42 research outputs found
Are Ethnic and Gender Specific Equations Needed to Derive Fat Free Mass from Bioelectrical Impedance in Children of South Asian, Black African-Caribbean and White European Origin? Results of the Assessment of Body Composition in Children Study
Background
Bioelectrical impedance analysis (BIA) is a potentially valuable method for assessing lean mass and body fat levels in children from different ethnic groups. We examined the need for ethnic- and gender-specific equations for estimating fat free mass (FFM) from BIA in children from different ethnic groups and examined their effects on the assessment of ethnic differences in body fat.
Methods
Cross-sectional study of children aged 8–10 years in London Primary schools including 325 South Asians, 250 black African-Caribbeans and 289 white Europeans with measurements of height, weight and arm-leg impedance (Z; Bodystat 1500). Total body water was estimated from deuterium dilution and converted to FFM. Multilevel models were used to derive three types of equation {A: FFM = linear combination(height+weight+Z); B: FFM = linear combination(height2/Z); C: FFM = linear combination(height2/Z+weight)}.
Results
Ethnicity and gender were important predictors of FFM and improved model fit in all equations. The models of best fit were ethnicity and gender specific versions of equation A, followed by equation C; these provided accurate assessments of ethnic differences in FFM and FM. In contrast, the use of generic equations led to underestimation of both the negative South Asian-white European FFM difference and the positive black African-Caribbean-white European FFM difference (by 0.53 kg and by 0.73 kg respectively for equation A). The use of generic equations underestimated the positive South Asian-white European difference in fat mass (FM) and overestimated the positive black African-Caribbean-white European difference in FM (by 4.7% and 10.1% respectively for equation A). Consistent results were observed when the equations were applied to a large external data set.
Conclusions
Ethnic- and gender-specific equations for predicting FFM from BIA provide better estimates of ethnic differences in FFM and FM in children, while generic equations can misrepresent these ethnic differences
Does neighborhood environment influence girls' pubertal onset? findings from a cohort study
<p>Abstract</p> <p>Background</p> <p>Pubertal onset occurs earlier than in the past among U.S. girls. Early onset is associated with numerous deleterious outcomes across the life course, including overweight, breast cancer and cardiovascular health. Increases in childhood overweight have been implicated as a key reason for this secular trend. Scarce research, however, has examined how neighborhood environment may influence overweight and, in turn, pubertal timing. The current study prospectively examined associations between neighborhood environment and timing of pubertal onset in a multi-ethnic cohort of girls. Body mass index (BMI) was examined as a mediator of these associations.</p> <p>Methods</p> <p>Participants were 213 girls, 6-8 years old at baseline, in an on-going longitudinal study. The current report is based on 5 time points (baseline and 4 annual follow-up visits). Neighborhood environment, assessed at baseline, used direct observation. Tanner stage and anthropometry were assessed annually in clinic. Survival analysis was utilized to investigate the influence of neighborhood factors on breast and pubic hair onset, with BMI as a mediator. We also examined the modifying role of girls' ethnicity.</p> <p>Results</p> <p>When adjusting for income, one neighborhood factor (Recreation) predicted delayed onset of breast and pubic hair development, but only for African American girls. BMI did not mediate the association between Recreation and pubertal onset; however, these associations persisted when BMI was included in the models.</p> <p>Conclusions</p> <p>For African American girls, but not girls from other ethnic groups, neighborhood availability of recreational outlets was associated with onset of breast and pubic hair. Given the documented risk for early puberty among African American girls, these findings have important potential implications for public health interventions related to timing of puberty and related health outcomes in adolescence and adulthood.</p
The Ups and Downs of Mutation Frequencies during Aging Can Account for the Apert Syndrome Paternal Age Effect
