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Unraveling the Complex Neuroscientific Explanations for Addiction

Addiction is a widespread and complex brain disorder, having a profound impact on individuals and societies globally. To effectively combat addiction, we must first understand the neurological mechanisms that underlie it. This article focuses on the significant role of dopamine, a neurotransmitter, involved in the development and maintenance of addiction. Dopamine is a neurotransmitter, a type of chemical messenger that transmits signals in the brain. It plays a crucial role in how we feel pleasure, making it a central component in our ability to think, plan, and find things interesting. Dopamine is primarily involved in the brain's reward system, underpinning the sensations of pleasure and reward (Schultz, 2015).

This article acknowledges the foundational role of dopamine, particularly considering the neurotransmitter's crucial role in reward-related processes and decision-making, mechanisms that have evolved under survival and reproductive pressures. Today, these mechanisms can lead us into harmful patterns of behavior in an erroneous pursuit of rewards (Volkow et al., 2017). However, for both pragmatic and epistemic reasons, this article will argue that the primary—if not the only—issue with neurobiology of addiction is its overemphasis on dopamine as the primary driver of addictive behaviors, excluding the essential role of other neurological, environmental, and psychosocial factors that contribute to addiction regardless of dopamine. This disproportionate focus on dopamine risks oversimplifying the complex etiology of addiction and may hinder the development of comprehensive and effective treatment strategies. Hence, it is problematic to hold the view that dopamine alone explains addiction. The main aim of this article is, therefore, to highlight the multifaceted nature of addiction and the contribution of various domains—not just neurobiology—to its understanding and treatment.

In the context of addiction, dopamine takes center stage. It is pivotal in the process of reinforcing rewarding behaviors, which is an essential aspect of survival. However, when substances such as drugs or alcohol artificially stimulate dopamine release, the brain's reward system gets hijacked. The result is a powerful sensation of pleasure or a "high," leading to the repeated use of the substance use to recreate this feeling. Over time, this behavior can lead to addiction (Volkow et al., 2017). The concept of Neurobiology of Addiction (hereafter, ‘NA’) is primarily rooted in the universally accepted premise that human behavior, including addiction, is significantly influenced by neurochemical processes, with dopamine playing a pivotal role (Volkow et al., 2017). This view posits that addictive behaviors and the neurophysiological changes that accompany them reflect fundamental aspects of our neurobiology, which have evolved over time. Of course, understanding the past is often instrumental in making sense of the present, just as understanding our neurobiology can illuminate the complexities of addiction.

Figure 1: Dr. Nora Volkow (National Institute on Drug Abuse, 2022)

Nora Volkow

We will primarily focus on the work of Nora Volkow, a leading authority in the field of addiction neuroscience. Volkow (2017), along with her colleagues, presents a compelling case for the primacy of dopamine in the neurobiology of addiction, arguing that it underlies the rewarding effects of drugs and the compulsion to seek them. This view anchors addiction to the dopamine-driven pursuit of rewards, often to the detriment of the individual.

Although Volkow is a key person in the field of understanding addiction, her theory may not fully capture the complexity of addiction. As such, this article seeks to present evidence from perspectives that do not solely focus on dopamine's role in addiction, including theories that emphasize the importance of other neurobiological, psychological, and environmental factors. These theories should be considered alongside the dopamine-centric view to provide a more nuanced understanding of addiction.

The article first outlines and introduces the NA view, including Volkow's perspective. Volkow's (2017) own explanation of addiction, based solely on dopamine, is then critically examined. The article proceeds to present objections to this perspective and discusses other theories of addiction. In sum, the goal is to illustrate how and why dopamine is not the only player in the complex neurobiology of addiction. Before delving into the core of the article, it is important to note that this piece acknowledges the ongoing debate regarding the precise definitions and use of terms such as 'addiction', 'dependence', and 'substance use disorder'. While this piece recognizes this terminological dispute, it will use these terms interchangeably, as it refers to different perspectives throughout the article.

Figure 2: Trapped individuals (Charity Atakunda, n.d.)

Dopamine's Role in Addiction

The Neurobiology of Addiction (NA) model primarily recognizes the critical role of dopamine in addiction. This neurotransmitter is widely known for its function in the brain's reward system, typically released during pleasurable activities. Nora Volkow and her colleagues have significantly contributed to our understanding of dopamine's role in addiction. They argue that the dopamine surge caused by drug use can "hijack" this reward system, leading to the intense desire and compulsive seeking associated with addiction (Volkow et al., 2017). In this model, drugs and other addictive substances are believed to drastically increase dopamine levels in the brain's reward circuits, far more than natural rewards like food or social interaction. This overstimulation creates a strongly reinforcing pattern: the brain remembers the intense pleasure and wants to repeat it, leading to compulsive drug use.

