Biomedical subjects
W H Dietz
Publications and source records attributed to W H Dietz.
Growth and development of term children born with low birth weight: effects of genetic and environmental factors.
OBJECTIVE: To evaluate the role of intrauterine growth retardation (IUGR) on childhood growth and development, controlling for environmental and genetic factors. METHODS: Women and infants enrolled in the National Collaborative Perinatal Project were analyzed. Weight, length, and IQ were assessed at birth and at 7 years in the entire National Collaborative Perinatal Project population in term infants born with and without IUGR ("population cohort"). To control for genetic and environmental factors, growth and development were also compared in 220 similar-sex term sibling pairs in which one sibling was born with IUGR and one was born without IUGR ("sibling cohort"). RESULTS: At 7 years of age heights and weights of infants born with IUGR remained approximately 0.5 SD less than infants born without IUGR (weight-for-age: p < 0.001, height-for-age: p < 0.001). In the entire National Collaborative Perinatal Project population, IQ (p < 0.001) and Bender-Gestalt (p < 0.001) scores were significantly lower in infants born with IUGR compared with those in infants born without IUGR. There were no significant differences in IQ or Bender-Gestalt scores between siblings born with and without IUGR. However, siblings with IUGR and large deficits in head circumference demonstrated both decreased IQ (p < 0.05) and Bender-Gestalt (p < 0.05) scores. CONCLUSION: Long-term growth deficits associated with IUGR appear largely independent of prenatal or postnatal environmental factors. IUGR had little impact on intelligence and motor development except when associated with large deficits in head circumference.
Role of the prenatal environment in the development of obesity.
Establishing that prenatal life is a critical or sensitive period for the development of obesity may focus basic research and clinical prevention efforts on this period. This review summarizes evidence that the intrauterine environment influences the risk of later obesity and considers the mechanisms by which this may occur. The association between birth weight and adult weight suggests that there are enduring effects of the intrauterine environment on later obesity risk. We examine whether the maternal factors of diabetes, obesity, and pregnancy weight gain alter the intrauterine environment and thereby increase the risk of later obesity in the offspring. Of these maternal factors, evidence is strongest for the role of maternal diabetes. No single mechanism explains how these maternal factors could change the intrauterine environment to increase obesity risk. However, all potential mechanisms involve an altered transfer of metabolic substrates between mother and fetus, which may influence the developing structure or function of the organs involved in energy metabolism.
Use of the body mass index (BMI) as a measure of overweight in children and adolescents.
Explore the source record for details and available documents.
Does energy expenditure affect changes in body fat in children?
Explore the source record for details and available documents.
Childhood weight affects adult morbidity and mortality.
Few studies have examined the long-term effects of childhood obesity on adult disease. Nonetheless, obesity present in childhood or adolescence seems to increase the likelihood of adult morbidity and mortality. In men who were obese during adolescence, all-cause mortality and mortality from cardiovascular disease and colon cancer were increased. In both men and women obese during adolescence, rates of cardiovascular disease and diabetes were increased. Among women but not men obese during adolescence, obesity has a variety of adverse psychosocial consequences. These include completion of fewer years of education, higher rates of poverty, and lower rates of marriage and household income. These effects seem related both to the persistence of obesity and to the effects of childhood or adolescent obesity on the quantity and location of body fat deposition. Approximately 50% of obese adolescents with a body mass index at or above the 95th percentile become obese adults. Furthermore, the risk factors for adult disease that are associated with obesity in children and adolescents persist into adulthood or increase in prevalence if weight gain occurs. Although both total body fat and regional fat deposition could account for the association of childhood or adolescent obesity with adult disease, no studies to date have examined cardiovascular risk factors and related them to visceral fat, controlled for total body fat.
Physical activity, genetic, and nutritional considerations in childhood weight management.
Almost one-quarter of U.S. children are now obese, a dramatic increase of over 20% in the past decade. It is intriguing that the increase in prevalence has been occurring while overall fat consumption has been declining. Body mass and composition are influenced by genetic factors, but the actual heritability of juvenile obesity is not known. A low physical activity (PA) is characteristic of obese children and adolescents, and it may be one cause of juvenile obesity. There is little evidence, however, that overall energy expenditure is low among the obese. There is a strong association between the prevalence of obesity and the extent of TV viewing. Enhanced PA can reduce body fat and blood pressure and improve lipoprotein profile in obese individuals. Its effect on body composition, however, is slower than with low-calorie diets. The three main dietary approaches are: protein sparing modified fast, balanced hypocaloric diets, and comprehensive behavioral lifestyle programs. To achieve long-standing control of overweight, one should combine changes in eating and activity patterns, using behavior modification techniques. However, the onus is also on society to reduce incentives for a sedentary lifestyle and over-consumption of food. To address the key issues related to childhood weight management, the American College of Sports Medicine convened a Scientific Roundtable in Indianapolis.
