Breaking the Broken Brain Model of Addiction
Brenna McMannon
Illustrations by: Sophie Sieckmann
What comes to mind when you hear the word “broken?” A broken bone, a broken heart, broken trust? We use the word in many different ways. What about a broken brain? The brain is an incredibly complex and malleable part of us, so is it even possible to break it? And why is this term used to talk about addiction? Addiction has shrugged off much of its original stigma as new studies have demonstrated its base in neuroscience. But understanding addiction means going beyond a purely neurological classification. While addictive behavior does correlate to neurological mechanisms, these processes are greatly influenced by one’s environment, mental health, stress levels, and developmental factors.
The molecules that form the basis of all brain function are known as neurotransmitters, which are chemical compounds that allow neurons (nerve cells) to send messages to each other. Dopamine is a neurotransmitter that is most active in the brain when modulating reward and addiction. Known as the “feel good” neurotransmitter, dopamine is released by the brain when you are having a pleasurable experience, such as eating your favorite meal or spending time with your favorite person. We even see this in rodents: they will consume alcohol because it increases their dopamine release [16]. Because dopamine plays a critical role in reward, it also plays a crucial role in addiction.
In order to fully understand the neurological side of addiction, we need to take a closer look at how dopamine is involved in reward processing in the brain. The area of the brain that is implicated the most in addiction is the nucleus accumbens (NAc), which is the center of the reward-related learning system. In this system, reward related-stimuli are sent as signals from the limbic system and converge in the NAc to be processed for motor functioning of the reward behavior [18]. Put more simply, your hand reaches for the cookie because you know it is going to be a pleasurable experience to eat the cookie. The NAc receives information from dopamine neurons in the ventral tegmental area of the brain (VTA). This is an important connection because most drugs of abuse modulate dopamine-based activity in the VTA, where neurons then send signals to the NAc. In other words, the more that a person’s behaviors engage the dopamine neurons in the VTA, the more that the NAc is going to be activated. Drugs of abuse tend to activate dopaminergic neurons in the VTA, triggering the reward pathway more frequently and making it more susceptible to stimulation. Over time, disruption of this pathway can result in the changes of motivated physical behaviors characteristic of addiction. Certain situations may trigger the reward pathway more, causing the physical action of the addictive behavior to occur more often. In the brain, these consequent motor functions are carried out through NAc activation and subsequent passing of information to the motor cortex, generating physical behaviors [3]. Addiction behavior is very much reward-based, which makes the reward pathway crucial to understanding the workings of addiction. In other words, if something makes you feel good, you will likely want to do it again.
Currently, many people accept the disease model, also known as the “broken brain” model, which focuses on the neurological mechanisms and effects of addiction-based behavior. This model uses a completely disease-based approach without acknowledging environmental and developmental factors that contribute to the learning of addictive behavior. Addiction research tends to hone in on dopamine signaling in the NAc because addiction tends to be correlated with disruptions in the reward circuit in the VTA and NAc regions of the brain [13]. Studies have shown that changes in neurotransmitter functions, specifically in dopamine circuits, contribute to abnormal brain function and increased addictive behavior [12]. In other words, the reward system works at the molecular level to affect changes in behavior Additionally, there is no evidence to suggest that there is only one part of the brain that is “broken” and causes someone to become an addict [18]. Although all of these are scientific claims, they only show us how the brain changes in response to learned addictive behaviors. The brain is incredibly plastic, meaning that it can change throughout your lifetime in response to experiences and the environment. Since addiction behavior is learned over time, the brain adapts and changes in response to learned behaviors. It is possible to acknowledge the science behind the disease model without dismissing it as the sole determinant of addiction.
Addiction is not purely a neurological disease, and we must change how we think about the development of addictive behavior. In her book, Unbroken Brain, Maia Szalavitz emphasizes the importance of recognizing addiction as a learned behavior. Szalavitz characterizes addiction as a developmental disorder rather than a neurological disease, defining it as a “learned relationship between the timing and pattern of the exposure to substances or other potentially addictive experiences and a person’s predispositions, cultural and physical environment, and social and emotional needs” [11]. In other words, you are not born destined to develop addictive behavioral patterns because your brain is not prewired with addictive tendencies. With this definition, Szalavitz rejects the notion of an “addictive personality,” asserting that the process of becoming addicted is much more complex and is rooted in the person’s individual, social, and cultural development.
Unfortunately, many do not understand the depth and complexity of addiction. Because people only see the external result of this learned behavior, they often assume that substance abuse is a personal and moral failure. In doing so, they fail to account for other factors –– such as a traumatic childhood or being bullied at school –– and make harmful assumptions about those who are struggling [17].