The brain's reward system, also known as the dopaminergic reward pathway, is a neural circuitry that reinforces behaviors that are essential for survival. This system primarily consists of the ventral tegmental area (VTA), nucleus accumbens (NAc), and prefrontal cortex (PFC), with dopamine serving as the critical neurotransmitter (Schultz, 2015). The VTA, located in the midbrain, is rich in dopamine-producing neurons. When an individual encounters a rewarding stimulus, such as food or a pleasant social interaction, these neurons are activated and release dopamine (Schultz, 2015). The VTA sends dopamine signals primarily to the NAc and PFC, but also to other regions such as the hippocampus and amygdala. The NAc is considered the pleasure center of the brain. Dopamine release in the NAc is associated with the sensation of pleasure. It helps to create a rewarding feeling that motivates the individual to repeat the behavior that led to the dopamine release. This is a crucial aspect of learning and behavior reinforcement. The NAc also plays a significant role in converting motivation into action - it's involved in the planning and execution of motor functions needed to pursue and acquire rewards (Floresco, 2015). The PFC is involved in decision-making and impulse control, among other executive functions. It uses information about rewards, including dopamine signals from the VTA, to help make decisions about which actions to take. Dopamine in the PFC is critical for focusing attention on rewarding stimuli and actions, and for maintaining the motivation to pursue them. It's also important for suppressing behavior towards non-rewarding or punishing stimuli (Volkow et al., 2016).

Figure 3: Dopamine (svtdesign, n.d.)

The initial stages of addiction are primarily characterized by the intense release of dopamine in response to the consumption of addictive substances. Many drugs, such as cocaine, amphetamines, and nicotine, stimulate the release of dopamine, leading to a surge in the nucleus accumbens (NAc), a key component of the reward system. This surge is significantly more substantial than the dopamine release associated with natural rewards, such as food or social interaction, leading to an intense sense of pleasure or euphoria (Volkow et al., 2017). This intense dopamine release strengthens the neural connections associated with drug-taking behavior, facilitating the learning of cues and contexts that predict drug availability. As a result, these cues and contexts can trigger intense cravings even in the absence of the drug, contributing to the compulsive drug-seeking behavior characteristic of addiction (Hyman et al., 2006).

Volkow's model

Volkow's perspective is supported by a wealth of empirical evidence demonstrating that drugs of abuse, such as cocaine and opioids, directly or indirectly increase dopamine levels in the nucleus accumbens (Koob & Volkow, 2010). This increase is much more dramatic than what is seen with natural rewards, contributing to the high addictive potential of these substances. Moreover, dopamine has been implicated in other crucial aspects of addiction, including the development of cravings and relapse. Cravings refer to the intense desire for a drug that individuals experience during abstinence. Relapse, on the other hand, refers to the return to drug use after a period of abstinence. Both are thought to be driven, at least in part, by changes in the dopamine system caused by chronic drug use. Notably, dopamine is also involved in the persistence of drug-seeking behavior despite negative consequences, a hallmark of addiction. Volkow and colleagues (2017) propose that drugs of abuse may interfere with the brain's ability to learn from negative outcomes, partly through their effects on the dopamine system. This may explain why individuals with addiction continue to use drugs even when they are aware of the adverse effects on their health, relationships, and other aspects of their life.

The NA model, with its focus on dopamine, provides a fundamental biological perspective on addiction. It highlights how drugs of abuse can co-opt our natural reward system, leading to the intense desire, compulsive use, and persistent drug-seeking behavior that define addiction.

Figure 4: Help Needed (Agapova, 2022).

The dopamine-centric view of addiction by Volkow, while foundational, may be an oversimplification. It primarily focuses on the biological aspects of addiction, centering almost exclusively on the brain's dopamine pathways. However, addiction is a multifaceted problem that extends beyond biology.

