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Constructin Addiction as a Brain Disease

1954 words (8 pages) Essay in Health

08/02/20 Health Reference this

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Throughout history addictions in the USA and Canada have been understood and approached in many different ways: The Moral model (addiction as a character flaw or moral failing); Choice model (addiction as a choice however harmful the behaviour); Psychosocial model (addiction as “an expression of social factors involving class, cultural, and socioeconomic processes” (Barnett et al, 2018 p. 678)). The last model, and what will be the focus of this paper, is the medical model, understanding addiction as a disease of the brain. What defines an addiction, and its causes, are greatly questioned with a lack of agreement between addiction experts (Fraser et al., 2017). 

Evidence for the Brain Disease Model

In 1997, the director of the US National Institute on Drug Abuse (NIDA), Alan Leshner, published an article which claimed addiction was best conceived of as a chronic, relapsing, brain disease (Leshner, 1997; Hall, Carter, Forlini, 2015). This article is understood to be a point in which BDMA really took hold but if we go back as far as the 17th century we can find ideas about BDMA and see how it gained in popularity in the mid-20th century (Barnett et al, 2018). This is, of course, in the context of the US and Canada; other countries, such as Finland and Sweden, drug and alcohol issues have been, and are, considered as social problems (Barnett et al, 2018).

In his report Leshner (1997) stated that while drug use is initially voluntary based, research has shown, with animal experiments, that chronic drugs use changes neurochemicals in the brain, creating a situation that it is very challenging for a person using drugs to discontinue use and explains why there is a high occurrence of relapse rates (Leshner, 1997; Hall, Carter, Forlini, 2015).

Neuroscience research, and the medical model, help to promote new opportunities of the treatment and prevention of substance addictions (Barnett et al, 2018; Hall, Carter, Forlini, 2015; Leshner, 1997), further information on behavioural addictions, and increase our understanding of biological processes comprised in voluntary behavioural control (Volkow et. al, 2016). This model also challenges the moral model and its entrenched values that assume addiction is a voluntary act of a person who is weak in character (Barnett et al, 2018; Volkow et. al, 2016). The mainstream medical model is a much more compassionate way of thinking, than addiction as a moral failure; we deal with bad decisions with punishment, however we, supposedly, do not punish people for the bad genetics they inherited, we offer them a chance in treatment.

Those who are proponents of BDMA state this furthers the destigmatizing of addiction by helping to dampen “the moral judgment attached to addictive behaviors of the individual, and foster more scientific and public health–oriented approaches to prevention and treatment” (Volkow et. al, 2016, p. 368). Looking at addictions with a BDMA lens also helps to find medical intervention to reduce craving which can decreases someone’s discomfort during the withdrawal phase and help to prevent relapse; it can help scientists legitimize research and ask for funding, which can in turn help to increase the number of researchers looking at addiction from this stand point (Hammer et al., 2013).

Such research has found links to drug use and the desensitization of reward circuits in the brain, which have a hindering effect on a person’s ability to feel pleasure and motivation from everyday activities; the increased force of “conditioned response and stress reactivity”, result in an increase in cravings for alcohol and other drugs, as well as “negative emotions when these cravings are not sated and the weakening of the brain regions involved in executive functions such as decision making, inhibitory control, and self-regulation that leads to repeated relapse” (Volkow et. al, 2016, p. 368).

Chronic drug use has been attributed to substantial changes in the body and brain on all levels: molecular, cellular, structural, and functional (Leshner, 1997). A brain that is addicted has been found to be specifically different from the non-addicted brain, “as manifested by changes in brain metabolic activity, receptor availability, gene expression, and responsiveness to environmental cues” (Leshner, 1997, p. 46). It is these changes to the brain that are seen to promote addiction as a brain disease (Leshner, 1997).

Addiction is not often an acute illness, as for most people, addiction is a chronic and relapsing disorder (Leshner, 1997). It is rare that after one period of treatment, a person will be able to abstain from the drug or behaviour for the rest of their lives (Leshner, 1997). Relapse rates for addictions have been found to be similar to other chronic illnesses such as Asthma, Hypertension, and Type 1 Diabetes (Zawertailo, 2018 p. 27). This is why those for the BDMA, state that addiction should be approached like any other chronic illness instead of an acute illness. As with “the case in other medical conditions in which voluntary, unhealthful behaviors contribute to disease progression (e.g., heart disease, diabetes, chronic pain, and lung cancer), evidence-based interventions aimed at prevention, along with appropriate public health policies, are the most effective ways of changing outcomes” (Volkow et. al 2016, p. 368). And these interventions come from the medical model and focus on changes in the brain. 

Criticism of the Brain Disease Model of Addiction.

Those who are critics of BDMA, claim that the BDMA does not give the full picture of addictions, especially leaving out the important effects of early childhood trauma on the brain, as well as historical, biopsychosocial conditions that leave a person more vulnerable to addictions (Maté, 2008). When focusing on the biological aspect of addiction it is easy to lose focus of other factors within someone’s life that helped create the addiction or helps to perpetuate the addiction and behaviour. As well as creating a situation in which policy makers focus on medical solutions to social problems and neglect public health population-based policies that have been proven to work in the past, such as higher taxes on cigarettes and alcohol, as well as restrictions on advertising of tobacco and alcohol and location in which people can smoke (Barnett et al, 2018; Hall, Carter, Forlini, 2015).