Early adiposity rebound and the risk of adult obesity.
OBJECTIVE: At 5 to 6 years of age, body fatness normally declines to a minimum, a point called adiposity rebound (AR), before increasing again into adulthood. We determined whether a younger age at AR was associated with an increased risk of adult obesity and whether this risk was independent of fatness at AR and parent obesity. DESIGN: A retrospective cohort study using lifelong height and weight measurements recorded in outpatient medical records. SETTING: Group Health Cooperative of Puget Sound (GHC), a health maintenance organization based in Seattle, Washington. PARTICIPANTS: All 390 GHC members (and their parents) born at GHC between January 1, 1965, and January 1, 1971, who had at least one recorded adult height and weight measurement plus two visits with recorded height and weight measurements in each of three age intervals: 1.5 to 4, 4 to 8, and 8 to 16 years. MAIN OUTCOME MEASURES: We calculated the mean body mass index (BMI) of each subject during young adulthood (age 21 to 29 years) and the BMI of the parents when each subject was 1.5 years of age. Adult obesity was defined as a BMI >/=27.8 for males and >/=27. 3 for females. Curves were fit to each subject's BMI values between ages 1.5 and 16 years, and the age and BMI at AR were calculated from these curves. Subjects were divided into tertiles of age at AR (early, middle, and late), BMI at AR, and parent BMI (heavy, medium, and lean). RESULTS: The mean age at AR was 5.5 years, and 15% of the cohort was obese in young adulthood. Adult obesity rates were higher in those with early versus late AR (25% vs 5%), those who were heavy versus lean at AR (24% vs 4%), those with heavy versus lean mothers (25% vs 5%), and those with heavy versus lean fathers (21% vs 5%). After adjusting for parent BMI and BMI at AR, the odds ratio for adult obesity associated with early versus late AR was 6.0 (95% CI, 1.3-26.6). CONCLUSION: An early AR is associated with an increased risk of adult obesity independent of parent obesity and the BMI at AR. Future research should examine the biological and behavioral determinants of AR.
Obesity evaluation and treatment: Expert Committee recommendations. The Maternal and Child Health Bureau, Health Resources and Services Administration and the Department of Health and Human Services.
OBJECTIVES: The development of recommendations for physicians, nurse practitioners, and nutritionists to guide the evaluation and treatment of overweight children and adolescents. METHODS: The Maternal and Child Health Bureau, Health Resources and Services Administration, the Department of Health and Human Services convened a committee of pediatric obesity experts to develop the recommendations. RESULTS: The Committee recommended that children with a body mass index (BMI) greater than or equal to the 85th percentile with complications of obesity or with a BMI greater than or equal to the 95th percentile, with or without complications, undergo evaluation and possible treatment. Clinicians should be aware of signs of the rare exogenous causes of obesity, including genetic syndromes, endocrinologic diseases, and psychologic disorders. They should screen for complications of obesity, including hypertension, dyslipidemias, orthopedic disorders, sleep disorders, gall bladder disease, and insulin resistance. Conditions that indicate consultation with a pediatric obesity specialist include pseudotumor cerebri, obesity-related sleep disorders, orthopedic problems, massive obesity, and obesity in children younger than 2 years of age. Recommendations for treatment evaluation included an assessment of patient and family readiness to engage in a weight-management program and a focused assessment of diet and physical activity habits. The primary goal of obesity therapy should be healthy eating and activity. The use of weight maintenance versus weight loss to achieve weight goals depends on each patient's age, baseline BMI percentile, and presence of medical complications. The Committee recommended treatment that begins early, involves the family, and institutes permanent changes in a stepwise manner. Parenting skills are the foundation for successful intervention that puts in place gradual, targeted increases in activity and targeted reductions in high-fat, high-calorie foods. Ongoing support for families after the initial weight-management program will help families maintain their new behaviors. CONCLUSIONS: These recommendations provide practical guidance to pediatric clinicians who evaluate and treat overweight children.
Predicting obesity in young adulthood from childhood and parental obesity.
