摘要：Objectives. I examined genetic influences on smoking among adolescents and differences in the heritability of smoking across states in the United States. Methods . With data from the National Longitudinal Study of Adolescent Health (participants aged 12–21 years), I used a multilevel twin- and sibling-pair (N = 2060 pairs) regression model. Results . Daily smoking (hereditability estimate [ h 2] = 0.54) and smoking onset ( h 2 = 0.42) were both highly heritable. Whereas the genetic influences on smoking onset were consistent across states, there was significant variation in these influences on daily smoking. Genetic influences on daily smoking were lower in states with relatively high taxes on cigarettes and in those with greater controls on the vending machines and cigarette advertising. Genetic influences were also negatively associated with rates of smoking among youths. Conclusions. At the state level, gene–environment interaction models are best characterized by the model of social control. State policies may influence genetic tendencies to smoke regularly, but they have not affected the genetic contributions to cigarette onset or experimentation. Future tobacco-control policies may emphasize the heritable endophenotypes that increase the likelihood that adolescents will initiate smoking. There is consistent evidence that genetic and social factors equally influence smoking behaviors. 1 – 11 However, little work has jointly considered the simultaneous effects of genetic and social factors on cigarette usage among adolescents and young adults. In work that does consider gene–environment interactions, the emphasis is typically on the social and demographic characteristics of individuals or families 9 , 12 – 16 rather than on the composition of larger social contexts at the national, regional, state, county, or neighborhood level, even though these social environments are more relevant to existing theory on gene–environment interactions. 17 The proportion of variance that is caused by genetic influences, called a heritability estimate, ( h 2), is believed to be just higher than 50% for smoking. 1 – 5 Heritability estimates are obtained by comparing the concordance of smoking among siblings and twins, such as the values presented in Table 1 . These results report the number of sibling or twin pairs from the National Longitudinal Study of Adolescent Health study (Add Health) in which neither, one, or both members of the pair are smokers. Evidence for genetic influences can be seen for both measures of smoking in which the correlation among monozygotic (identical) twins is significantly higher compared to the correlation among dizygotic (fraternal) twins. Genetic influences are formally characterized in Table 2 using quantitative genetic methods. According to these results, 42% of the variance of smoking onset and 54% of the variance of daily smoking is because of additive genetic effects. These estimates are in line with other research in this area. 2 , 12 , 18 Estimates for the heritability of daily smoking range from 40% to 70%, 9 , 19 and the literature on gene–environment interactions provides insights about the social contexts that may enhance heritability and those in which genetic influences should be muted. 17 TABLE 1 Descriptive Statistics for Smoking Onset and Daily Smoking Status Among Twin and Sibling Pairs (N = 2060): National Longitudinal Study of Adolescent Health, Wave 2, September 1994–April 1995 Smoking Onset Daily Smoking Total No. Neither, No. One, No. Both, No. r Neither, No. One, No. Both, No. r Monozygotic twins 248 113 68 67 0.63 186 31 31 0.83 Dizygotic twins 378 159 132 87 0.42 280 65 33 0.65 Full siblings 1066 396 384 286 0.42 716 248 102 0.51 Half siblings 368 118 146 104 0.32 240 92 36 0.47 Open in a separate window TABLE 2 Quantitative Genetic Parameter Estimates for Smoking Onset and Daily Smoking Status Among Twin and Sibling Pairs (N = 2060): National Longitudinal Study of Adolescent Health, Wave 2, September 1994–April 1995 Smoking Onset, Variance (95% CI) Daily Smoking, Variance (95% CI) Heritability 0.42 (0.15, 0.66) 0.54 (0.29, 0.74) Shared environment 0.21 (0.06, 0.36) 0.29 (0.14, 0.44) Nonshared environment 0.37 (0.10, 0.19) 0.17 (0.09, 0.29) Open in a separate window Note. Heritability estimates and 95% confidence intervals (in parentheses) were calculated by using Mx version 1.7.03 (Medical College of Virginia, Richmond, VA). This freely available structural equation modeling package contains a number of standard procedures to decompose phenotypic variance into genetic and environmental components. A modified version of the script ctVCut2c.mx was used to estimate the parameters presented. Shanahan and Hofer 17 reviewed the literature on gene–environment interactions and pointed out that genetic influences on a variety of different behaviors are attenuated by social control. The institutional perspective emphasizes limits on the locations in which smoking is permitted, limits on the sale of tobacco products, educational programs, and taxes. These policies influence smoking in general, but they may be particularly effective in reducing the phenotypic expression of genetic factors that predispose people to initiate smoking or, following initiation, to become daily smokers. 20 The other control model emphasizes antismoking norms and values that limit genetic influences on smoking. 5 , 21 There are also reasons to believe that environmental characteristics may increase the relative influence of genes on the risk of smoking. According to the social trigger model, latent (e.g., genetic) tendencies to smoke are most likely to differentiate between individuals within environments in which there are social pressures to smoke cigarettes. Therefore, the heritability of smoking should increase with increased prevalence of smoking, decreased social sanctions against smoking, and increased expectations of tobacco use. Boardman et al. 22 showed that the heritability of daily smoking is significantly higher within schools in which the most popular students smoke the most compared with schools in which there were less clear prosmoking norms. Finally, according to the social distinction model, genetic vulnerability to tobacco use may manifest more clearly within environments in which smoking is less common. Raine 23 called this the “social push perspective” and suggested that we should examine genetic associations in benign environments or those that lack social factors that encourage smoking. The literature on gene–environment interactions may shed new light on tobacco-control policies. Specifically, policies may influence the smoking rates of a state, but they may do little to influence the genetic factors that encourage individuals to either begin smoking or to smoke regularly. If this is the case, then focused policies aimed at the biophysical causes of cigarette consumption can be developed. The influence of social controls may be very different for different endophenotypes—such as personality characteristics or nicotine metabolism—that are linked with cigarette initiation or daily use. Therefore, the examination of the genetic influences on smoking across states may provide a new perspective on the nature, scope, and effectiveness of tobacco-control policies. I build upon existing research on gene–environment interactions by examining the ways in which institutional and social characteristics of states moderate genetic predispositions toward cigarette use. My main assertion is that heritability estimates denote averages and that genetic tendencies to smoke should vary across discrete social environments; we should only expect consistent genetic associations within comparable social environments.
