We have since conducted several studies that have disentangled family history into elements of genetic liability, nurture and density of risk (e.g., References 23, 24, 25). We were also able to examine the risk posed by early initiation of alcohol use on later drinking milestones using several analytic paradigms (e.g., References 29, 30). More recently, our longitudinal design has facilitated characterizations of remission and recovery in AUD (e.g., References 31, 32, 33). A detailed description of these findings is outlined in the accompanying review (2. Sample and Clinical Data). In conclusion, alcoholism is a complex disease influenced by a combination of genetic and environmental factors.
The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) provides eleven criteria, of which at least two must be present over twelve months for an alcoholism diagnosis. Most clinicians use the term “alcohol use disorder” to help emphasize the disease value of the disorder and reduce inhibitions to seek medical help. Starting to drink at an early age and mental illnesses such as anxiety, depression, bipolar disorder, ADHD, and schizophrenia, also put an individual at a higher risk of developing the condition.
However, it should be borne in mind that no matter how sophisticated genetic techniques might become, further advances in detecting genotype – phenotype associations are hampered by the fact that alcoholism is a heterogeneous phenotype. One way around this has been the use of intermediate phenotypes, including electrophysiological and imaging, that reflect mediating factors in behavior and are likely to be influenced by variation at fewer genes. Finally, the diagnostic criteria for the alcoholism phenotype (now called alcohol use disorder (AUD)) have just been radically revised in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) 3.
However, researchers need more information before concluding about alcohol tolerance and CYP2E1. Other genetic factors and environment likely play a bigger role than any single gene in whether or not a person develops AUD. A 2018 study also showed that genetic factors account for 40 to 60 percent of the reasons people develop AUD.14 Since that study, specific genes have been identified that link with the development of the disorder. Until we get there, research will continue focusing on identifying genetic variants and possible mechanisms behind risk.
Psychological, social, and environmental factors also influence the likelihood of developing the addiction. Insight, Not DestinyThe coga project has been structured around families, but this type of research has also strengthened understanding of the relative importance of specific gene variants as risk factors in different ethnic groups. The knowledge that such genes are likely to be influencing dependence in patients belonging to one of these populations is another tool that can be used to assess the nature of an individual’s problem and to tailor treatment accordingly. Family TiesAt coga’s outset, researchers at sites around the country sought to identify families severely affected by alcoholism. Finding the genes involved in our responses to alcohol and understanding their is alcholism genetic effects may thus illuminate a broader array of conditions, too.
No person is guaranteed to develop an addiction, just as nobody drug addiction is completely immune to it. Studies suggests that triggers in your environment can alter the way your genes express themselves—effectively turning genes on or off. What’s even more interesting is that you may be able to partially pass these changes on. Your life experience, and that of your family, may in some ways change your DNA.
Studies have shown that individuals with a family history of alcoholism are at a higher risk of developing the disease themselves. This suggests that genetic factors play a crucial role in the development of alcoholism. It is likely that, as for most complex diseases, alcohol dependence and AUDsare due to variations in hundreds of genes, interacting with different socialenvironments. An additional challenge in the search for genetic variants that affectthe risk for AUDs is that there is extensive clinical heterogeneity among thosemeeting criteria.