Volkow, N. D., & O’Brien, C. P. (2007). Issues for DSM-V: should obesity be included as a brain disorder?. American Journal of Psychiatry, 164(5), 708–710. https://doi.org/10.1176/ajp.2007.164.5.708 From the research article’s abstract: “Obesity (body mass index >30), has increased significantly over the past 30 years (approximately 50% per decade) (1), afflicting 32.2% of adults in the United States (2) . Obesity increases risk for cardiovascular disease, diabetes, cancer, and other diseases, resulting in annual health care costs conservatively estimated for the United States at $70 to $100 billion a year (3) as well as reductions in life expectancy by 5 to 20 years (4) . These facts highlight the urgent need to develop strategies to prevent and treat those afflicted. Although there have been major scientific advances in the treatment of the medical complications of obesity (i.e., diabetes, hypertension hypercholesterolemia), the morbidity from this disorder is hampered by the failure of interventions to sustain weight loss.
The Neurobiology of Addiction: Implications for Voluntary Control of Behavior
Hyman S. E. (2007). The neurobiology of addiction: implications for voluntary control of behavior. The American journal of bioethics : AJOB, 7(1), 8–11. https://doi.org/10.1080/15265160601063969 From the neurobiology article’s key finding: “Addicted individuals have substantial impairments in cognitive control but this ‘loss of control’ is not complete or simple.”
Involvement of the endocannabinoid system in drug addiction
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.”
Body mass predicts orbitofrontal activity during visual presentations of high-calorie foods
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.”
How can drug addiction help us understand obesity?
Volkow, N. D., & Wise, R. A. (2005). How can drug addiction help us understand obesity?. Nature Neuroscience, 8(5), 555–560. https://doi.org/10.1038/nn1452 From the research article’s abstract: “To the degree that drugs and food activate common reward circuitry in the brain, drugs offer powerful tools for understanding the neural circuitry that mediates food-motivated habits and how this circuitry may be hijacked to cause appetitive behaviors to go awry.”
Toward a Syndrome Model of Addiction: Multiple Expressions, Common Etiology
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.”
Exposure to appetitive food stimuli markedly activates the human brain
Wang, G. J., Volkow, N. D., Telang, F., Jayne, M., Ma, J., Rao, M., Zhu, W., Wong, C. T., Pappas, N. R., Geliebter, A., & Fowler, J. S. (2004). Exposure to appetitive food stimuli markedly activates the human brain. NeuroImage, 21(4), 1790–1797. https://doi.org/10.1016/j.neuroimage.2003.11.026 From the research article’s abstract: “Objective: The increased incidence of obesity most likely reflects changes in the environment that had made food more available and palatable. Here we assess the response of the human brain to the presentation of appetitive food stimuli during food presentation using PET and FDG. Method: Metabolic changes in response to food presentation were done in 12 healthy normal body weight subjects who were food deprived before the study. Results: Food presentation significantly increased metabolism in the whole brain (24%, P < 0.01) and these changes were largest in superior temporal, anterior insula, and orbitofrontal cortices. The increases in the right orbitofrontal cortex were the ones that correlated significantly with the increases in self-reports of hunger and desire for food. Discussion: The marked increase in brain metabolism by the presentation of food provides evidence of the high sensitivity of the human brain to food stimuli. This high sensitivity coupled with the ubiquitousness of food stimuli in the environment is likely to contribute to the epidemic of obesity.
Motivational/solution-focused intervention improves HbA1c in adolescents with Type 1 diabetes: a pilot study
Viner, R. M., Christie, D., Taylor, V., & Hey, S. (2003). Motivational/solution-focused intervention improves HbA1c in adolescents with Type 1 diabetes: a pilot study. Diabetic Medicine, 20(9), 739-742. https://doi.org/10.1046/j.1464-5491.2003.00995.x From the research article’s abstract: “Aims We piloted a motivational and solution-focused therapy group intervention to improve glycaemic control in young people 11–17 years with poorly controlled Type 1 diabetes (mean annual HbA1c > 8.5%). Methods Seventy-seven subjects agreed to be assessed for a pilot non-randomized controlled trial. Subjects completed psychological questionnaires and were given feedback designed to encourage entry into the intervention. Twenty-one young people opted to enter the intervention groups (cases). Two intervention groups consisting of five to six subjects were conducted in each age band 10–13 years and 14–17 years. Twenty of those who did not opt to join the groups were randomly selected to act as controls. Cases and controls were well matched for age, HbA1c, duration of diabetes and socio-economic status. Results The intervention produced a significant improvement of 1.5% in HbA1c in cases (P < 0.05) at 4–6 months post intervention compared with no change in controls. This improvement was partly maintained at 7–12 months post intervention.
Recognition of alcohol and substance abuse
Mersy, D. J. (2003). Recognition of alcohol and substance abuse. American Family Physician, 67(7), 1529–1532. https://pubmed.ncbi.nlm.nih.gov/12722853/ From the research article’s abstract: “Ten percent of the population abuses drugs or alcohol, and 20 percent of patients seen by family physicians have substance-abuse problems, excluding tobacco use. These patients can be identified by relying on regular screening or a high index of suspicion based on “red flags” that can be noted in various clinical situations. The modified CAGE questionnaire is an excellent screening instrument, but several alternatives are available. The best screening test is one that the physician will routinely use well. Laboratory indicators such as gamma-glutamyl transpeptidase, mean corpuscular volume, and carbohydrate-deficient transferrin are nonspecific but can add to the evidence of alcohol abuse. If problem alcohol use is diagnosed, even brief physician advice can be helpful. If the problem has progressed to addiction, referral to an addiction specialist or treatment center is recommended.
Brain dopamine and obesity
Wang, G. J., Volkow, N. D., Logan, J., Pappas, N. R., Wong, C. T., Zhu, W., Netusil, N., & Fowler, J. S. (2001). Brain dopamine and obesity. Lancet (London, England), 357(9253), 354–357. https://doi.org/10.1016/s0140-6736(00)03643-6 From the research article’s abstract: “Background The cerebral mechanisms underlying the behaviours that lead to pathological overeating and obesity are poorly understood. Dopamine, a neurotransmitter that modulates rewarding properties of food, is likely to be involved. To test the hypothesis that obese individuals have abnormalities in brain dopamine activity we measured the availability of dopamine D2 receptors in brain. Methods Brain dopamine D2 receptor availability was measured with positron emission tomography (PET) and [C-11]raclopride (a radioligand for the dopamine D2 receptor). Bmax/Kd (ratio of the distribution volumes in striatum to that in cerebellum minus 1) was used as a measure of dopamine D2 receptor availability. Brain glucose metabolism was also assessed with 2-deoxy-2[18F]fluoro-D-glucose (FDG). Findings Striatal dopamine D2 receptor availability was significantly lower in the ten obese individuals