Alcoholism: Evidence For The Disease Model

Alcoholism, or alcohol use disorder (AUD), is a complex condition that has been the subject of extensive research and debate. The disease theory of alcoholism proposes that problem drinking is caused by a disease of the brain, involving altered brain structure and function. This theory has been supported by advancements in neuroscience, which have provided evidence of observable brain changes associated with addiction. On the other hand, some critics argue that alcoholism does not adhere to a typical disease model and challenge the effectiveness of standard medical treatments. The disease model has also been criticised for potentially reducing personal responsibility and increasing the likelihood of relapse. Alternative perspectives, such as the biopsychosocial model, consider the interplay of biological, psychological, and sociocultural factors in the development of alcoholism. While the disease model has stimulated research and understanding in various fields, the ongoing debate highlights the need for comprehensive approaches that address the multifaceted nature of alcoholism.

Genetic influences and biological risk factors

Alcoholism, or alcohol dependence, is a complex genetic disease. While there is no single "gene for alcoholism", variations in a large number of genes can affect an individual's risk of developing an alcohol use disorder (AUD). Research suggests that 40% to 60% of people with AUD have genes that increase their risk of developing an addiction. However, having these genes does not guarantee that an individual will develop an AUD.

Genetic factors influence not only the risk of alcohol dependence but also the level of alcohol consumption and the risk for alcohol-associated diseases, including cirrhosis and upper GI cancers. For example, the ADH1B gene has been identified as having a strong effect on the risk for alcoholism. This gene is involved in how the body metabolizes alcohol. Other genes, such as ALDH2, also play a role in alcohol metabolism, and certain variants of this gene can cause a buildup of acetaldehyde when alcohol is consumed, leading to facial flushing, nausea, and tachycardia. The CHNR5, GCKR, and DRD2 genes have also been identified as candidates for being inheritable addiction genes.

In addition to these genetic influences, biological risk factors related to deficiencies in various neurochemicals also play a role in alcoholism. Ethanol, the type of alcohol present in alcoholic beverages, affects the fluidity of cell membrane lipids, leading to membrane dysfunction. It also adversely affects the activity of monoamine oxidase and adenylate cyclase, enzymes that play important roles in the brain's information processing system.

Environmental and social factors also interact with genetic factors to influence the development of alcoholism. For example, individuals who live in an unhealthy environment or experience trauma, especially during childhood, may be more prone to heavy drinking patterns and an increased risk of AUD. The interplay of genetic and environmental factors can also contribute to the development of mental health conditions such as anxiety and depression, which further raise the risk of AUD.

Additionally, epigenetics, the combination of genes and environment, plays a significant role in AUDs. The drinking habits of parents and the pressure to consume alcohol within one's environment can increase the chances of developing alcohol-related issues.

The brain disease model of addiction

Advances in neuroscience have helped us understand how drugs affect the brain, and the brain disease model has contributed to improvements in understanding and treating substance use disorders. This model has led to the development of different medication and non-medication-based treatments that target vulnerable areas of the brain affected by substance use.

Nevertheless, research does not support these criticisms. The brain disease model considers the environment and individual differences in the development of addiction as a brain disease. It acknowledges that addiction is a complex disease with physical, social, and psychological components, and that factors such as unaddressed trauma, family history of drug use, early exposure, exposure to high-risk environments, and certain mental illnesses increase vulnerability to addiction.

While the brain disease model of addiction has its limitations, it has stimulated promising areas of inquiry into addictive behaviors across various fields, including medicine, neurobiology, neuroscience, pharmacology, and the social sciences.

The disease model's critics and counterarguments

The disease model of alcoholism has faced criticism from various physicians, scientists, and addiction experts on logical, empirical, and other grounds. Critics argue that the disease model removes stigma and personal responsibility, which increases alcoholism and drug abuse, and thus the need for treatment. This argument is supported by a study that found a correlation between a stronger belief in the disease theory of alcoholism and a higher commitment to total abstinence, resulting in a higher likelihood of a full-blown relapse.