To make matters worse, while drug policies in the U.S. may cause people to feel like action is being taken, these policies fail to address the real problem at hand: the original afflictions that led people to seek refuge in drugs in the first place [11]. Consider the “War on Drugs” enacted by President Nixon in the 1970s, which set a precedent for the intense criminalization of drugs in the future and further damaged society’s relationship with addiction. These policies framed substance use disorders as criminal and the people who struggled with them as morally inept. This mindset preceded years of harmful drug policies that disproportionately impacted and continue to affect the vulnerable and low-income communities that they should be working to serve. Because individuals within these communities frequently face stressful situations, they are more prone to resort to substances in search of an escape. Furthermore, it has been shown that increased stress levels are associated with a higher risk of developing a substance use disorder [2]. We know that high levels of stress hormones can cause damage to the hippocampus, a brain structure that plays a prominent role in learning and memory [10]. The hippocampus has also been found to play a role in the development of mood disorders [9]. Therefore, experiencing higher levels of stress puts people at higher risk of developing mental disorders. Because of this, we cannot apply the same substance abuse rehabilitation treatment offered in wealthy areas to people with a lower socioeconomic status. We, as a society, cannot create a “one size fits all” solution. Different environments invite different risk factors; lower socioeconomic status is correlated with increased risk of developing addictive behavior [2]. It doesn’t make sense to enforce a policy without thoroughly comprehending and addressing the root causes of the issue; this is akin to slapping a bandaid on an internal wound. It’s not going to stop the bleeding.
Understanding addiction is also important for college-age students, as the majority of people who develop substance-use addictions do so in their early to mid-twenties when they are going through big life changes, like moving out of their childhood home or going to college [5]. In fact, 90% of all substance use addiction begins in adolescence [4]. On the molecular level, dopamine may also play a role in this age-dependent vulnerability. There is evidence that the risk-taking and unpredictable behavior associated with adolescence is due, in part, to dopamine overactivity in the brain [15]. Young adults may experience higher levels of other mental health afflictions, like depression, anxiety, and acute or chronic stress, which puts them at a higher risk for developing addictive behavior [6]. The prevalence of mental health disorders is an important factor to consider in the learning of addiction and its neural mechanisms.
The overlap of addiction and other mental problems is called comorbidity, and it turns out to be fairly common. In fact, 32% of people with a substance use disorder also have a major depressive disorder (MDD), and their overall risk of relapsing is increased because of this comorbidity [18]. Scientists believe that the comorbidity between depression and substance use disorders is due to parallel mechanisms involving dopamine in response to stress. Specifically, they may share a common pathway through the nucleus accumbens [18]. Further studies have found similar brain imaging results and common changes in stress responses in people with MDD and substance use disorder [1]. Depression and substance use disorders are dangerously linked, increasing the risks of each of them when combined [18]. The interconnectedness of addiction and mood disorders, specifically depression, is an important example of how dangerous it is to oversimplify the mechanisms of addiction.
Another oversimplification would be to claim that physiological changes are the only qualifiers of disease. Scientists that support the disease model base their argument on the physiological changes observed in the brains of people with addictive behaviors. They use tissue damage in the brain as evidence for the model, claiming that it is specifically caused by drug use and increases compulsive behavior [14]. Therefore, the disease model argument is based simply on the premise that addiction changes the brain. However, this claim cannot be fully discredited; it is just not the whole story. In fact, the brain changes all the time; it’s called neuroplasticity.
In order to fully understand how addiction is learned, we must look deeper into developmental and environmental factors and how they affect neuroplasticity. The brain is made up of billions of synapses, or neural connections, that are all interconnected and make us who we are. This synaptic web is also incredibly sensitive to our environment and individual experiences and undergoes structural changes in response to events and behaviors. Over time, the synaptic pathways that we use more frequently become more prominent and sensitive when they are repeatedly activated [7]. These pathways become more solidified and less subject to change, usually as a result of learning and repeated behavior or thought. This process of synaptic strengthening is responsible for much of the neuroplasticity that occurs in the brain. In other words, doing something more often makes the behavior easier and easier because the brain has essentially “carved out” and solidified this neural pathway.
Our experiences throughout life change the way the neurons in our brain fire, making us more or less likely to engage in risky behaviors in the future. As discussed before, people living in stressful environments are at higher risk of engaging in addictive behaviors in the future. This is because the connections in their brains have been changed over time based on their experiences and environment. For this reason, addiction behavior is learned, and as with all habits, it is hard to break [7]. The synaptic connections in the reward pathway strengthen through repetitions of the behavior, making it easier to activate the reward pathway.
The disease model claims that addictive behavior causes changes and damage to the brain, while the development model claims that these changes are actually a result of the learned behavior. Yes, the brain does undergo physical changes because of addiction. But the brain is always changing [8]. There are so many different factors that are responsible for someone developing a substance use disorder. Different environmental factors make people more vulnerable to depression and stress, which cause their brains to be more susceptible to engaging in addictive behavior. Over time, this behavior becomes learned and the reward pathway in the brain becomes strengthened. It takes less stimulation for dopamine neurons in the VTA to be activated and send signals to the nucleus accumbens, generating the addictive behavior.
Although we know that addictive behavior is learned and strengthened through neural pathways in the brain, we should still reject the purely neurological disease classification. Addiction doesn’t change the way the brain works in the same way that diabetes changes the way the pancreas works [7]. Your brain has been adapting and changing your entire life; it is designed to change. Yes, the brain is a complex structure and there is much that we still do not know, but we know how behaviors are learned and we know that it is not because something is “broken.”
