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Background: Eating behavior and thus dietary intake affect the development of obesity-related diseases such as diabetes, hypertension, and hyperlipidemia. Objective: We investigated the genetic underpinnings of eating behavior. Design: We administered a standardized eating behavior inventory to 624 adults from 28 families participating in the Amish Family Diabetes Study. Three quantifiable components of eating behavior were measured: restraint, disinhibition, and hunger. Associations between eating behavior scores and physical characteristics were evaluated. Heritability analysis and a genome-wide multipoint linkage analysis were performed. Results: Eating behavior scores were associated with obesity and obesity-related phenotypes. Heritability estimates were 0.28 [+ or -] 0.09 for restraint, 0.40 [+ or -] 0.10 for disinhibition, and 0.23 [+ or -] 0.09 for hunger (P < 0.001). The linkage analysis showed 4 regions of suggestive linkage. We observed suggestive evidence for linkage of restraint scores to 2 chromosomal regions, near markers D3S1304 [LOD (log of odds) = 2.5, P = 0.0003] and D6S276 (LOD = 2.3, P = 0.0006). We previously reported that D3S1304 is linked to a locus influencing percentage body fat in this same population (LOD = 1.6), suggesting that this behavioral phenotype may be secondary to obesity. The maximum LOD scores for disinhibition were 1.6 (P = 0.003) near marker D7S657 and 1.4 (P = 0.005) near marker D16S752. The maximum LOD score for hunger was 1.4 (P = 0.005) near marker D3S1278. Conclusion: Significant familial effects on eating behavior and suggestive genetic linkage were found in Amish adults. Am J Clin Nutr 2002;75:1098-1106. KEY WORDS Restraint, obesity, behavioral genetics, Amish, heritability, linkage analysis

Stimulation of [Β.sub.3]-adrenoceptors by selective agonists improves insulin action and stimulates energy metabolism in various rodent models of obesity and type 2 diabetes. Whether selective [Β.sub.3]-adrenoceptor stimulationexerts metabolic actions in [...]

It is controversial whether food intake in humans is under day-to-day regulation to maintain constant body glycogen stores. In eight white males with a mean ([+ or -] SD) age of 30 [+ or -] 4 y, body weight of 82 [+ or -] 20 kg, and percentage body fat of 22 [+ or -] 5%, exercise and diets were used to produce either high (HG) or low glycogen (LG) stores in a randomized crossover design. After each treatment a vastus lateralis muscle biopsy was obtained. Subsequent ad libitum food intake was measured with an automated food-selection system during 2 d in a respiratory chamber. Despite a 46 [+ or -] 21% difference in muscle glycogen between the two treatments, ad libitum 2-d food intakes (energy, weight, or macronutrients) were similar between treatments (HG: 23.80 [+ or -] 4.67 MJ/d; LG: 21.20 [+ or -] MJ/d). However, energy intake on the second day of ad libitum feeding was negatively correlated with carbohydrate balance on the first day, adjusted for the effect of total energy intake and treatment. Adjusted carbohydrate balance on day 1 only explained 9% of the variance in energy intake on day 2. The 24-h respiratory quotient on the first day after treatment was higher after the HG than after the LG treatment: 0.94 [+ or -] 0.04 and 0.88 [+ or -] (P [is less than] 0.001). The findings suggest that 1) body glycogen stores play at most a minor role in short-term food intake regulation, and 2) in the short term, imbalances in glycogen stores are corrected by adjustments of macronutrient oxidation rates.