Firstly, not all addictive substances increase dopamine levels in the reward circuits. For instance, benzodiazepines, a class of drugs often misused, primarily act on the GABAergic system, yet they can lead to addiction (Schumann et al., 2019). Moreover, some behaviors that can lead to addiction, like gambling, do not involve substances at all, although they may also involve dopamine in some capacity (Potenza, 2008). Secondly, the dopamine-centric view may not fully account for the progression from casual use to addiction. Many individuals use addictive substances casually without developing an addiction. If dopamine were the sole factor in addiction, we would expect everyone who experiences a dopamine surge from substance use to become addicted, which is not the case (Volkow et al., 2016).

Broadening the Perspective: Other Factors in Addiction

While the Neurobiology of Addiction model, with its focus on dopamine, offers an essential understanding of addiction, a more nuanced perspective necessitates the consideration of a broader range of factors. Multiple layers of influence, from neurobiology to genetics and environment to psychology, work in concert to create the intricate web of addiction.

The neurobiology of addiction is not solely about dopamine. Other neurotransmitters like GABA, glutamate, and serotonin have crucial roles in the addictive process. For instance, the glutamatergic system, which is primarily involved in neural activation and synaptic plasticity, plays a significant part in the formation of memories related to drug use. This contributes to cravings and the likelihood of relapse as individuals are reminded of the pleasurable experiences associated with substance use (Kalivas, 2009).

Figure 5: Addiction (Molyneux, 2020)

The role of genetics in addiction is increasingly recognized. Genetic predispositions can influence an individual's susceptibility to addiction, with certain genes and gene variants associated with an increased risk. These genetic factors can affect how an individual responds to substances, the level of pleasure they derive from substance use, and their ability to quit (Agrawal & Lynskey, 2008). However, it's important to note that genetics alone doesn't determine whether someone will develop an addiction. It's the interplay between genetics and environment that largely shapes this risk.

Environmental factors significantly influence the onset and course of addiction. This encompasses a wide range of influences, including socioeconomic status, peer pressure, availability and accessibility of drugs, and exposure to stress or traumatic events. For example, individuals in disadvantaged socioeconomic circumstances or those exposed to high levels of stress may be more prone to substance abuse as a coping mechanism. Similarly, peer pressure can significantly influence initial experimentation with substances (Ducci & Goldman, 2012).

Psychological factors, including mental health conditions, personality traits, and coping strategies, can also significantly contribute to addiction. Comorbidity, where a person has two or more disorders, is common in addiction. Mental health disorders, such as depression and anxiety, often co-occur with substance abuse disorders, creating a cycle where each disorder exacerbates the other. Certain personality traits, such as impulsivity or a high need for sensation, can also increase the risk of addiction. Moreover, ineffective coping strategies can lead individuals to turn to substance use as a means of dealing with life's stresses (Swendsen et al., 2010).

Figure 6: Coping mechanisms (Porter, 2023)


In conclusion, addiction is a complex and multifaceted condition that goes beyond the confines of a single neurotransmitter or neurobiological process. While the dopamine-centric perspective, as championed by Nora Volkow and others, offers critical insights into the neurobiology of addiction, it is far from the whole story. Our understanding of addiction deepens when we account for other neurobiological factors, such as the roles played by neurotransmitters like GABA, glutamate, and serotonin. Similarly, the influence of genetic factors is undeniable, with specific genes and gene variants associated with an increased risk of addiction. Moreover, environmental and psychological factors offer another level of complexity. Social and environmental elements, including socioeconomic status, peer pressure, drug availability, and exposure to trauma, significantly shape the risk and course of addiction. Psychological factors, such as comorbid mental health conditions, personality traits, and coping strategies, are also integral in understanding why some individuals develop addiction while others do not.

The landscape of addiction is intricate and multifactorial. Therefore, to effectively address addiction, we must approach it from a holistic perspective that acknowledges the interplay of neurobiological, genetic, environmental, and psychological factors. Only then can we devise more comprehensive and effective strategies for prevention and treatment, ultimately assisting individuals on their journey to recovery. The complexity of addiction may be daunting, but it is in understanding this complexity that we find the most promise for meaningful solutions.

Bibliographical References

Agrawal, A., & Lynskey, M. T. (2008). Are there genetic influences on addiction: evidence from family, adoption and twin studies. Addiction, 103(7), 1069-1081.

Ducci, F., & Goldman, D. (2012). The genetic basis of addictive disorders. Psychiatric Clinics, 35(2), 495-519.

Floresco, S. B. (2015). The nucleus accumbens: an interface between cognition, emotion, and action. Annual review of psychology, 66, 25-52.

Hyman, S. E., Malenka, R. C., & Nestler, E. J. (2006). Neural mechanisms of addiction: the role of reward-related learning and memory. Annual review of neuroscience, 29, 565-598.

