Why “Just Say No” Programs Don’t Prevent Alcohol Misuse
September 21st, 2017
Youth programs with a “just say no” approach to preventing substance use have proven largely ineffective. Researchers have known this for over a decade, but now studies are helping to explain why. Alcohol misuse results from a complex interplay of genetic, environmental, and developmental factors, those studies find. There is no one reason problems develop “and no one-size-fits all solution to solving them,” according to Jeanne Savage and colleagues in a review of research on alcohol misuse for Policy Insights from the Behavioral and Brain Sciences. For educators and clinicians, that news is mixed. On the one hand, it makes alcohol problems complicated to treat. On the other, it shows their trajectory is malleable and therefore preventable.
Alcohol misuse (AM), defined as “the excessive, inappropriate, or harmful consumption of alcohol that causes negative consequences,” costs individuals, families, employers, and society almost $250 billion a year, and immeasurable stress and suffering. Policies and programs have aimed to prevent and treat those problems with mixed success. Savage and colleagues hope those efforts can be improved by incorporating research from behavioral genetics, a field that examines how genes and behaviors influence one another.
Behavioral genetics studies show there are many factors influencing AM, including individual personality traits, social and environmental influences, age, race, social class, and the heritability of certain genes. Each of these factors is complicated in itself. For example, although half the risk for AM can be attributed to genetics, there is no single marker responsible, but rather a constellation of several genes that have small and cumulative effects on risk. The precipitating factors are further complicated by the fact that they interact. For example, genetic factors matter more at some ages than others. At age 13, the heritability of AM is basically zero, but by age 24, it’s about 50%. Conversely, environmental factors play a larger role in adolescence. Even then there are age differences: parental monitoring of children’s behavior decreases the genetic risk for AM in early adolescence, while peer substance use plays a larger moderating role in later adolescence.
The authors write that one of the big takeaway messages from the research is the need to understand that the influence of genes varies in different environments and at different ages – and vice versa. So far, few intervention programs have taken a broad perspective, but Savage and colleagues point to a few promising exceptions. One is a school-based program called Preventure. Based on research showing how different personality traits impact risk for AM, it teaches adolescents coping strategies for stress, depression, and other triggers based on their individual personality traits. Another effective program tailors prevention education to college students with a genetic predisposition to have a low level of tolerance for alcohol.
The authors are careful to point out that large-scale prevention programs are still needed, but recommend that those programs take a multi-pronged and community-wide approach. Because decisions about alcohol use are about more than just peer pressure, programs to prevent them should do more than teach young people to just say no.
Drawn from “Alcohol Misuse Across the Life Span: Insights From Developmental Studies in Behavior Genetics” by Jeanne E. Savage, Elizabeth C. Long, Sally I-Chun Kuo, Megan E. Cooke, Jinni Su, Peter B. Barr, and Jessica E. Salvatore from Policy Insights from the Behavioral and Brain Sciences.