Childhood Body Mass Index Gain Research Articles

Early life body size and its associations with adult bladder cancer

Background: Adult overweight is a potential bladder cancer (BC) risk factor, but little is known about size earlier in life.Aim: To investigate if birth weight, childhood body mass index (BMI), height and growth are associated with adult BC.Subjects and methods: Anthropometric information from birth and ages 7–13 on 315,763 individuals born 1930–1989 in the Copenhagen School Health Records Register was linked to national registers. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated by Cox regression.Results: 1145 individuals (839 men) were diagnosed with BC. Sex differences were not detected. Childhood BMI had positive associations and height had inverse associations with BC; at age 13, HR = 1.10 (95% CI: 1.02–1.18) per BMI z-score and HR = 0.94 (95% CI: 0.89–1.00) per height z-score. A pattern of above-average increases in BMI from 7 to 13 years had higher hazards of BC than average increases. Above-average growth in height was not significantly associated with BC. Compared with birth weights of 3.5 kg, low (2.5 kg) and high (4.5 kg) values were associated with increased hazards of BC; HR = 1.26 (95% CI: 1.01–1.58) and HR = 1.36 (95% CI: 1.09–1.70), respectively.Conclusions: A high BMI, a short height, excess BMI gain in childhood and low and high birth weights are associated with increased hazards of BC.

Adolescent body composition and associations with body size and growth from birth to late adolescence. The Tromsø study: Fit Futures-A Norwegian longitudinal cohort study.

Fat and fat-free masses and fat distribution are related to cardiometabolic risk. to explore how birth weight, childhood body mass index (BMI) and BMI gain were related to adolescent body composition and central obesity. In a population-based longitudinal study, body composition was measured by dual-energy X-ray absorptiometry in 907 Norwegian adolescents (48% girls). Associations between birth weight, BMI categories, and BMI gain were evaluated by fitting linear mixed models and conditional growth models with fat mass index (FMI, kg/m2 ), fat-free mass index (FFMI, kg/m2 ) standard deviation scores (SDS), and central obesity at 15 to 20years, as well as change in FMI SDS and FFMI SDS between ages 15 to 17 and 18 to 20 as outcomes. Birth weight was associated with FFMI in adolescence. Greater BMI gain in childhood, conditioned on prior body size, was associated with higher FMI, FFMI, and central overweight/obesity with the strongest associations seen at age 6 to 16.5years: FMI SDS: β=0.67, 95% CI (0.63-0.71), FFMI SDS: 0.46 (0.39, 0.52), in girls, FMI SDS: 0.80 (0.75, 0.86), FFMI SDS: 0.49 (0.43, 0.55), in boys. Compared with birth and early childhood, high BMI and greater BMI gain at later ages are strong predictors of higher fat mass and central overweight/obesity at 15 to 20years of age.

Parental nonstandard work schedules during infancy and children’s BMI trajectories

BACKGROUND: Empirical evidence has demonstrated adverse associations between parental nonstandard work schedules (i.e., evenings, nights, or weekends) and child developmental outcomes. However, there are mixed findings concerning the relationship between parental nonstandard employment and children’s body mass index (BMI), and few studies have incorporated information on paternal work schedules. OBJECTIVE: This paper investigated BMI trajectories from early to middle childhood (ages 3–11) by parental work schedules at 9 months of age, using nationally representative cohort data from the United Kingdom. This study is the first to examine the link between nonstandard work schedules and children’s BMI in the United Kingdom. METHODS: We used data from the Millennium Cohort Study (2001‒2013, n = 13,021) to estimate trajectories in BMI, using data from ages 3, 5, 7, and 11 years. Joint parental work schedules and a range of biological, socioeconomic, and psychosocial covariates were assessed in the initial interviews at 9 months. RESULTS: Compared to children in two-parent families where parents worked standard shifts, we found steeper BMI growth trajectories for children in two-parent families where both parents worked nonstandard shifts and children in single-parent families whose mothers worked a standard shift. Fathers’ shift work, compared to standard shifts, was independently associated with significant increases in BMI. CONCLUSIONS: Future public health initiatives focused on reducing the risk of rapid BMI gain in childhood can potentially consider the disruptions to family processes resulting from working nonstandard hours. CONTRIBUTION: Children in families in which both parents work nonstandard schedules had steeper BMI growth trajectories across the first decade of life. Fathers’ nonstandard shifts were independently associated with increases in BMI.

The effect of differing patterns of childhood body mass index gain on adult physiology in American Indians.

