Long before the human genome was sequenced, and in the decades preceding current imaging technology, the association between Major Depressive Disorder (MDD) and Alcohol Dependence (AD) was assumed by most psychiatrists and psychologists. But not how you might think. AD and all SUDs were thought of as “secondary conditions” resulting from untreated depression, unresolved psychodynamic conflicts or trauma that could be treated by intensive psychotherapy, psychoanalysis, electroconvulsive therapy, and then the cognitive therapies including client-centered therapy. All designed to untangle or unlock the secrets behind the individual’s obsession with alcohol or drugs and their seemingly incontrollable compulsion to intoxicate.

By the late 60s, the nature and effects of alcoholism was being taught to physicians, not in medical school, but by patients in recovery. Thankfully, enlightened and often humbled doctors observed the success of a handful of treatment programs based on the 12-steps of AA. The idea that AD was a “primary” disorder was a radical departure from the medical community’s pedagogy, but not to the millions of persons who attained recovery, most without the benefit of trained physicians.

Understanding Alcoholism and Depression

Today, we understand the primary nature of SUDs and are still learning the pathophysiology, but the etiology remains most elusive. Certainly depression, in all its manifestations, is not uncommon among persons with SUD. Instead of arguing about the chicken or the egg, enlightened medical professionals understand that addiction and psychiatric disease often co-occur, as many chronic conditions do. Yet treatment has not kept up with the research, and therefore, often does not adequately address both conditions. Clinicians, depending on their training will treat the alcohol dependence, or the major depressive disorder, but seldom both. While it has been observed that treating AD may degrade the symptoms of MDD, or dysthymia in some persons, post-treatment surveys suggest that untreated or undertreated depression is a cause of relapse.

Understanding the common genetic and the functional neurobiology that influence the onset of MDD and AD may help change clinical practice and training bias. Adoption studies with family members and monozygotic twins have shed light on this issue. Association analyses (Rogers, et al 2017) were reviewed between MDD polygenic risk score (PRS) and AD case-control status. Genome-wide association study (GWAS) data sets were collected from 1.) Collaborative Study on the Genetics of Alcoholism (COGA), 2.) The Study of Addiction, Genetics, and Environment (SAGE), 3.) The Yale-Penn genetic study of substance dependence, and 4.) The National Health and Resilience in Veterans Study (NHRVS). From these data, meta-analysis of 9,240 patients with MDD and 9,519 controls from the Psychiatric Genomics Consortium were applied to calculate PRS at thresholds from P < .05 to P ≤ .99 in each AD, GWAS data set.

The results from this well-designed and well-powered analysis support previous evidence that common vulnerabilities exist for depression and SUDs. The results confirm what many clinicians have observed, SUDs can cause depression and depression increases the risk for SUDs. Individuals with elevated polygenic risk for MDD are more likely to develop AD.

Why Does This Matter?

It should not concern clinicians which condition came first—and genetically-speaking, the risk factors were most likely present in utero. Therefore, SUD professionals should thoroughly screen, and when necessary, aggressively treat co-occurring depression. In addition, continuous monitoring of both conditions is absolutely necessary in preventing relapse.