The disease model would like you to think that addiction is just like any other disease, because something broken simply needs to be fixed. This couldn’t be further from the truth. In the case of substance use disorders, there is no quick fix; there is no obvious solution. But this is not to say that there is no route for recovery. In fact, there are many rehabilitation methods that work for several people. The key to treatment of addictive behavior is recognizing that each person’s recovery must cater to their unique situation, based on their developmental and environmental conditions. There is no “one size fits all solution.” The more that we learn about addiction, the better we get at developing solutions for people who are struggling. And it is becoming abundantly clear that our society should be more focused on prevention: providing equal opportunities to kids in schools at a young age, making resources available to children living in less than ideal environments, and working to manage and alleviate stress. No one should ever feel broken. This is where it starts.
REFERENCES
1. Brady, K. T., & Sinha, R. (2007). Co-occurring mental and substance use disorders: The neurobiological effects of chronic stress. Focus, 5(2), 229-239. doi:10.1176/foc.5.2.foc229.
2. Compton, W. M., Thomas, Y. F., Stinson, F. S., & Grant, B. F. (2007). Prevalence, correlates, disability, and comorbidity of DSM-IV drug abuse and dependence in the United States. Archives of General Psychiatry, 64(5), 566-576. doi:10.1001/archpsyc.64.5.566.
3. Dafny, N., & Rosenfeld, G. (2017). Neurobiology of drugs of abuse. Conn's Translational Neuroscience, 715-722. doi:10.1016/b978-0-12-802381-5.00052-x
4. Heyman, G. M. (2013). Addiction and choice: Theory and new data. Frontiers in Psychiatry, 4. doi:10.3389/fpsyt.2013.00031.
5. Krohn, M. D., Lizotte, A. J., & Perez, C. M. (1997). The interrelationship between substance use and precocious transitions to adult statuses. Journal of Health and Social Behavior, 38(1), 87-103. doi:10.2307/2955363.
6. Kuo, P., Gardner, C. O., Kendler, K. S., & Prescott, C. A. (2006). The temporal relationship of the onsets of alcohol dependence and major depression: Using a genetically informative study design. Psychological Medicine, 36(8), 1153-1162. doi:10.1017/s0033291706007860.
7. Lewis, M. (2017). Addiction and the brain: Development, not disease. Neuroethics, 10(1), 7-18. doi:10.1007/s12152-016-9293-4.
8. Mcewen, B. S. (2012). The ever-changing brain: Cellular and molecular mechanisms for the effects of stressful experiences. Developmental Neurobiology, 72(6), 878-890. doi:10.1002/dneu.20968.
9. McEwen, B. S., Nasca, C., & Gray, J. D. (2016). Stress effects on neuronal structure: hippocampus, amygdala, and prefrontal cortex. Neuropsychopharmacology, 41(1), 3-23. doi:10.1038/npp.2015.171.
10. Sapolsky, R. M. (1993). Potential behavioral modification of glucocorticoid damage to the hippocampus. Behavioural Brain Research, 57(2), 175-182. doi:10.1016/0166-4328(93)90133-b.
11. Szalavitz, M. (2017). Unbroken brain: A revolutionary new way of understanding addiction. New York: Picador St. Martin's Press.
12. Volkow, N. D., & Li, T. (2004). Drug addiction: The neurobiology of behaviour gone awry. Nature Reviews Neuroscience,5(12), 963-970. doi:10.1038/nrn1539.
13. Volkow, N. D., Michaelides, M., & Baler, R. (2020). The neuroscience of drug reward and addiction. Physiological Reviews, 99(4), 2115-2140. doi:10.1152/physrev.00014.2018.
14. Volkow, Nora D., George F. Koob, and A. Thomas McLellan. (2016). Neurobiologic advances from the brain disease model of addiction. New England Journal of Medicine, 374, 363–371. doi:10.1056/NEJMra1511480.
15. Wahlstrom, D., White, T., & Luciana, M. (2010). Neurobehavioral evidence for changes in dopamine system activity during adolescence. Neuroscience & Behavioral Reviews, 34(5), 631-648. doi:10.1016/j.2009.12.007.
16. Weiss, F., Lorang, M., Koob, G., & Bloom, F. (1993). Oral alcohol self-administration stimulates dopamine release in rat nucleus accumbens: Genetic and motivational determinants. The Journal of Pharmacology and Experimental Therapeutics, 267(1), 250-258. PMID: 8229752
17. Wolke, D., Copeland, W. E., Angold, A., & Costello, E. J. (2013). Impact of bullying in childhood on adult health, wealth, crime, and social outcomes. Psychological Science, 24(10), 1958-1970. doi:10.1177/0956797613481608.
18. Xu, L., Nan, J., & Lan, Y. (2020). The nucleus accumbens: A common target in the comorbidity of depression and addiction. Frontiers in Neural Circuits,14(37). doi:10.3389/fncir.2020.00037.