by metabolic or medication effect. Acute toxicity of serotonin is displayed when the endogenous serotonin level is raised by exogenous factors (drugs, food (banana or walnuts), tryptophan) or by serotonin hyperproduction (carcinoid tumor). The most common clinical symptoms observed are: nausea, vomiting, headache, diarrhea and uremic anorexia. Animal I.V. LD50 varied between 12.8 mg/kg bodyweight for the guinea pig to 81 mg/kg body weight for the mouse. Chronic serotonin toxicity is seen in
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