We Only Eat What We Like, Part 5 – Pleasure Pathways and Possible Addiction
For References, please see the previous articles, same title. The reward/reinforcement circuitry of the mammalian brain consists of synaptically interconnected neurons associated with the medial forebrain bundle, linking the ventral tegmental area, nucleus accumbens, and ventral pallidum.
Electrical stimulation of this circuit supports intense self-stimulation in animals and, in humans, produces intense pleasure or euphoria. This circuit is strongly implicated in the neural substrates of drug addiction and in such addiction-related phenomena as withdrawal dysphoria and craving. But this circuit is also implicated in the pleasures produced by natural rewards (e.g., food, sex). Cannabinoids are euphorigenic in humans and have addictive liability in vulnerable persons, but were long considered “anomalous” drugs of abuse, lacking pharmacological interaction with these brain reward substrates. It is now clear, however, that cannabinoids activate these brain substrates and influence reward-related behaviors [Gardner et al. 1998].
Tobacco is worse than anthrax in the social psyche of the healthists. However, a recent Swedish study [Hjern et al. 2001] confirms that the herb of Jean Nicot can reduce the allergic burden in both children and adults.
The method was a cross-sectional study of present and former smoking habits in relation to atopic disorders from data on 6909 young and middle-aged adults (16-49 years) and their 4472 children (3-15 years) from the Swedish Survey of Living Conditions in 1996-97. The authors observed that the prevalence of allergic asthma and allergic rhino-conjunctivitis decreased, in a dose-response manner (P = 0.03 and P = 0.004, respectively), with increasing exposure to tobacco smoke in the adult study population. This pattern was little changed when potential confounders (sex, age, education, domicile, country of birth) were entered into a multivariate analysis: the adjusted odds ratio (OR) for allergic rhino-conjunctivitis was 0.5 (0.4-0.7) for those who smoked at least 20 cigarettes a day and OR 0.7 (0.6-0.9) for those smoking 10-19 cigarettes, compared with those who reported that they never had smoked Former smokers had a tendency for a slightly lower risk: OR 0.9 (0.8-1.0). In a multivariate analysis, children of mothers who smoked at least 15 cigarettes a day tended to have lower odds for suffering from allergic rhino-conjunctivitis, allergic asthma, atopic eczema and food allergy, compared to children of mothers who had never smoked (ORs 0.6-0.7). Children of fathers who had smoked at least 15 cigarettes a day had a similar tendency (ORs 0.7-0.9).
This study demonstrates an association between current exposure to tobacco smoke and a low risk for atopic disorders in smokers themselves and a similar tendency in their children. Smoking habits and atopic disorder in parents should not be considered independent variables in epidemiological studies of the connection between exposure to tobacco smoke and atopy in children.