Abstract:A sample of Swedish urban schoolchildren (357 girls, 373 boys) born in 1954/55 followed from 10 to 18 years were grouped according to peak height velocity age (PHV age) into early, average and late maturers. Mean heights differed between the maturity groups at ages from 10.0 to 14.0 years for girls and 10.5 to 17.0 years for boys. Mean weights differed between the maturity groups at all ages up to 16.0 years for girls and up to 18.0 years for boys. The earlier the maturity process, the heavier for given height… Show more
“…Thus, MPV during adolescence decreases gradually as the timing of MPV becomes later. Such tendency was also shown by Lindgren (1978), among others, who showed significant differences in respective mean velocities at PHV in early, average, and late maturers. (1-4) There exists a function (t) ʰ V 0 such that { (t − k) : k ʰ z} is an orthogonal basis of V 0 .…”
“…Thus, MPV during adolescence decreases gradually as the timing of MPV becomes later. Such tendency was also shown by Lindgren (1978), among others, who showed significant differences in respective mean velocities at PHV in early, average, and late maturers. (1-4) There exists a function (t) ʰ V 0 such that { (t − k) : k ʰ z} is an orthogonal basis of V 0 .…”
“…28,33 Longitudinal data on growth of Swedish schoolchildren showed that increased body weight was associated with earlier peak height velocity in both genders. 34 The gain of 1 unit of BMI between 2 and 8 years of age was associated with an average of 0.11 years earlier for peak height velocity. 35 There are only few studies, which have investigated the hormonal regulation of the acceleration of bone age in obese children.…”
Objective: To investigate clinical and laboratory markers of pubertal development in a large sample of obese children and adolescents. Methods: Analysis of parameters of sexual maturation in 1232 obese individuals (582 boys) aged 6-18 years (mean 13.072.42 years). Clinical evaluation of pubertal stage and determination of bone age in a subset (227 patients).Results: Mean Height -standard deviation scores (height-SDS) was positive during childhood and reached zero approximately at age 14 years followed by a turn to negative mean height-SDS in both genders. Accordingly, bone age was accelerated until age 14. No significant differences in average time points of occurrence of pubic hair stages PH 2 to PH 4 in boys and PH 2 to PH 5 in girls were observed as compared to references of the First Zurich Longitudinal Study. In girls, breast stage B 3 was reached earlier (11.6 vs 12.2 years, P ¼ 0.03). In boys, mean volume of testis revealed no significant deviation from reference. Mean dehydroepiandrosterone sulfate (DHEAS) levels were elevated in boys (within age ranges 8-10 years and 12-16 years, Po0.02) and in girls (within age ranges 6-8 years and 12-18 years, Po0.005) and mean testosterone levels in boys 412 years were lower as compared to reference ranges (all P-values o0.0001). Conclusion: The study data suggest normal development of pubarche and gonadarche in obese German boys and normal timing of pubarche in girls. Breast development in obese girls seems to be slightly advanced. In obese boys, an obvious dissociation of clinical and laboratory parameters of pubertal development was observed. Despite significantly increased height-SDS and increased DHEAS levels, gonadal development was normal and testosterone levels were decreased. Elevated DHEAS levels in both genders may contribute to the acceleration of bone maturation, a lower final body height and could increase cardiovascular risk.
“…[77][78][79][80][81][82][83][84] Similar findings are observed in boys as measured by growth spurt or genital and pubic hair maturation. 81,[85][86][87] Body size measures also have been associated with early puberty, 82,86,88 as have dietary and physical activity exposures and pubertal timing. 79,[89][90][91][92][93][94] Environmental exposure to persistent halogenated organic chemicals such as PCBs, dichlorodiphenyltrichloroethane/dichlorodiphenyldichloroethylene (DDT/DDE), and brominated flame retardants have been associated with pubertal alterations, as have dioxin, hexachlorobenzene (HCB), endosulfan, and heavy metals, but to a lesser extent ( Table 2).…”
Serono Symposia International convened an expert panel to review the impact of environmental influences on the regulation of pubertal onset and progression while identifying critical data gaps and future research priorities. An expert panel reviewed the literature on endocrine-disrupting chemicals, body size, and puberty. The panel concluded that available experimental animal and human data support a possible role of endocrine-disrupting chemicals and body size in relation to alterations in pubertal onset and progression in boys and girls. Critical data gaps prioritized for future research initiatives include (1) etiologic research that focus on environmentally relevant levels of endocrine-disrupting chemicals and body size in relation to normal puberty as well as its variants, (2) exposure assessment of relevant endocrine-disrupting chemicals during critical windows of human development, and (3) basic research to identify the primary signal(s) for the onset of gonadotropinreleasing hormone-dependent/central puberty and gonadotropin-releasing hormone-independent/peripheral puberty. Prospective studies of couples who are planning pregnancies or pregnant women are needed to capture the continuum of exposures at critical windows while assessing a spectrum of pubertal markers as outcomes. Coupled with comparative species studies, such research may provide insight regarding the causal ordering of events that underlie pubertal onset and progression and their role in the pathway of adult-onset disease.
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