Identifying groups of individuals with similar patterns of body mass index (BMI) change during childhood may increase understanding of the relationship between childhood BMI and adult health. Discrete classes of BMI z-score change were determined in 1,920 American Indian children with at least four non diabetic health examinations between the ages of 2 and 18 years using latent class trajectory analysis. In subsets of subjects, data were available for melanocortin-4 receptor (MC4R) sequencing; in utero exposure to type 2 diabetes (T2D); or, as adults, oral glucose tolerance tests, onset of T2D, or body composition. Six separate groups were identified. Individuals with a more modern birth year, an MC4R mutation, or in utero exposure to T2D were clustered in the two groups with high increasing and chronic overweight z-scores (P < 0.0001). The z-score classes predicted adult percent fat (P < 0.0001, partial r(2) = 0.18 adjusted for covariates). There was a greater risk for T2D, independent from adult BMI, in three classes (lean increasing to overweight, high increasing, and chronic overweight z-scores) compared to the two leanest groups (respectively: HRR= 3.2, P = 0.01; 6.0, P = 0.0003; 11.6, P < 0.0001). Distinct patterns of childhood BMI z-score change associate with adult adiposity and may impact risk of T2D.

Body mass index in school-aged children and the risk of routinely diagnosed non-alcoholic fatty liver disease in adulthood: a prospective study based on the Copenhagen School Health Records Register

ObjectiveThe relation between childhood overweight and adult non-alcoholic fatty liver disease (NAFLD) is largely unknown. We investigated if weight and weight gain in childhood increases the risk of being diagnosed...

PS-355 The Different Contributions Of Body Mass Index And Height During The Life Cycle In Predicting Adult Hypertension

Background and aims Birthweight and weight gain have been associated with high adult blood pressure (BP). Less well known is the association between height gain across the life cycle and hypertension (HT). The objective of the present study is to assess the independent association of body mass index (BMI) and length at birth and BMI and height gains from birth to childhood, and from childhood to adulthood with adult blood pressure and HT. Methods A prospective cohort of all living born in Ribeirao Preto, Brazil, was assessed at birth (1978/79), school-age (1987/89) and adulthood (2002/04). Data on neonatal variables, socioeconomic position and anthropometry of all three moments as well as adult risk factors for HT were present for 1141 subjects. Conditional weight analysis was performed to assess the independent association of BMI and height repeated-in-time measurements on adult HT. Results After adjustments BMI at birth (inversely: RR = 0.58; 95% CI 0.35–0.96), BMI gain in adolescence (RR = 3.39; 95% CI 1.87–6.16) and height gain in childhood (RR = 1.95; 95% CI 1.12–3.38) were associated with adult HT. Adult systolic BP was associated with BMI at birth, BMI and height gains in childhood and adolescence. Diastolic BP was associated with BMI at birth, BMI gain in childhood and adolescence, and with height gain in childhood. Conclusion Lower BMI at birth, higher height gain between birth and school age and higher BMI gain during the second decade of life were associated with adult HT. BMI and height also predict both systolic and diastolic blood pressure. Supported CNPq, FAPESP, FAEPA.

Growth from birth to adulthood and peak bone mass and density data from the New Delhi Birth Cohort

Growth in early life may predict adult bone health. Our data showed that greater height and body mass index (BMI) gain in utero and infancy are associated with higher peak bone mass, and greater BMI gain in childhood/adolescence with higher peak bone density. These associations are mediated by attained adult height and BMI. To study the relationship of height and BMI during childhood with adult bone mineral content (BMC), areal density (aBMD) and apparent density (BMAD, estimated volumetric density). Participants comprised 565 men and women aged 33-39 years from the New Delhi Birth Cohort, India, whose weight and height were recorded at birth and annually during infancy (0-2 years), childhood (2-11 years) and adolescence (11 years-adult). Lumbar spine, femoral neck and forearm BMC and aBMD were measured using dual X-ray absorptiometry; lumbar spine and femoral neck BMAD were calculated. Birth length, and height and height gain during infancy, childhood and adolescence were positively correlated with adult BMC (p≤0.01 all sites except birth length with femoral neck). Correlations increased with height from birth to 6 years, then remained constant for later height measurements. There were no associations with BMAD. BMI at birth, and during childhood and adolescence was also positively correlated with BMC (p < 0.01 all sites). BMI at 11 years, and BMI gain in childhood and adolescence, were correlated with aBMD and BMAD (p < 0.001 for all); these correlations strengthened with increasing age of BMI measurement. The associations with height and BMI in early life became non-significant after adjustment for adult height and BMI. Greater skeletal growth and BMI gain in utero and during infancy are associated with higher peak BMC, and greater BMI gain in childhood and adolescence is associated with higher peak aBMD and BMAD. These associations are mediated by the attainment of adult height and BMI, respectively.