Maté (2008) states that while he thinks addiction is a brain disease, it is not the type described above and he questions to origin of the brain disease. Whereas, the research on BDMA focuses on the changes that occur within the brain after long term drug use, Maté (2008) and others (Dube et al., 2003; Enoch, 2011; Lewis, 2017; Lindberg, & Zeid, 2017; Racine, Sattler, & Escande, 2017) look at how the brain develops in interaction with the environment a child grows up in and how that impacts the development of addiction.  Evidence has been found to link stress early in life and substance use later in life (Lindberg, & Zeid, 2017) and many studies have found a correlation between early trauma and the occurrence of substance use disorders in adulthood (Lindberg, & Zeid, 2017; SAMHSA, 2016), especially when using the Adverse Childhood Events (ACE) questionnaire (Dube et al., 2003).

Lewis (2017) states that BDMA is flawed because the changes in the brain observed when a person has an addiction are close to what is “generally observed when recurrent, highly motivated goal seeking results in the development of deep habits, Pavlovian learning, and prefrontal disengagement” (p. 7). Other studies “do not show whether addiction is a cause or a consequence of differences in brain structure and function or some combination of the two” (Hall, Carter, Forlini, 2015, p.107).

Other criticisms of the BDMA are: other experiments with rats BDMA show differences in results, such as when put in enriched environments rats have different patterns of drug self-administration after a stressful event and some rats were found to abstain from drugs when given the choice of natural rewards (such as food or pair bonding) (Hall, Carter, Forlini, 2015); Recreational drug users respond to small changes in personal situations and some people recover without treatment (Hall, Carter, Forlini, 2015); And also unlike other diseases there is a lack of molecular diagnosis for addiction (Hammer et al., 2013).

Hammer et al. (2013) state that we must be aware that depicting addiction as a disease does not mean it is seen as neutral, as how a disease is understood is part of our cultural and societal outlook (Acker, 2010) and is constructed by both social and biological features. As we have seen with the changes in the DSM over the years, what is pathologized changes with time and knowledge. This brings us to another criticisms which is that currently in the DSM 5 addiction is characterized by behavioral criteria, not biological creating a confusing space where we diagnosis one as having a substance use disorder by their actions, and how these behaviour impacts their lives, yet under the BDMA focus treatments on the changes in the brain.

Conclusion. This paper has discussed both the evidence for and criticisms against BDMA and the possible impacts that the BDMA has on policy, treatment, and recovery. Between all of this it is important to remember that addiction is a “complex biological, psychological, and social disorder that needs to be addressed by various clinical and public health approaches” (Hall, Carter, Forlini, 2015) and research from all disciplines are needed to help provide insights to decrease the harm of drug misuse.

References

  • Acker, C. J. 2010. How crack found a niche in the American ghetto. Biosocieties 5(1): 70–88.
  • Barnett, A. I., Hall, W., Fry, C. L., Dilkes‐Frayne, E., & Carter, A. (2018). Drug and alcohol treatment providers’ views about the disease model of addiction and its impact on clinical practice: A systematic review. Drug and alcohol review, 37(6), 697-720.
  • Dube, S. R., Felitti, V. J., Dong, M., Chapman, D. P., Giles, W. H., & Anda, R. F. (2003). Childhood abuse, neglect, and household dysfunction and the risk of illicit drug use: the adverse childhood experiences study. Pediatrics, 111(3), 564-572.
  • Enoch, M. (2011). The role of early life stress as a predictor for alcohol and drug dependence. Psychopharmacology, 214(1), 17–31.
  • Fraser, S., Pienaar, K., Dilkes-Frayne, E., Moore, D., Kokanovic, R., Treloar, C., & Dunlop, A. (2017). Addiction stigma and the biopolitics of liberal modernity: A qualitative analysis. International Journal of Drug Policy, 44, 192-201.
  • Hammer, R., Dingel, M., Ostergren, J., Partridge, B., McCormick, J., & Koenig, B. A. (2013). Addiction: Current criticism of the brain disease paradigm. AJOB Neuroscience, 4(3), 27-32.
  • Hall, W., Carter, A., & Forlini, C. (2015). The brain disease model of addiction: is it supported by the evidence and has it delivered on its promises?. The Lancet Psychiatry, 2(1), 105-110.
  • Leshner, A. I. (1997). Addiction is a brain disease, and it matters. Science, 278(5335), 45-47.
  • Lewis, M. (2017). Addiction and the brain: development, not disease. Neuroethics, 10(1), 7-18.
  • Lindberg, M. A., & Zeid, D. (2017). Interactive pathways to substance abuse. Addictive behaviors, 66, 76-82.
  • Maté, G. (2008). In the realm of hungry ghosts. Toronto: Vintage Canada.
  • Racine, E., Sattler, S., & Escande, A. (2017). Free will and the brain disease model of addiction: The not so seductive allure of neuroscience and its modest impact on the attribution of free will to people with an addiction. Frontiers in psychology, 8, 1850.
  • Substance Abuse and Mental Health Services Administration. (2016). 2015 National Survey on Drug Use and Health.
  • Volkow, N. D., Koob, G. F., & McLellan, A. T. (2016). Neurobiologic advances from the brain disease model of addiction. New England Journal of Medicine, 374(4), 363-371.
  • Zawertailo, L. (2018). The Nature of Drug Addiction [PowerPoint presentation].
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