OBJECTIVE:To prospectively examine the relation between television watching and body fat change in children from preschool to early adolescence. METHODS: In a longitudinal study, 106 children were enrolled during preschool years (mean age 4.0 y) and followed into early adolescence (mean age 11.1 y). Parents completed an annual questionnaire on the child's television and video habits. Body mass index (BMI), triceps skinfolds, and sum of five skinfolds were recorded yearly at annual clinic visits. Longitudinal statistical analyses were carried out using mixed modeling procedures to control for potential confounding by a number of factors. RESULTS: Television watching was an independent predictor of the change in the child's BMI, triceps, and sum of five skinfolds throughout childhood. Its effect was only slightly attenuated by controlling for the baseline body fat, level of physical activity (as measured repeatedly by Caltrac accelerometer), percent of calories from fat, total calorie intake, or the parents' BMI or education. By age 11, children who watched 3.0 h or more of television per day had a mean sum of skinfolds of 106.2 mm, compared with a mean sum of skinfolds of 76.5 mm for those who watched less than 1.75 h per day (P ¼ 0.007). Furthermore, the adverse effect of television viewing was worse for those children who were also sedentary or had a higher-fat diet. CONCLUSIONS: Children who watched the most television during childhood had the greatest increase in body fat over time. Healthy lifestyle education designed to prevent obesity and its consequences should target television-watching habits of children.

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BACKGROUND: It is unclear whether the increased risk of colon cancer associated with obesity differs for men and women, by distribution of body fat, or by location of the tumor. The primary goal of this study was to address these questions. METHODS: Eligible subjects from the Framingham Study cohort were classified according to body mass index (BMI) and waist size during two age periods: 30-54 y (n ¼ 3764) and 55-79 y (n ¼ 3802). All eligible men and women were cancer-free at baseline and had complete information on the following potential confounders: age, sex, education, height, activity, smoking, and alcohol. There were 157 incident lifetime cases of colon cancer among those followed beginning at 30-54 y of age and 149 lifetime cases among those whose follow up began at 55-79 y. Subjects were stratified further by gender, activity, and tumor location. The Cox Proportional Hazards Models were used to adjust for possible confounding by the above-described factors. RESULTS: A BMI Z30 led to a 50% increased risk (95% CI: 0.92-2.5) of colon cancer among middle-aged (30-54 y) and a 2.4-fold increased risk (95% CI: 1.5-3.9) among older (55-79 y) adults. The BMI effect was stronger for men than for women and for cases occurring in the proximal colon. These adverse effects generally diminished when waist was added to the multivariable models. A larger waist size (Z99.1 cm (39 in) and 101.6 cm (40 in) for women and men, respectively) was associated with a twofold increased risk of colon cancer; this risk increased linearly with increasing waist size and was evident for both proximal and distal colon cancer. There was no attenuation of these effects when BMI was added to the multivariable models. A larger waist had a particularly adverse effect among sedentary subjects (relative risk (RR) ¼ 4.4 for middle-aged adults; RR ¼ 3.0 for older adults). CONCLUSION: These findings suggest that waist circumference is a stronger predictor of colon cancer risk than is BMI, and that central obesity is responsible for an increased risk of cancer of both the proximal and distal colon.

Objective: To explore mean food group intakes associated with central obesity anthropometry among children and adolescents enrolled in the Third National Health and Nutrition Examination Survey (NHANES III). Design: Cross-sectional study. Setting: Representative sampling of the US population (1998)(1999)(2000)(2001)(2002). Subjects: Subjects were 3761 children (5-11 years) and 1803 adolescents (12-16 years) with single 24 h dietary recalls and anthropometric measures of central body fat (waist circumference and sum of subscapular and suprailiac skinfold thicknesses). Results: Results were controlled for confounding by age, height, race/ethnicity, Tanner stage, television viewing and parental education. In younger children, there was no relationship between central adiposity and mean intakes of dairy, fruit, vegetables or grains, while a positive association with meat intake was found among boys. In adolescent boys and girls, central body fat measures were inversely associated with mean dairy and grain intakes. Adolescent boys in the highest quartile of central adiposity consumed less fruit and fewer vegetables; those in the lowest central adiposity quartile consumed less meat. Finally, adolescents who met the criteria for central obesity (waist circumference $85th percentile for age and sex) reported consuming significantly less total dairy (as well as milk and cheese separately), total grains (whole and refined) and total fruit and vegetables. There was no association with meat consumption. To test the stability of these findings, the final analysis was replicated in 2541 same-aged adolescents from NHANES 1999-2002; the results were very similar. Conclusions: These cross-sectional analyses suggest that intakes of dairy, grains and total fruits and vegetables are inversely associated with central obesity among adolescents.

This study was designed to evaluate the effects of maternal obesity and diabetes mellitus on the risk of nonchromosomal congenital defects. We used data from 22,951 pregnant women enrolled in a prospective cohort study of early prenatal exposures and pregnancy outcome. The relative risks [prevalence ratios (PRs)] of major nonchromosomal congenital defects associated with obesity and diabetes, alone or in combination, were calculated using multiple logistic regression analysis. In this study, in the absence of diabetes, obese women (body mass index > or =28) had no higher risk, overall, of having an offspring with a major defect [PR = 0.95; 95% confidence interval (CI) = 0.62-1.5]. Their offspring, however, did have a higher prevalence of certain types of defects, including orofacial clefts; club foot; cardiac septal defects; and, to a lesser extent, hydrocephaly and abdominal wall defects. Women with pre-existing or gestational diabetes who were not obese also had no excess risk overall of having offspring affected by a major defect (PR = 0.98; 95% CI = 0.43-2.2), although they did have a higher prevalence of musculoskeletal defects. The pregnancies of women who were both obese and diabetic were 3.1 times as likely (95% CI = 1.2-7.6) to result in an offspring with a defect than were those of nonobese, nondiabetic women, which suggests that obesity and diabetes mellitus may act synergistically in the pathogenesis of congenital anomalies. The defects were largely craniofacial or musculoskeletal.