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Additionally, many neurotransmitters are involved in the experience of reward (dopamine, opioids, GABA, serotonin, endocannabinoids, and glutamate; Blum et al., 2020). Thus deficiencies in any combination of these neurochemicals may contribute to a predisposition to addiction. It is important to note that one person’s reaction to the reward experience may be quite different from another’s.

At a population-level analysis, we must acknowledge that results of a variable-centered approach such as this work only represent findings based on a population average. More specialized approaches, such as person-centered ones, are necessary to study specific at-risk groups and opioid misuse and/or use disorder [72]. Thus, these findings serve as a population-level risk profile using the most recent US nationally representative data to inform epidemiological trends and possible large-scale interventions. Advances in neuroscience are changing how mental health issues such as addiction are understood and addressed as a brain disease. Although a brain disease model legitimizes addiction as a medical condition, it promotes neuro-essentialist thinking, categorical ideas of responsibility and free choice, and undermines the complexity involved in its emergence.

Box 1 What’s in a name? Differentiating hazardous use, substance use disorder, and addiction

Early residential laboratory studies on alcohol use disorder indeed revealed orderly operant control over alcohol consumption [106]. Furthermore, efficacy of treatment approaches such as contingency management, which provides systematic incentives for abstinence [107], supports the notion that behavioral choices in patients with addictions remain sensitive to reward contingencies. Epidemiologically, it is well established that social determinants of health, including major racial and ethnic disparities, play a significant role in the risk for addiction [75, 76]. Contemporary neuroscience is illuminating how those factors penetrate the brain [77] and, in some cases, reveals pathways of resilience [78] and how evidence-based prevention can interrupt those adverse consequences [79, 80]. In other words, from our perspective, viewing addiction as a brain disease in no way negates the importance of social determinants of health or societal inequalities as critical influences. In fact, as shown by the studies correlating dopamine receptors with social experience, imaging is capable of capturing the impact of the social environment on brain function.

  • According to Borrell-Carrio (2004) in The Biopsychological model 25 years later, “biological, genetic, personality, psychological, cognitive, social, cultural and environmental factors” are the main cause of the addiction disorder.
  • As globalization continues, COVID-19 is unlikely to be the last pandemic, and there will undoubtedly be subsequent global economic crises.
  • The critical role of alternative reinforcers was elegantly brought into modern neuroscience by Ahmed et al., who showed that rats extensively trained to self-administer cocaine would readily forego the drug if offered a sweet solution as an alternative [103].
  • As Searle (2004) argues, “there is a striking difference between the passive character of perceptual consciousness and the active character of what we might call ‘volitional consciousness’“ (41).

In addition, our coworkers could also be considered a social factor when they encourage us to drink or use drugs to help alleviate stress and anxiety related to our jobs. While they might mean well, their encouragement could be the factor that sets us on the path to addiction. Both of these hypotheses reflect a perspective in which biological and psychosocial processes are inherently and intrinsically interactive.