I have often wondered why addictions, such as alcoholism, do not receive the same sympathy afforded to other disorders. The stigma surrounding addiction tends to place blame solely on the individual, viewing them as morally deficient or lacking the willpower and resilience to overcome their struggles. During my studies in Psychology, I learned about the neurobiological and genetic predispositions that contribute to alcohol addiction, which reinforced my understanding of the issue. Let us delve deeper into why the disease model should represent alcoholism and examine the limitations of the character flaw model.
The Disease Model vs the Character Flaw Model for Alcoholism
The Disease Model defines alcoholism as a brain disorder, linking it to neurobiological changes that arise from chronic alcohol consumption. Both genetic and environmental factors significantly contribute to an individual’s predisposition to addiction. Once addiction takes root, it disrupts self-regulation, making it exceedingly difficult to quit, even for those with strong willpower (Carson, 2025). In contrast, the character flaw model perceives alcoholism as a voluntary behavior stemming from inadequate self-control, implying that individuals could stop drinking if they simply exercised greater willpower or possessed better morals (Carson, 2025). This stigmatizing view of addiction, framing it as a “flawed character,” may be intended to inspire change, but it often serves to worsen the issue.
Why is the Character Flaw Model Flawed?
The idea that addiction is solely a result of a person’s willpower and that it should be easy to resist is misleading. If that were the case, people with severe addictions would find it easier to quit. However, psychological studies indicate otherwise. Many alcoholics report failed attempts to stop drinking despite facing severe consequences, suggesting that their struggles are more aligned with a compulsive disorder than a simple matter of choice (Leshner, 1997). Additionally, social and behavioral conditioning plays a significant role; alcohol consumption is integrated into various cultures worldwide (Carson, 2025). Behavioral conditioning can lead to cravings triggered by cues, such as being in a bar or experiencing stress, undermining the notion of purely voluntary behavior (Robinson & Berridge, 2003).
Neurobiological Changes Support the Disease Model
Research shows that alcohol consumption leads to dopamine dysregulation. Alcohol increases dopamine release in the nucleus accumbens, reinforcing addictive behavior. Over time, the brain’s reward system becomes less responsive to natural rewards, making alcohol the primary motivator (Volkow et al., 2016). In chronic alcoholics, the prefrontal cortex, which is responsible for self-control and decision-making, tends to shrink, reducing their ability to resist cravings (Goldstein & Volkow, 2011). Continued alcohol use can result in neuroadaptation, which leads to tolerance and withdrawal symptoms, indicating physiological dependence (Koob & Volkow, 2016).
Genetic and Physiological Factors Support the Disease Model
Research indicates that genetic factors contribute to alcohol consumption (Hooley et al., 2019). Twin and adoption studies estimate that genetics account for 40-60% of the risk for alcoholism (Prescott & Kendler, 1999). There are also observable physiological differences in the brains of certain individuals; those with naturally lower availability of dopamine receptors are more susceptible to addiction (Volkow et al., 2006).
Conclusion
While personal responsibility is a significant aspect of recovery, the disease model provides a more comprehensive understanding of alcoholism. It reduces stigma, encourages people to seek treatment, and aligns with scientific insights regarding brain changes. This model acknowledges the brain’s alterations and supports genetic and neurochemical evidence, explaining why willpower alone often fails in the context of addiction. It reframes addiction as a chronic, relapsing brain condition rather than a moral failing, fostering a more compassionate and effective approach to recovery (Wallace, 1990).
References
Carson, S. H. (2025, July 18). Psychopathology [lecture recording], Canvas. https://canvas.harvard.edu/
Hooley, J. M., Butcher, J. N., Nock, M., & Mineka, S. (2019). Abnormal psychology (18th ed.). Pearson.
Leshner AI. Addiction is a brain disease, and it matters. Science. 1997 Oct 3;278(5335):45-7. doi: 10.1126/science.278.5335.45. https://pubmed.ncbi.nlm.nih.gov/9311924/
Robinson, T. E., & Berridge, K. C. (2003). Addiction. Annual Review of Psychology, 54, 25-53. https://doi.org/10.1146/annurev.psych.54.101601.145237
Volkow ND, Koob GF, McLellan AT. Neurobiologic Advances from the Brain Disease Model of Addiction. N Engl J Med. 2016 Jan 28;374(4):363-71. doi: 10.1056/NEJMra1511480. https://pubmed.ncbi.nlm.nih.gov/26816013/
Goldstein RZ, Volkow ND. Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications. Nat Rev Neurosci. 2011 Oct 20;12(11):652-69. doi: 10.1038/nrn3119. https://pubmed.ncbi.nlm.nih.gov/22011681/
Koob GF, Volkow ND. Neurobiology of addiction: a neurocircuitry analysis. Lancet Psychiatry. 2016 Aug;3(8):760-773. doi: 10.1016/S2215-0366(16)00104-8. https://pubmed.ncbi.nlm.nih.gov/27475769/
Prescott CA, Kendler KS. Genetic and environmental contributions to alcohol abuse and dependence in a population-based sample of male twins. Am J Psychiatry. 1999 Jan;156(1):34-40. doi: 10.1176/ajp.156.1.34. https://pubmed.ncbi.nlm.nih.gov/9892295/
Volkow ND, Wang GJ, Telang F, Fowler JS, Logan J, Childress AR, Jayne M, Ma Y, Wong C. Cocaine cues and dopamine in dorsal striatum: mechanism of craving in cocaine addiction. J Neurosci. 2006 Jun 14;26(24):6583-8. doi: 10.1523/JNEUROSCI.1544-06.2006. https://pubmed.ncbi.nlm.nih.gov/16775146/
Wallace J. The new disease model of alcoholism. West J Med. 1990 May;152(5):502-5. https://pmc.ncbi.nlm.nih.gov/articles/PMC1002402/