Some critics, like addiction expert Stanton Peele and alcohol researcher Nick Heather, have authored books intending to disprove the disease model. They argue that the disease model removes personal responsibility, which increases alcoholism.

Another criticism of the disease model is that it implies that problem drinkers are incapable of returning to 'normal' problem-free drinking, and therefore treatment should focus on total abstinence. However, critics have presented evidence of controlled drinking in formerly dependent drinkers to dispute this claim. For example, a 1962 study by Dr. D. L. Davies found that seven out of ninety-three problem drinkers were able to return to "controlled drinking" (less than seven drinks per day for at least seven years).

Critics also argue that alcoholism does not follow the model of a 'disease' and is not amenable to standard medical treatment. Dr. Bankole Johnson, Chairman of the Department of Psychiatry at the University of Virginia, states that many doctors are reluctant to prescribe drugs to treat alcoholism because they believe it is a moral disorder rather than a disease. Furthermore, critics argue that medical research on alcoholism does not support the disease model.

While the disease model of alcoholism has its critics, it is important to note that the American Medical Association (AMA), the largest association of physicians, declared that alcoholism was an illness in 1956. Additionally, the AMA further endorsed the dual classification of alcoholism under both psychiatric and medical sections in 1991.

The family disease model

Codependency is characterised by enabling behaviours that perpetuate substance abuse and shield the addicted individual from the negative consequences of their actions. For example, family members may facilitate access to alcohol, keep the addiction a secret, or provide care and attention when the affected individual is under the influence, while alienating them when they are sober.

The family systems model of addiction, which emerged in the 1970s, shares similarities with the family disease model. However, it views substance use as a means to maintain homeostasis within the family, rather than solely focusing on enabling behaviours. This theory suggests that substance use is initiated or maintained when the addicted individual or the family as a whole is facing developmental or internal difficulties.

While the family disease model has provided a framework for understanding and supporting families affected by alcoholism, it is important to acknowledge the complex interplay of biological, psychological, and sociocultural factors that contribute to alcoholism. Additionally, critics of the disease model argue that it removes personal responsibility, reduces stigma, and may even increase alcoholism and drug abuse.

Furthermore, the medical community has been reluctant to fully embrace the disease model of alcoholism due to conflicting views on the nature of the disease and the effectiveness of standard medical treatments. While some physicians and researchers have rejected the disease model, others have made significant contributions to advancing this understanding. The American Medical Association (AMA) recognised alcoholism as an illness in 1956 and endorsed its dual classification under psychiatric and medical sections in 1991.

The disease model's influence on research and clinical practice

The disease model of alcoholism has had a significant influence on both research and clinical practice. The model proposes that alcoholism is a disease of the brain, characterised by altered brain structure and function, and has stimulated research in various fields, including medicine, neurobiology, neuroscience, pharmacology, and the social sciences.

Neuroscientific research has particularly benefited from the disease model, as it has helped identify observable brain changes associated with addiction. For example, research has shown that ethanol affects the fluidity of cell membrane lipids, leading to membrane dysfunction and impaired control. This has contributed to the understanding of addiction as a chronic brain disorder, similar to other diseases such as diabetes or heart disease. Furthermore, the identification of neural systems and structures changed by alcohol use has facilitated the development of targeted medication and non-medication-based treatments.

The disease model has also influenced clinical practice by shifting the perception of addiction away from a moral failing towards a medical condition. This shift has reduced stigma and encouraged a more compassionate approach to treatment. Additionally, the disease model has emphasised the importance of abstinence in treating alcoholism, although some critics argue that this may not be the only successful approach. The model has also led to a better understanding of the role of genetic and environmental factors in the development of alcoholism, with research indicating that alcoholism is 50-60% genetically determined and 40-50% influenced by environmental factors.

However, the disease model has faced criticism from some experts who argue that it removes personal responsibility and may increase alcoholism by providing a medical explanation. Critics also highlight the importance of psychological and social factors in understanding and treating addiction, which they believe have been overlooked in favour of a solely biological perspective. Nevertheless, the disease model has undoubtedly shaped the current landscape of research and clinical practice related to alcoholism and substance use disorders.

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