The prevalence of smoking in our society is subject to many social influences. Heavy and regular smoking and the development of nicotine dependence, however, are determined not only by social factors but also by individual psychological and biological factors. Recent epidemiological and molecular genetic studies have provided evidence that nicotine dependence is, at least partially, genetically determined. Regular smoking and more particularly heavy smoking have been attributed with a high probability to genetic factors. The development of nicotine dependence results from the direct effect of nicotine on nicotinergic acetylcholine receptors, and perhaps more importantly, the dopaminergic transmitter system. The nucleus accumbens, an important part of the dopaminergic reward system, appears to play a particularly important role in nicotine dependence. A possibly relevant genetic variability in the dopaminergic system was found in the D2 dopamine receptor gene (DRD2) of alcoholics and heavy smokers. Animal studies have shown that variations in the structure of the nicotinergic acetylcholine receptor might interfere with the development of nicotine dependence. Other possible candidate genes for receptors in the serotonergic, adrenergic and dopaminergic system are being examined as potential contributors to the development of nicotine or tobacco dependence. Furthermore, reduced metabolism of nicotine into cotinine may also reduce risk for nicotine dependence. Although current research findings cannot fully explain how nicotine or tobacco dependence develops, it has advanced understanding of dependence disorders.
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