Apert syndrome is almost always caused by a spontaneous mutation of paternal origin in one of two nucleotides in the fibroblast growth factor receptor 2 gene (FGFR2). The incidence of this disease increases with the age of the father (paternal age effect), and this increase is greater than what would be expected based on the greater number of germ-line divisions in older men. We use a highly sensitive PCR assay to measure the frequencies of the two causal mutations in the sperm of over 300 normal donors with a wide range of ages. The mutation frequencies increase with the age of the sperm donors, and this increase is consistent with the increase in the incidence rate. In both the sperm data and the birth data, the increase is non-monotonic. Further, after normalizing for age, the two Apert syndrome mutation frequencies are correlated within individual sperm donors. We consider a mathematical model for germ-line mutation which reproduces many of the attributes of the data. This model, with other evidence, suggests that part of the increase in both the sperm data and the birth data is due to selection for mutated premeiotic cells. It is likely that a number of other genetic diseases have similar features
Report of the first case of precocious puberty in Rett syndrome
Rett syndrome is an X-linked dominant disorder frequently caused by the mutations in the methyl-CpG-binding protein 2 gene (MECP2). Its prevalence in the population is 1/15,000-20,000. Patients with Rett syndrome present apparently normal psychomotor developments during the first 6-18 months of life. Subsequently, they show a short period of developmental stagnation followed by a rapid regression in language and motor development. Precocious puberty is characterized by premature breast and pubic hair development, and advanced bone age development at 8 years of age. We present a case of Rett syndrome and precocious puberty in a 6-year-old girl. At the age of 6, the first signs of precocious puberty appeared (Tanner stage 3). Laboratory measurements were detected as follows: luteinizing hormone (LH), 0.2 mIU/mL; follicle-stimulating hormone (FSH), 1.1 mIU/mL; estradiol, 36 pg/mL; bone age, 9 years. The response to luteinizing hormone releasing hormone (gonadotropin-releasing hormone stimulation test) was characteristic for true precocious puberty (LH, 32 mIU/mL; FSH, 26 mIU/mL). This is the first reported case of precocious puberty related to Rett syndrome
Pathway-Based Analysis of the Liver Response to Intravenous Methylprednisolone Administration in Rats: Acute Versus Chronic Dosing
Testosterone, Obesity and Insulin Resistance in Young Males: Evidence for an Association between Gonadal Dysfunction and Insulin Resistance During Puberty
Normal sonographic liver and spleen dimensions in a central European pediatric population
Women’s reproductive health factors and body adiposity: findings from the UK Biobank
Objective: To conduct a comprehensive examination of the association between women’s reproductive health factors and measures of body adiposity in a contemporary Western population. Methods: A cross-sectional analysis of 502 664 individuals from the UK Biobank was conducted. Multivariable linear regression models were used to examine the association of age at menarche, age at first birth, parity and age at menopause with measures of general and central body adiposity, adjusted for age, smoking and socioeconomic status. The association between number of children and body adiposity in men was also assessed. Results: Age at menarche was inversely associated with body mass index (BMI); adjusted mean BMI was 29.0 kg m–2 in women with menarche before the age of 12 years, compared with 26.5 kg m–2 in those who had menarche after 14 years of age. Age at first birth was linearly and inversely associated with BMI: 0.16 kg m–2 lower BMI per year increase in age of first birth. Each additional live birth or child fathered was associated with a 0.22 kg m–2 higher BMI in women and a 0.14 kg m−2 higher BMI in men. There was no evidence for an association between age at menopause and BMI. Corresponding associations for other markers of general or abdominal adiposity were similar to those for BMI. Findings were broadly similar in analyses stratified by age, smoking status, socioeconomic status, ethnic background, and history of diabetes or cardiovascular disease. Conclusions: In women from a contemporary Western population, earlier age at menarche and age at first birth, and higher number of total live births were associated with higher levels of body adiposity. Prospective evaluations of the association between reproductive health factors, adiposity and the onset of cardiometabolic diseases are needed to assess causality, and to explore the mechanisms involved