Kalivas, P. W. (2009). The glutamate homeostasis hypothesis of addiction. Nature Reviews Neuroscience, 10(8), 561-572.

Koob, G. F., & Volkow, N. D. (2010). Neurocircuitry of addiction. Neuropsychopharmacology, 35(1), 217-238.

Potenza, M. N. (2008). The neurobiology of pathological gambling and drug addiction: an overview and new findings. Philosophical Transactions of the Royal Society B: Biological Sciences, 363(1507), 3181-3189.

Schumann, G., Bonomo, Y., Aarø, L. E., Abebe, D., Bannink, R., Best, D., ... & Jernigan, D. (2019). The cross-cultural importance of research on adolescent drug use and problematic use. Nature.

Schultz, W. (2015). Neuronal reward and decision signals: from theories to data. Physiological reviews, 95(3), 853-951.

Swendsen, J., Conway, K. P., Degenhardt, L., Glantz, M., Jin, R., Merikangas, K. R., ... & Kessler, R. C. (2010). Mental disorders as risk factors for substance use, abuse and dependence: results from the 10-year follow-up of the National Comorbidity Survey. Addiction, 105(6), 1117-1128.

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.

Volkow, N. D., Wang, G. J., Fowler, J. S., & Tomasi, D. (2012). Addiction circuitry in the human brain. Annual review of pharmacology and toxicology, 52, 321-336.

Volkow, N. D., Fowler, J. S., Wang, G. J., Baler, R., & Telang, F. (2009). Imaging dopamine's role in drug abuse and addiction. Neuropharmacology, 56, 3-8.

Volkow, N. D., Wang, G. J., Fowler, J. S., Tomasi, D., & Telang, F. (2011). Addiction: beyond dopamine reward circuitry. Proceedings of the National Academy of Sciences, 108(37), 15037-15042.

Volkow, N. D., Wang, G. J., Telang, F., Fowler, J. S., Logan, J., Childress, A. R., & Wong, C. (2008). Dopamine increases in striatum do not elicit craving in cocaine abusers unless they are coupled with cocaine cues. Neuroimage, 39(3), 1266-1273.

Volkow, N. D., Wang, G. J., Telang, F., Fowler, J. S., Logan, J., Jayne, M., & Wong, C. (2007). Profound decreases in dopamine release in striatum in detoxified alcoholics: possible orbitofrontal involvement. Journal of Neuroscience, 27(46), 12700-12706.

Wiers, R. W., Gladwin, T. E., Hofmann, W., Salemink, E., & Ridderinkhof, K. R. (2013). Cognitive bias modification and cognitive control training in addiction and related psychopathology: Mechanisms, clinical perspectives, and ways forward. Clinical Psychological Science, 1(2), 192-212.

Wise, R. A., & Koob, G. F. (2014). The development and maintenance of drug addiction. Neuropsychopharmacology reviews, 39(1), 254.

Koob, G. F., & Le Moal, M. (2005). Plasticity of reward neurocircuitry and the ‘dark side’ of drug addiction. Nature neuroscience, 8(11), 1442-1444.

Leshner, A. I. (1997). Addiction is a brain disease, and it matters. Science, 278(5335), 45-47.

Nestler, E. J. (2005). Is there a common molecular pathway for addiction? Nature Neuroscience, 8(11), 1445-1449.

Sinha, R. (2008). Chronic stress, drug use, and vulnerability to addiction. Annals of the New York Academy of Sciences, 1141(1), 105-130.

Volkow, N. D., & Li, T. K. (2004). Drug addiction: the neurobiology of behaviour gone awry. Nature reviews. Neuroscience, 5(12), 963–970.

Breiter, H. C., Gollub, R. L., Weisskoff, R. M., Kennedy, D. N., Makris, N., Berke, J. D., ... & Hyman, S. E. (1997). Acute effects of cocaine on human brain activity and emotion. Neuron, 19(3), 591-611.

Visual Sources

Figure 1: Nora Volkow. (2022). National Institute on Drug Abuse. Figure 2: Charity Atakunda. (n.d.).

Figure 3: Svtdesign. (n.d.). Dopamine. Freepic.

Figure 4: Agapova, M. (2022). Help Needed. Verywellmind.

Figure 5: Molyneux, A. (2020). Addiction. Delamere.

Figure 6: Porter, L. (2023). Coping Mechanisms. Verywellmind.


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