Both of these models attribute a causal influence of the social environment in limiting or exacerbating genetic influences. Shared behavioral expectations and corresponding sanctions cause genes to operate differently by either blocking or enabling their expression. If the social environment makes smoking difficult for everyone, it inhibits the potential for genes to affect smoking; if the social environment presents new choices, it facilitates the potential for genes to affect smoking. But a noncausal model of gene–environment interaction is also possible. The social push model (Raine 2002) posits that changes in social norms regarding smoking can affect the relevance of genetic influences by minimizing or maximizing “noise” that has the potential to overwhelm and hide the influences. On one hand, genetic associations are most clearly observable in benign environments that lack social factors encouraging genetically influenced addictive behaviors. When social noise is minimized, it allows for “biology to shine through” (Raine 2002:14). Conversely, when social factors “push” certain behaviors, then biological factors are harder to identify. As Raine makes clear, the social push perspective does not mean that the environment actually
