Abstract/Text: The origins of adult disease are considered to relate to fetal undernutrition, and this concept is termed "developmental origins of adult health and disease" (DOHaD). Here, we describe several epidemiological studies performed in Japan and discuss whether DOHaD is applicable to children in present day Japan. In a study of healthy children and young adults, it was found that systolic blood pressure, total cholesterol and adiponectin were associated with birth weight. Hyperinsulinemia, high blood pressure, elevated transaminase levels and prevalence of metabolic syndrome in obese children were inversely correlated with birth weight and positively correlated with current weight and waist circumference. Birth weight was related to the development of type 2 diabetes in children. DOHaD is therefore considered to be applicable in Japan. The key considerations of DOHaD are the following two mismatches. The first mismatch pertains to growth and development in response to environmental influences, especially those of nutrition. The second mismatch pertains to the prenatal versus postnatal environment. We consider that the chance of children in present day Japan developing adult diseases is determined by the above mismatches. Pediatricians and schoolteachers should therefore understand the concept of DOHaD, so that they can educate both children and their families regarding an appropriate diet to reduce the likelihood of developing adult diseases in later life.

Abstract/Text: To follow and predict the evolution of adiposity during growth, individual adiposity curves, assessed by the weight/height2 index, were drawn for 151 children from the age of 1 month to 16 yr. Adiposity increases during the 1st yr and then decreases. A renewed rise, termed here the adiposity rebound, occurs at about 6 yr. Individual weight/height2 curves may differ regarding their percentile range level and age at adiposity rebound. The present study shows a relationship between the age at adiposity rebound and final adiposity. An early rebound (before 5.5 yr) is followed by a significantly higher adiposity level than a later rebound (after 7 yr). This phenomenon is observed whatever the subject's adiposity at 1 yr. The present observations might be connected with the cellularity of adipose tissue.

Abstract/Text: OBJECTIVE: To prospectively assess the association of the metabolic syndrome in childhood with adult metabolic syndrome and type 2 diabetes mellitus (T2DM) 25 to 30 years later.
STUDY DESIGN: Data from the National Heart Lung and Blood Institute Lipid Research Clinics (LRC) Princeton Prevalence Study (1973-1976) and the Princeton Follow-up Study (PFS, 2000-2004) were used. Body mass index (BMI = kg/m(2)) was used as the obesity measure in childhood because waist circumference was not measured at the LRC. The adult T2DM status of participants and their parents was obtained by participant report or fasting blood glucose >/=126 mg/dL. A logistic analysis for clustered samples was used to predict adult metabolic syndrome and T2DM, taking into account sibling correlations in the cohort. Pediatric metabolic syndrome, age at PFS, sex, race, change in BMI percentile, parental history of diabetes, and the interaction of pediatric metabolic syndrome and parental diabetes were explanatory variables.
RESULTS: Ages ranged from 5 to 19 years in the LRC and from 30 to 48 years in the PFS. Pediatric metabolic syndrome, parental diabetes, age at follow-up, and change in age-specific BMI percentile were significant predictors of metabolic syndrome in adulthood, and pediatric metabolic syndrome, age at follow-up, black race, and parental diabetes were significant predictors of T2DM.
CONCLUSIONS: Evaluating 5- to 19-year-old children for metabolic syndrome and family history of diabetes could identify children at increased risk of adult metabolic syndrome and T2DM, allowing prospective primary prevention of these outcomes.

Abstract/Text: The purpose of this study was to determine the relationship between BMD and childhood obesity. We examined 1070 obese children (722 boys and 348 girls) aged 7 to 15 years. Their mean relative weight, as a percentage of the standard weight for age, height, and sex, was 152.9 +/- 14%. BMD was assessed, by a digital image processing method, in the second metacarpal bone of the left hand. We compared our results with those of healthy nonobese Japanese children based on both chronological and bone age. Mean BMD values for bone age in the obese children were significantly higher than those in control groups in boys aged 11 years and under and girls 9 years and under. On the other hand, in boys over 12 years old, BMD values for bone age were lower than those in the control groups. In girls over 11 years old, BMD values tended to be lower than those in the control groups. In conclusion, we studied the BMD of obese children from the point of view of advanced bone age. Our results showed that BMD was higher than in prepubertal obese children, but a low BMD value was found after puberty, due to poor gain of BMD during puberty. It is important to prevent obesity in childhood in order to prevent the low BMD after puberty.