Evaluation of the Brain Disease Model of Addiction (BDMA)

Critically evaluate the disease model of addiction and how people may differ in their vulnerability for substance use in relation to genetic, environmental, social and developmental factors.

Brain Disease Model of Addiction

The Brain Disease Model of Addiction (BDMA) states that addiction is a brain disease characterised by altered brain structure and functioning. It is a biological and chemical issue that has genetic and environmental origins. The medical community has projected that since addiction is a brain disease, treatment is needed for the addict to recover from their disease. Addiction does not discriminate, it can affect anyone because the substance is highly addictive.

The American National Institute on Drug Abuse (2008) defines addiction as “A chronic, relapsing brain disease characterised by compulsive drug seeking and use, despite harmful consequences.”.  This biological perspective aimed to eradicate the stigma and negative connotations associated with using drugs (Seear 2017), however, evidence shows that the BDMA has only increased the stigma, leaving addict more vulnerable and marginalised than ever before (Heather 2017). Critics believe that classifying an addict as someone suffering from a disease allows them to play the victim and not take responsibility of their actions. Critics also believe that this encourages relapse. However, others argue that the addict must accept responsibility for their actions in order to get proper treatment in order to recover, therefore they are not playing a victim at all. The BDMA implies that since addictions is a disease, one can go into remission but will always be an addict. This theory has been disproved by neuroimaging research. Neuroplasticity is the ability of the brain to change throughout a person’s life. Neurons can compensate for injury and disease and change in response to this.

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In 1997, Leshner argued that drug use is initially voluntary, but he used his animal studies to prove that chronic drug use essentially turned on a neurochemical switch in the brain that made it extremely difficult for addicted people to stop using drugs. This explains the high number of addicts that relapse after receiving treatment for addiction. Leshner has since conducted multiple neuroimaging studies of addicts, which conclude that drug use ‘hijacks’ the brains reward system, thus proving addiction is a disease. Leading critics of the BDMA challenge this claim that addiction is a chromic and relapsing disease by citing epidemiological evidence that many addicts recover without ever receiving treatment. It has also been found that most people who meet diagnostic criteria for dependence in epidemiological surveys are not drug dependent at the time of the interview, and have, in fact, stopped using drugs many years before. (Heyman 2009).

It has been argued that the high rates of recovery following the BDMA is due to the varying severity of addiction (Suliman 2010). Suliman argued that addicts with less severe addictions are most likely to recover

There are multiple things that make someone vulnerable when it comes to using drugs. These include genetic, environmental, social and developmental factors.

Genetic predisposition

Twin studies indicate that genetic factors make a significant contribution in developing an addiction. (20). It has been found that the heritability of alcohol, nicotine and cannabis dependence range between 40% and 60% (Ball 2008). Genome Wide Association Studies have found substantial links between genetic markers and addiction risk. It has also been found that there are risk alleles that influence drug metabolism and have an effect of the mesolimbic reward system. This is proof that addiction is the consequence of extensive drug use acting n the brains of genetically vulnerable individuals (Kendler et al 2012).

However, some people suggest that addiction is not a disorder that is limited to people who possess an ‘addiction gene’. A high number of alleles are involved in the genetic susceptibility to addiction, but individually these alleles very weakly predict addiction risk (Satel 2013).  Hall (2008) found that genetic risk scores based combinations of multiple risk alleles do predict addiction risk, but no better that family history. Roberts et al (2012) Argues that it is near impossible to predict who will develop an addiction , even when using whole genome sequencing information

Environmental and social factors also raise one’s risk of addiction. Lack of parental involvement has been found to lead to a greater risk-taking or experimentation with drugs. People who experience abuse and neglect from parents are also found to be more vulnerable to drug abuse, using drugs and alcohol to cope with their emotions. Social factors such as peer pressure and social media is another thing that makes people vulnerable to addiction. Pressure from friends to fit in and the need to belong and feel connected to like minded people is a strong factor in the maintenance of addiction (Jaffe 2018).

Often, underlying mental health difficulties contribute to addiction.

Childhood trauma has been strongly linked to addiction. The National Institute of Health reported that more than one third of children who report abuse or trauma, have a substance abuse problem before their eighteenth birthday. In addition, it has been revealed that 55% to 60% of post-traumatic stress disorder sufferer develop some form of addiction during their lifetime.

References

• Leshner A. Addiction is a brain disease, and it matters. Science 1997; 278:45-47.
• 2.  Dackis C, O'Brien C. Neurobiology of addiction: treatment and public policy ramifications. Nat Neurosci 2005; 8:1431-36
• Leshner A. Addiction is a brain disease, and it matters. Science 1997; 278:45-47.
• Dackis C, O'Brien C. Neurobiology of addiction: treatment and public policy ramifications. Nat Neurosci 2005; 8:1431-36
• Satel  S,  Lilienfeld  S.  Brainwashed:  the  seductive  appeal  of  mindless neuroscience. New York: Perseus Books Group, 2013. 23.  Heyman  G.  Addiction:  a  disorder  of  choice.  Cambridge,  MA:  Harvard University Press, 2009.
• 24.  Kincaid H,  Sullivan J.  Medical models  of  addiction.  In:  Ross  D,  Kincaid H, Spurrett  D,  Collins P,  eds.  What is addiction?  Cambridge,  MA:  MIT, 2010: 353.
• Satel  S,  Lilienfeld  S.  Brainwashed:  the  seductive  appeal  of  mindless neuroscience. New York: Perseus Books Group, 2013.
• Heyman  G.  Addiction:  a  disorder  of  choice.  Cambridge,  MA:  Harvard University Press, 2009.
• Kincaid H,  Sullivan J.  Medical models  of  addiction.  In:  Ross  D,  Kincaid H,
• Spurrett  D,  Collins P,  eds.  What is addiction?  Cambridge,  MA:  MIT, 2010:353.
• Ball D. Addiction science and its genetics. Addiction 2008; 103:360-7.
• Kendler  K,  Chen  X,  Dick  D,  et  al.  Recent  advances  in  the  genetic epidemiology and molecular genetics of substance use disorders. Nat Neurosci 2012; 15:181-89
• Satel  S,  Lilienfeld  S.  Brainwashed:  the  seductive  appeal  of  mindless neuroscience. New York: Perseus Books Group, 2013.
• Satel  S,  Lilienfeld  S.  Brainwashed:  the  seductive  appeal  of  mindless neuroscience. New York: Perseus Books Group, 2013.
• ncbi.nlm.nih.gov – Behavioural consequences of child abuse.