Early age at menarche increases future disease risk. Secular decline in age at menarche has been attributed to body size characteristics, diet, and energy expenditure. Risk factors for puberty have been less frequently explored.
A cross-sectional study of 186 New York Metropolitan Area, 9-year-old girls (54 African-American, 70 Hispanic, 62 Caucasians) used interviewer-administered questionnaires to assess exposures. Height and weight were measured. Pediatricians assessed pubertal development according to Tanner stages.
African-Americans were more likely than Caucasians to have achieved puberty as determined by breast or hair development (stage 2 or higher) [age-adjusted odds ratios and 95% confidence intervals = 4.91 (2.15-11.19) and 4.25 (1.85-9.77), respectively]. Pubertal development was similar among Hispanics and Caucasians. Adiposity and height were significantly positively associated with breast or hair development. More sedentary activity hours non-significantly increased the likelihood of hair development. Lower energy, but higher polyunsaturated fat, consumption were suggestive of an association with breast development. Vitamin C and hair development were inversely related. No other nutrients or physical activity measures were related to pubertal development.
Results are consistent with height and adiposity being associated with pubertal development. Sedentary activity or diet might possibly influence maturation.
"Endocrine disruption by dietary fat and obesity, or exposure to AHR ligands can alter mammary gland development during puberty. Dietary fat induces early breast development (Britton et al. 2004), and girls with higher body fat have earlier breast development than do their lean counterparts (Carmichael 2006; Himes et al. 2004; Ogden et al. 2006). Conversely, as serum dioxin concentrations increase in girls, their pubertal breast development is delayed (Den Hond et al. 2002). "
[Show abstract][Hide abstract] ABSTRACT: Increased fat intake is associated with obesity and may make obese individuals uniquely susceptible to the effects of lipophilic aryl hydrocarbon receptor (AHR) ligands.
We investigated the consequences of high-fat diet (HFD) and AHR ligands on body composition, mammary development, and hepatic P450 expression.
Pregnant C57BL/6J (B6) and DBA/2J (D2) dams, respectively expressing high- or low-responsive AHR, were dosed at mid-gestation with TCDD. At parturition, mice were placed on an HFD or a low-fat diet (LFD). Body fat of progeny was measured before dosing with 7,12-dimethylbenz[a]anthracene (DMBA). Fasting blood glucose was measured, and liver and mammary glands were analyzed.
Maternal TCDD exposure resulted in reduced litter size in D2 mice and, on HFD, reduced postpartum survival in B6 mice. In D2 mice, HFD increased body mass and fat in off-spring, induced precocious mammary gland development, and increased AHR expression compared with mice given an LFD. Maternal TCDD exposure increased hepatic Cyp1a1 and Cyp1b1 expression in offspring on both diets, but DMBA depressed Cyp1b1 expression only in mice fed an HFD. In D2 progeny, TCDD exposure decreased mammary terminal end bud size, and DMBA exposure decreased the number of terminal end buds. Only in D2 progeny fed HFD did perinatal TCDD increase blood glucose and the size of mammary fat pads, while decreasing both branch elongation and the number of terminal end buds.
We conclude that despite having a low-responsive AHR, D2 progeny fed a diet similar to that consumed by most people are susceptible to TCDD and DMBA exposure effects blood glucose levels, mammary differentiation, and hepatic Cyp1 expression.
Environmental Health Perspectives 09/2009; 117(9):1414-9. DOI:10.1289/ehp.0800530 · 7.98 Impact Factor
"Sedentary activity or higher polyunsaturated fat might possibly influence maturation, though no other nutrients or physical activity measures were related to pubertal development (Britton et al., 2004). Similar findings are reported by Koo et al. (2002), Koprowski et al. (1999) and Meyer et al. (1990). "
[Show abstract][Hide abstract] ABSTRACT: This paper provides empirical evidence on several dimensions of the potential socio-economic and physical consequences for girls of adolescent marriage using data from rural Bangladesh. I explore the commonly cited hypotheses that women attain less schooling, experience more frequent reproductive health complications, have higher fertility and experience lower levels of equality in marriage as a result of marrying young. I isolate the causal effect of marriage timing on adult outcomes by exploiting variation in the timing of menarche as an instrumental variable for age of first marriage. My results indicate that marriage age matters: Each additional year that marriage is delayed is associated with an estimated reduction of 0.27 pregnancies. This is achieved primarily through an increase in age of first pregnancy, providing additional health benefits in the form of lower incidence of stillbirths and miscarriages among younger cohorts of women. Delayed marriage is also associated with a significant increase in female schooling, adult literacy, and quality of marital life. Though they are substantial, the benefits appear to come at a high cost to families: dowry payments increase an estimated 40% of baseline cost with each additional year that marriage is postponed. workshop participants for useful comments and suggestions. Financial support is gratefully acknowledged from the Robert Wood Johnson Foundation. Please direct correspondence to <email@example.com>.
[Show abstract][Hide abstract] ABSTRACT: Breast development, one of the first signs of puberty, is closely associated with age at menarche; and early menarche is in turn a well-established risk factor for female breast cancer. We examined the relationships between the onset of puberty and gene variants for certain enzymes that regulate hormone metabolism among 137 healthy nine-year-old girls from two pediatric clinics. High-activity CYP17 alleles, involved in estrogen formation, and high-activity CYP1A2 and CYP1B1 alleles, whose gene products metabolize estradiol, were not associated with pubertal stage. High activity CYP3A4, but not CYP3A5, which primarily metabolizes testosterone, showed a striking association with the onset of puberty (adjusted odds ratio, 3.21; 95% confidence interval, 1.62-6.89 for the genotype 0-1-2 rapid alleles). Of the homozygous CYP3A4*1B/1B girls, 90% had reached puberty; whereas, for the low-activity homozygous CYP3A4*1A/1A individuals, only 40% had done so. In heterozygotes, 56% had reached puberty. CYP1B1, CYP3A4, and CYP3A5 rapid variants were more common in African-American than in Hispanic or Caucasian girls.
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