Body mass index and marijuana use.
ABSTRACT Though marijuana has been reported to stimulate appetite, we searched for a correlation between obesity and decreased marijuana use. We examined charts of all females referred for morbid obesity/weight management in a 12-month period. BMI and substance use data were collected from 297 charts. While 29% of the sample with BMI < 30 (n = 7) used marijuana in the past year, only 21% of those with BMI 30-39 (n = 84), 16% of those with BMI 40-49 (n = 110) and 14% (n = 96) of those with BMI > 50 used marijuana in the past year. Linear regression revealed a negative correlation between BMI group and percent marijuana use (R-squared = 0.96; P = 0.0173). These findings provide support for overeating as competition for drugs and alcohol in brain reward sites.
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ABSTRACT: Data suggest that low levels of dopamine D2 receptors and attenuated responsivity of dopamine-target regions to food intake is associated with increased eating and elevated weight. There is also growing (although mixed) evidence that genotypes that appear to lead to reduced dopamine signaling (e.g., DRD2, DRD4, and DAT) and certain appetite-related hormones and peptides (e.g., ghrelin, orexin A, leptin) moderate the relation between dopamine signaling, overeating, and obesity. This chapter reviews findings from studies that have investigated the relation between dopamine functioning and food intake and how certain genotypes and appetite-related hormones and peptides affect this relation.01/2011; 6:81-93. DOI:10.1007/7854_2010_89
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ABSTRACT: Recent studies demonstrated that alcohol dependence and excessive alcohol consumption are associated with increased rates of obesity. In healthy light-drinkers, we and others have observed associations between elevated body mass index (BMI) and reductions in brain volumes, lower concentrations of N-acetyl-aspartate (NAA, marker of neuronal viability) and choline-containing compounds (Cho, involved in membrane turnover), and lower glucose utilization, particularly in frontal lobe-a brain region that is particularly vulnerable to the effects of alcohol dependence. Here, we evaluated whether BMI in alcohol-dependent individuals was independently associated with regional measures of brain structure, metabolite concentrations, and neocortical blood flow. As part of a study on the effects of alcohol dependence on neurobiology, we analyzed retrospectively data from 54 alcohol-dependent males, abstinent from alcohol for about 1 month and with BMI between 20 and 37 kg/m(2) by structural MRI, perfusion MRI (blood flow), and proton magnetic resonance spectroscopic imaging. After correction for age, smoking status, and various measures of alcohol consumption, higher BMI was associated with lower concentrations of NAA, Cho, creatine and phosphocreatine (Cr, involved in high energy metabolism), and myo-inositol (m-Ino, a putative marker of astrocytes) primarily in the frontal lobe, in subcortical nuclei, and cerebellar vermis (p < 0.004). Regional brain volumes and perfusion were not significantly related to BMI. Furthermore, comorbid conditions, clinical laboratory measures, and nutritional assessments were not significant predictors of these MR-based measures. The results suggest that BMI, independent of age, alcohol consumption, and common comorbidities, is related to regional NAA, Cho, Cr, and m-Ino concentrations in this cohort of alcohol-dependent individuals. Additionally, as some common comorbid conditions in alcohol dependence such as cigarette smoking are associated with BMI, their associations with regional brain metabolite levels in alcohol-dependent individuals may also be influenced by BMI.Alcoholism Clinical and Experimental Research 12/2010; 34(12):2089-96. DOI:10.1111/j.1530-0277.2010.01305.x
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ABSTRACT: Recent studies indicate that decreased central dopamine is associated with diet-induced obesity in humans and in animal models. In the current study, the authors assessed the hypothesis that diet-induced obesity reduces mesolimbic dopamine function. Specifically, the authors compared dopamine turnover in this region between rats fed a high-fat diet and those consuming a standard low-fat diet. The authors also assessed behavioral consequences of diet-induced obesity by testing the response of these animals in a conditioned place paradigm using amphetamine as a reinforcer and in an operant conditioning paradigm using sucrose reinforcement. Results demonstrate that animals consuming a high-fat diet, independent of the development of obesity, exhibit decreased dopamine turnover in the mesolimbic system, reduced preference for an amphetamine cue, and attenuated operant responding for sucrose. The authors also observed that diet-induced obesity with a high-fat diet attenuated mesolimbic dopamine turnover in the nucleus accumbens. These data are consistent with recent hypotheses that the hormonal signals derived from adipose tissue regulate the activity of central nervous system structures involved in reward and motivation, which may have implications for the treatment of obesity and/or addiction.Behavioral Neuroscience 01/2009; 122(6):1257-63. DOI:10.1037/a0013111