ABSTRACT
Smokers are less educated and are more likely to discount future rewards than nonsmokers. We assessed the relationship between delay discounting and education level in 77 smokers entering smoking cessation treatment. There was an effect of education on computer task and the questionnaire measures of discounting, with participants having no college discounting delayed rewards significantly (P < .01) more than those attending college. Subjects discounted small rewards more than large rewards for both tasks (P < .001). Results show that education level is inversely associated with discounting in smokers.
Subject(s)
Reward , Smoking/psychology , Adolescent , Adult , Educational Status , Female , Humans , Impulsive Behavior , Male , Smoking CessationABSTRACT
BACKGROUND: Food reinforcement and dopaminergic activity may influence food consumption, but research on whether they interact has not been performed. OBJECTIVE: We assessed the effects of food reinforcement and the interaction of food reinforcement with the dopamine transporter (SLC6A3) genotype and the dopamine D(2) receptor (DRD(2)) genotype on energy consumption. DESIGN: We studied food-consumption and reinforcing-value-of-food tasks in 88 smokers of European ancestry before they enrolled in smoking-cessation treatment. In the food-consumption task, subjects tasted and consumed 8 snack foods ad libitum. The reinforcing-value-of-food task assessed how hard subjects would work for food. RESULTS: Significant interactions between dopamine genotypes and food reinforcement were observed. Subjects high in food reinforcement who lacked an SLC6A3*9 allele consumed significantly more calories (>150 kcal; P = 0.015) than did subjects low in food reinforcement or those high in food reinforcement who carried at least one SLC6A3*9 allele. Similarly, subjects high in food reinforcement who carried at least one DRD(2)*A1 allele consumed >130 kcal more (P = 0.021) than did subjects low in food reinforcement or those high in food reinforcement who lacked a DRD(2)*A1 allele. There was also a main effect of food reinforcement on energy intake (P = 0.005), with subjects high in food reinforcement consuming 104 kcal (or 30%) more than did subjects low in food reinforcement. CONCLUSIONS: Food reinforcement has a significant effect on energy intake, and the effect is moderated by the dopamine loci SLC6A3 and DRD(2).
Subject(s)
Dopamine/metabolism , Energy Intake/physiology , Membrane Glycoproteins , Membrane Transport Proteins/genetics , Nerve Tissue Proteins/genetics , Receptors, Dopamine D2/genetics , Reinforcement, Psychology , Smoking Cessation , Adult , Alleles , Analysis of Variance , Bupropion/therapeutic use , Conditioning, Operant , Diet , Dopamine/genetics , Dopamine Plasma Membrane Transport Proteins , Dopamine Uptake Inhibitors/therapeutic use , Energy Intake/genetics , Female , Food , Genotype , Humans , Male , Polymorphism, Genetic , SmokingABSTRACT
Both the hedonic ratings and the reinforcing value of food have been considered to be determinants of food intake. The objective of this study was to compare the pleasurable ratings and the reinforcing value of food as determinants of energy intake. Seventy-four smokers were studied in food consumption and reinforcing value of food tasks prior to enrolling in a smoking-cessation treatment program. For the food consumption task, the participants tasted and consumed food ad lib from eight snack foods. The reinforcing value of the food task assessed how hard subjects would work for a preferred snack food. Results showed that food reinforcement was related to laboratory food intake, with those high in food reinforcement consuming significantly more calories (+114.4 kcal, P<.01) than did the participants low in food reinforcement. Food reinforcement was related to food intake for the preferred food as well as to total energy intake. Hedonics for the preferred food was related to food reinforcement but not to either measure of laboratory energy intake. In multiple-regression models, food reinforcement and the interaction of food reinforcement by sex were significant predictors of energy intake for the preferred food and for total energy intake, along with baseline hunger. In conclusion, energy intake in smokers in a laboratory setting is more strongly related to food reinforcement than to the hedonic ratings of food.
Subject(s)
Eating/psychology , Food Preferences/physiology , Reinforcement, Psychology , Smoking/psychology , Adult , Body Mass Index , Energy Intake/physiology , Female , Humans , Male , Regression Analysis , Sex Characteristics , Smoking Cessation , WorkABSTRACT
OBJECTIVE: Rapid synaptic dopamine transport or reduced brain dopamine receptor signaling may influence energy intake. Methylphenidate, a dopamine reuptake inhibitor, increases brain synaptic dopamine and produces anorexia, suggesting that it may reduce energy intake. We investigated the effects of two doses of short-acting methylphenidate on energy intake over one meal in obese adult males. RESEARCH METHODS AND PROCEDURES: Nine obese males (>85th BMI percentile) ingested a placebo or a moderate dose (0.5 mg/kg) or a high dose (1.0 mg/kg) of methylphenidate in a within-subject double-blind acute laboratory study. One hour after ingestion, pizza consumption was measured in a naturalistic laboratory setting. RESULTS: Participants reduced energy intake by 23% for the moderate dose vs. the placebo (p < 0.02), but there was no significant difference for the high dose vs. the moderate dose (p > 0.05). Participants consumed 34% fewer kilocalories after ingesting the lowest effective dose of methylphenidate compared with placebo (725.7 +/- 404.5 vs.1095 +/- 271.1 kcal, p < 0.01). Seven of nine subjects responded to the moderate dose. The increase in perceived drug effect above placebo was correlated with the reduction in energy intake for both the moderate (r = -0.85, p = 0.004) and the high (r = -0.75 p = 0.021) doses. Hunger scores were not different across drug doses or placebo before drug administration. DISCUSSION: Methylphenidate reduced energy intake of a highly palatable food over one meal by one-third in obese adult males. Dopamine transport inhibition may be an effective component of a comprehensive treatment for obesity.
Subject(s)
Dopamine Uptake Inhibitors/pharmacology , Eating/drug effects , Methylphenidate/pharmacology , Obesity/drug therapy , Adult , Cross-Over Studies , Dopamine Uptake Inhibitors/administration & dosage , Dose-Response Relationship, Drug , Double-Blind Method , Eating/physiology , Energy Intake/drug effects , Energy Intake/physiology , Humans , Male , Methylphenidate/administration & dosage , Satiation/drug effects , Satiation/physiologyABSTRACT
OBJECTIVE: To assess the association between a polymorphism related to dopamine function, dopamine transport (SLC6A3), and obesity in smokers. RESEARCH METHODS AND PROCEDURES: Logistic regression was used to assess the relationship between this genetic polymorphism and obesity (body mass index > or = 30 kg/m(2)) from a sample of 510 smokers who smoked at least 10 cigarettes per day and who were participating in a study designed to examine genetic and nongenetic predictors of response to a pharmacological treatment. RESULTS: The likelihood of obesity in African Americans (N = 90) with the 10/10 SLC6A3 genotype was 5.16 times that of African Americans with 9/9 or 9/10 SLC6A3 genotypes (odds ratio = 5.16, confidence interval = 1.60 to 16.65). There was no association of the SLC6A3 genotype with obesity for non-Hispanic whites (N = 420). DISCUSSION: These results suggest that variants of the dopamine transporter gene may be related to obesity in African-American smokers. Possible mechanisms responsible for the association between dopamine transport and obesity in African-American smokers are discussed.