BACKGROUND: Childhood obesity increases the risk of obesity in adulthood, but how parental obesity affects the chances of a child's becoming an obese adult is unknown. We investigated the risk of obesity in young adulthood associated with both obesity in childhood and obesity in one or both parents. METHODS: Height and weight measurements were abstracted from the records of 854 subjects born at a health maintenance organization in Washington State between 1965 and 1971. Their parents' medical records were also reviewed. Childhood obesity was defined as a body-mass index at or above the 85th percentile for age and sex, and obesity in adulthood as a mean body-mass index at or above 27.8 for men and 27.3 for women. RESULTS: In young adulthood (defined as 21 to 29 years of age), 135 subjects (16 percent) were obese. Among those who were obese during childhood, the chance of obesity in adulthood ranged from 8 percent for 1- or 2-year-olds without obese parents to 79 percent for 10-to-14-year-olds with at least one obese parent. After adjustment for parental obesity, the odds ratios for obesity in adulthood associated with childhood obesity ranged from 1.3 (95 percent confidence interval, 0.6 to 3.0) for obesity at 1 or 2 years of age to 17.5 (7.7 to 39.5) for obesity at 15 to 17 years of age. After adjustment for the child's obesity status, the odds ratios for obesity in adulthood associated with having one obese parent ranged from 2.2 (95 percent confidence interval, 1.1 to 4.3) at 15 to 17 years of age to 3.2 (1.8 to 5.7) at 1 or 2 years of age. CONCLUSIONS: Obese children under three years of age without obese parents are at low risk for obesity in adulthood, but among older children, obesity is an increasingly important predictor of adult obesity, regardless of whether the parents are obese. Parental obesity more than doubles the risk of adult obesity among both obese and nonobese children under 10 years of age.
Effects of intrauterine growth retardation in premature infants on early childhood growth.
OBJECTIVE: To evaluate in preterm infants the role of intrauterine growth retardation and infant body proportionality on subsequent childhood growth. METHODS: Preterm infants (818) prospectively enrolled in the Infant Health and Development Program were studied from birth to 36 months of corrected age. Weights and lengths were recorded at eight intervals. Growth parameters were compared in preterm infants with differing body symmetry at birth, defined by length-for-age and weight-for-age. Infants with both low length-for-age and low weight-for-age at birth were categorized as symmetrically growth retarded, and infants with normal length-for-age and low weight-for-age were categorized as asymmetrically growth retarded. RESULTS: Infants born with low length-for-age demonstrated increased growth velocity until 8 months of corrected age (p <0.001). However, infants born with low weight-for-age demonstrated decreased weight-gain velocity compared with preterm infants with appropriate weight for gestational age (AGA) until 40 weeks of corrected age (p <0.001). Heights and weights of infants with either symmetric or asymmetric intrauterine growth retardation remained significantly retarded compared with AGA preterm patients and the National Child Health Survey (NCHS) reference population (p <0.001). Infants born short but with normal weight did not significantly differ from AGA preterm infants in either weight or length at 36 months of corrected age. Preterm infants with both symmetric and asymmetric growth retardation demonstrated limited catch-up growth in weight until age 4 months and then paralleled the AGA preterm patients and the NCHS reference population. Very low birth weight (< or = 1250 gm), gestational age, and a broad-based day-care intervention did not influence growth outcome after control for the presence of intrauterine growth retardation. CONCLUSIONS: Preterm infants with both symmetric and asymmetric intrauterine growth retardation demonstrate limited catch-up growth. Intrauterine growth deficits persist into early childhood.
Body fatness and bioelectrical impedance in non-obese pre-menarcheal girls: comparison to anthropometry and evaluation of predictive equations.
OBJECTIVES: To determine in non-obese pre-menarcheal girls if bioelectrical impedance (BIA) is a better predictor of body fatness than triceps skinfold (TSF) or body mass index (BMI) and to cross-validate published equations for determination of fat-free mass (FFM) from BIA in pre-menarcheal girls. DESIGN: Cross-sectional analysis of data from 132 non-obese pre-menarcheal girls. The relationship of percent body fat (%BF), derived from isotopic dilution of H2 18O to TSF, BMI, and %BF by BIA, calculated from measures of height, weight and resistance was examined by correlation analysis. SETTING: Massachusetts Institute of Technology (MIT) Clinical Research Center in Cambridge, MA, USA. SUBJECTS: Pre-menarcheal girls aged 8-12 y were recruited from local schools, MIT summer day camp and by word of mouth. RESULTS: TSF accounted for 68% of the explained variance (R2) in the prediction of %BF measured by H2 18O, compared to 38% for BMI and 70% for BIA. Prediction of FFM by comparison of published equations was evaluated in this population. The predictive ability differed by Tanner stage. Kushner's equation (Kushner et al, 1992), based solely on height2/resistance was the only equation that provided estimates that did not differ significantly from measured values among all Tanner stages. CONCLUSIONS: BIA appears to be a valid and reliable measure of FFM but is no better than TSF in predictions of body fat.