Pubertal timing and body mass index gain from birth to maturity in relation with femoral neck BMD and distal tibia microstructure in healthy female subjects

SummaryChildhood body mass index (BMI) gain is linked to hip fracture risk in elderly. In healthy girls, menarcheal age is inversely related to BMI gain during childhood and to femoral neck areal bone mass density (aBMD) and distal tibia structural components at maturity. This study underscores the importance of pubertal timing in age-related fragility fracture risk.IntroductionRecent data point to a relationship between BMI change during childhood and hip fracture risk in later life. We hypothesized that BMI development is linked to variation in pubertal timing as assessed by menarcheal age (MENA) which in turn, is related to peak bone mass (PBM) and hip fracture risk in elderly.MethodsWe studied in a 124 healthy female cohort the relationship between MENA and BMI from birth to maturity, and DXA-measured femoral neck (FN) aBMD at 20.4 year. At this age, we also measured bone strength related microstructure components of distal tibia by HR-pQCT.ResultsAt 20.4 ± 0.6 year, FN aBMD (mg/cm2), cortical thickness (μm), and trabecular density (mg HA/cm3) of distal tibia were inversely related to MENA (P = 0.023, 0.015, and 0.041, respectively) and positively to BMI changes from 1.0 to 12.4 years (P = 0.031, 0.089, 0.016, respectively). Significant inverse (P < 0.022 to <0.001) correlations (R = −0.21 to –0.42) were found between MENA and BMI from 7.9 to 20.4 years, but neither at birth nor at 1.0 year. Linear regression indicated that MENA Z-score was inversely related to BMI changes not only from 1.0 to 12.4 years (R = −0.35, P = 0.001), but also from 1.0 to 8.9 years, (R = −0.24, P = 0.017), i.e., before pubertal maturation.ConclusionBMI gain during childhood is associated with pubertal timing, which in turn, is correlated with several bone traits measured at PBM including FN aBMD, cortical thickness, and volumetric trabecular density of distal tibia. These data complement the reported relationship between childhood BMI gain and hip fracture risk in later life.

Predicting adult metabolic syndrome from childhood body mass index: follow-up of the New Delhi birth cohort

Objectives:To assess whether serial measurements of childhood body mass index (BMI) give clinically useful predictions of the risk of developing adult metabolic syndrome and impaired glucose tolerance or type 2...

Childhood body mass index gain during the summer versus during the school year

The nationwide increase in obesity affects all population sectors, but the impact on children is of special concern because overweight children are prone to becoming overweight adults. Contrary to the opinion of experts, research suggests that schools may be more part of the solution than the problem. Recent seasonal comparison research (comparing children's outcomes during the summer and during school year) reports that children gain body mass index (BMI) nearly twice as fast during the summer as during the school year. Whereas most children experience healthier BMI gain during the school year than the summer, this is especially the case for black and Hispanic children and for children already overweight.

Bmi in childhood and its association with height gain, timing of puberty, and final height.

No large population-based study has addressed the question of how overnutrition is related to subsequent height gain in childhood, timing of puberty, and final height. The present data represent a large Swedish population-based longitudinal growth study. Height gain in childhood, timing of reaching peak height velocity and height gain during adolescence, and final height were regarded as the short-term, interim, and long-term outcomes of childhood nutritional status, i.e. body mass index (BMI) change between 2 and 8 y. Midparental height was adjusted as the genetic influence on linear growth of the child. Childhood BMI gain was related to an increased height gain during the same period, i.e. an increase of 1 BMI unit was associated with an increase in height of 0.23 cm in boys and 0.29 cm in girls. A higher BMI gain in childhood was related to an earlier onset of puberty; the impact on the timing of puberty was 0.6 y in boys and 0.7 y in girls. Each increased unit of BMI gain in childhood also reduced the height gain in adolescence, 0.88 cm for boys and 0.51 cm for girls. No direct correlation was shown between childhood BMI gain and final height. We conclude that overnutrition between 2 and 8 y of age will not be beneficial from a final height point of view, as the temporary increase in height gain in childhood will be compensated by an earlier pubertal maturity and a subnormal height gain in adolescence.