Maldonado, R., Valverde, O., & Berrendero, F. (2006). Involvement of the endocannabinoid system in drug addiction. Trends in Neurosciences, 29(4), 225–232. https://doi.org/10.1016/j.tins.2006.01.008 From the research article’s abstract: “Recent studies have shown that the endocannabinoid system is involved in the common neurobiological mechanism underlying drug addiction. This system participates in the primary rewarding effects of cannabinoids, nicotine, alcohol and opioids, through the release of endocannabinoids in the ventral tegmental area. Endocannabinoids are also involved in the motivation to seek drugs by a dopamine-independent mechanism, demonstrated for psychostimulants and opioids. The endocannabinoid system also participates in the common mechanisms underlying relapse to drug-seeking behaviour by mediating the motivational effects of drug-related environmental stimuli and drug re-exposure. In agreement, clinical trials have suggested that the CB1 cannabinoid antagonist rimonabant can cause smoking cessation. Thus, CB1 cannabinoid antagonists could represent a new generation of compounds to treat drug addiction.”

Killgore, W. D. S., & Yurgelun-Todd, D. A. (2005). Body mass predicts orbitofrontal activity during visual presentations of high-calorie foods. NeuroReport, 16(8), 859–863. https://doi.org/10.1097/00001756-200505310-00016 From the research article’s abstract: “Little is known about the relationship between weight status and reward-related brain activity in normal weight humans. We correlated orbitofrontal and anterior cingulate cortex activity as measured by functional magnetic resonance imaging with body mass index in 13 healthy, normal-weight adult women as they viewed images of high-calorie and low-calorie foods, and dining-related utensils. Body mass index correlated negatively with both cingulate and orbitofrontal activity during high-calorie viewing, negatively with orbitofrontal activity during low-calorie viewing, and positively with orbitofrontal activity during presentations of nonedible utensils. With greater body mass, activity was reduced in brain regions important for evaluating and modifying learned stimulus–reward associations, suggesting a relationship between weight status and responsiveness of the orbitofrontal cortex to rewarding food images.”

Shaffer, H. J., LaPlante, D. A., LaBrie, R. A., Kidman, R. C., Donato, A. N., & Stanton, M. V. (2004). Toward a syndrome model of addiction: Multiple expressions, common etiology. Harvard Review of Psychiatry, 12(6), 367-374. https://doi.org/10.1080/10673220490905705 From the research article’s abstract: “Research about alcohol, tobacco, illegal drug use, gambling, and eating disorders have revealed commonalities that support the use of the syndrome model of addiction. Yet no coherent framework exists to explicate the syndrome. This article introduces a syndrome model of addiction that holds that all addictions reside on an etiological spectrum of disorders. The model proposes that addictions are more alike than unalike and all addictions share common etiological factors associated with genetic influences, neurobiological deficiencies, repeated behaviors, and psychological and social stressors. The model also suggests that just as there are multiple pathways to addictions, there are multiple pathways away from addictions. Prevention and treatment implications of the model are examined.”