Validity of reported energy intake in preadolescent girls.
Energy intake and energy expenditure were assessed in 109 girls aged 8-12 y. Intake was estimated from a 7-d dietary record based on household measures. Expenditure was measured with the doubly labeled water technique during 2-wk period. Overall, the mean (+/-SD) energy intake was 7.0 +/- 1.67 MJ/d and the mean energy expenditure was 8.03 +/- 1.28 MJ/d. The mean difference between intake and expenditure was 1.03 +/- 1.77 MJ/d (P < 0.0001). The mean proportion of actual intake reported was 88.3 +/- 21.0%. Multivariate-regression analysis showed that age and total daily energy expenditure were significantly and independently related to the reporting error. Coefficients for age and total daily energy expenditure were both positive, indicating that as age and daily energy expenditure increased, the magnitude of the error of reporting increased. Income, ethnicity, parental obesity, and body fat were not significantly related to accuracy of reporting. The use of food records to determine energy intake appears to provide more accurate results in younger than in older girls, and the accuracy of the method apparently decreases as energy expenditure increases.
Periods of risk in childhood for the development of adult obesity--what do we need to learn?
The prenatal period, the period of adiposity rebound and adolescence appear to represent critical periods for the development of obesity that persists into adulthood. Nonetheless, relatively little is known about the extent to which incident obesity at each of these intervals contributes to the prevalence of adult obesity. Similarly, little is known about the mechanisms that operate at each of these critical periods to entrain adult obesity.
Television viewing as a cause of increasing obesity among children in the United States, 1986-1990.
BACKGROUND AND METHODS: The prevalence of obesity among children and adolescents has increased, and television viewing has been suggested as a cause. We examined the relation between hours of television viewed and the prevalence of overweight in 1990, and the incidence and remission of overweight from 1986 to 1990 in a nationally representative cohort of 746 youths aged 10 to 15 years in 1990 whose mothers were 25 to 32 years old. Overweight was defined as a body mass index higher than the 85th percentile for age and gender. RESULTS: We observed a strong dose-response relationship between the prevalence of overweight in 1990 and hours of television viewed. The odds of being overweight were 4.6 (95% confidence interval, 2.2 to 9.6) times greater for youth watching more than 5 hours of television per day compared with those watching 0 to 2 hours. When adjustments were made for previous overweight (in 1986), baseline maternal overweight, socioeconomic status, household structure, ethnicity, and maternal and child aptitude test scores, results were similar (odds ratio, 5.3; 95% confidence interval, 2.3 to 12.1). We also found significant relations between television viewing and increased incidence and decreased remission of overweight during this 4-year period, adjusted for baseline covariates. The adjusted odds of incidence were 8.3 (95% confidence interval, 2.6 to 26.5) times greater for youth watching more than 5 hours of television per day compared with those watching for 0 to 2 hours. Estimates of attributable risk indicate that more than 60% of overweight incidence in this population can be linked to excess television viewing time. CONCLUSION: Television viewing affects overweight among youth, and reductions in viewing time could help prevent this increasingly common chronic health condition.
Is reduced metabolic rate associated with obesity?
Explore the source record for details and available documents.
The role of lifestyle in health: the epidemiology and consequences of inactivity.
Explore the source record for details and available documents.
Effect of age on body water and resting metabolic rate.
BACKGROUND: We previously reported that differences in fat-free mass (FFM) estimated by isotope dilution of 18O-labeled water could not fully account for lower resting metabolic rates (RMR) in old men and women compared to RMR in young men. METHODS: Since age-related changes in the distribution of water between extracellular and intracellular spaces could lead to overestimation of FFM in the old, we reanalyzed our data using estimates for total body and intracellular water (TBW and ICW, respectively) derived from published equations and included data from adolescent boys and girls studied under similar conditions. RESULTS: In both sexes, the age-related reduction in RMR remained significant after adjustment for estimated body water compartments (p < .05). While adjusted RMR differed in boys and girls (p < .0001), it did not in old men and women (p = .15). CONCLUSION: We conclude that aging per se reduces RMR in lean tissue, a difference which cannot be fully explained by changes in body water or its distribution. Investigators should be cautious when selecting models and equations to estimate body water compartments.