During the past two decades, many investigators have measured the thermic effect of food (TEF) in humans and have speculated on its role in the development of obesity. In this study we compared different ways of computing TEF from daily energy expenditure measurements in a respiratory chamber, evaluated the determinants of TEF, and more importantly assessed for the first time the relation between TEF and change in body weight. In 471 subjects, TEF was 1697 [+ or -] 857 kJ/d (x [+ or -] SD), ie, 18 [+ or -] 9% of energy intake. In 114 subjects studied more than once, intraindividual TEF variability was very high (CV = 48%). TEF correlated positively with the level of spontaneous physical activity (SPA) and negatively with fasting plasma glucose and insulin concentrations. TEF correlated inversely with age (males only) and body weight, percent body fat, and waist-to-hip ratio (females only). The level of SPA and fasting plasma glucose concentration were the only significant determinants of TEF, explaining 15% of its variance. In 137 subjects in whom body weight was measured [greater than or equal to] 6 mo after TEF measurement (mean follow-up duration of 2.9 [+ or -] 1.7 y), a low TEF was not predictive of body weight gain. We conclude that, despite the low reproducibility of TEF from use of a respiratory chamber, data in a large number of subjects suggest that TEF is increased by higher SPAs and that insulin resistance is associated with a low TEF. More important, longitudinal data indicate that the variability in TEF is not associated with changes in body weight. Am J Clin Nutr 1995;61:1013-9.

Background: Recent reports have identified a lower resting metabolic rate in African Americans than in whites, but most studies included only females and used short-term measurements with ventilated-hood systems. Objective: Our objective was to compare 24-h measurements of energy metabolism between African American and white women and men using a respiratory chamber. Design: Thirty-eight African American ([bar] x [+ or -] SD: 32 [+ or -] 7 y of age, 24 [+ or -] 10% body fat) and 288 white (31 [+ or -] 7 y of age, 26 [+ or -] 12% body fat) subjects spent 24 h in a respiratory chamber for measurement of 24-h energy expenditure (24EE), sleeping metabolic rate (SMR), 24-h respiratory quotient (24RQ), and substrate oxidation rates. Results: After adjustment for sex, age, and body composition (by hydrodensitometry), African Americans had lower SMR (-301 [+ or -] 105 kJ/d; P [is less than] 0.01) and higher 24RQ (0.014 [+ or -] 0.004; P [is less than] 0.001) than whites, whereas 24EE was similar. A sex-specific analysis, using a subset of 38 whites with an equal sex distribution and similar age and body weight, revealed that African American women had lower SMR (-442 [+ or -] 182 kJ/d; P [is less than] 0.05) and lower 24EE (-580 [+ or -] 232 kJ/d; P [is less than] 0.05), but similar 24RQ values compared with white women. African American men tended to have lower SMRs than white men (-355 [+ or -] 188 kJ/d; P = 0.07), but had higher 24RQ values, accounting for a 992 [+ or -] 327-kJ/d lower 24-h fat oxidation rate (P [is less than] 0.005). Conclusions: These data not only confirm the findings of a lower metabolic rate in African American than in white women, but also suggest that fat oxidation is lower in African American men than in white-men. Am J Clin Nutr 1999;70:13-20.

Toxoplasma gondii(T. gondii) infects central nervous tissue and is kept in relative dormancy by a healthy immune system. Sleep disturbances have been found to precipitate mental illness, suicidal behavior and car accidents, which have been previously linked to T. gondii as well.We speculated that if sleep disruption, particularly insomnia, would mediate, at least partly, the link between T. gondiiinfection and related behavioral dysregulation, then we would be able to identify significant associations between sleep disruption and T. gondii. The mechanisms for such an association may involve dopamine (DA) production by T. gondii, or collateral effects of immune activation necessary to keep T. gondiiin check. Sleep questionnaires from 2031 Old Order Amish were analyzed in relationship to T. gondii-IgG antibodies measured by enzyme-linked immunosorbent assay (ELISA). Toxoplasma gondiiseropositivity and serointensity were not associated with any of the sleep latency variables or Epworth Sleepiness Scale (ESS). A secondary analysis identified, after adjustment for age group, a statistical trend toward shorter sleep duration in seropositive men (p=0.07). In conclusion, it is unlikely that sleep disruption mediates links between T. gondiiand mental illness or behavioral dysregulation. Trending gender differences in associations between T. gondiiand shorter sleep need further investigation.