Methods: Anthropometric data from three contemporary Danish population-based studies were combined. References for height were based on healthy Caucasian children born at term. A total of 12 671 height measurements (8055 in boys and 4616 in girls) were included. Reference charts were developed using the generalised additive models for location, scale and shape.Results: From prepubertal ages, a secular increase in height was observed for both genders. The differences were most pronounced in puberty, and final heights were increased by 1.4 cm in boys and 2.9 cm in girls compared to 1982 references. In boys, but not girls an upward shift in body mass index (BMI) above median levels was found. Reference curves for height were superimposable with standard curves based on the selective WHO criteria. Danish children were longer/taller and heavier and they had larger head circumferences than those reported in the recent multiethnic WHO standards.

BACKGROUND AND OBJECTIVES: Studies of adolescents often use self-assessment of pubertal maturation, the reliability of which has shown conflicting results. We aimed to examine the reliability of child and parent assessments of healthy boys and girls.METHODS: A total of 898 children (418 girls, 480 boys, age 7.4-14.9 years) and 1173 parents (550 daughters, 623 sons, age 5.6-14.7 years) assessed onset of puberty or development of breasts, genitals, and pubic hair according to Tanner stages by use of a questionnaire and drawings. Physicians' assessments were blinded and set as the gold standard. Percentage agreement, k, and Kendall's correlation were used to analyze the agreement rates.RESULTS: Breast stage was assessed correctly by 44.9% of the girls (k = 0.28, r = 0.74, P , .001) and genital stage by 54.7% of the boys (k = 0.33, r = 0.61, P , .001). For pubic hair stage 66.8% of girls (k = 0.55, r = 0.80, P , .001) and 66.1% of boys (k = 0.46, r = 0.70, P , .001) made correct assessments. Of the parents, 86.2% correctly assessed onset of puberty in girls (k = 0.70, r = 0.71, P , .001) and 68.4% in boys (k = 0.30, r = 0.37, P , .001). Children who underestimated were younger and children who overestimated older than their peers who made correct assessments. Girls and their parents tended to underestimate, whereas boys overestimated their pubertal stage.CONCLUSIONS: Pubertal assessment by the child or the parents is not a reliable measure of exact pubertal staging and should be augmented by a physical examination. However, for large epidemiologic studies self-assessment can be sufficiently accurate for a simple distinction between prepuberty and puberty.WHAT'S KNOWN ON THIS SUBJECT: Many population-based studies including pubertal children are based on self-assessment of pubertal maturation, the reliability of which is uncertain.WHAT THIS STUDY ADDS: Self-assessment is not reliable for precise pubertal staging. Simple distinctions between prepuberty and puberty showed moderate agreement with clinical examinations. Parents and girls tended to underestimate and boys to overestimate pubertal development by up to 50% and 30%, respectively.

SF %BF showed the highest correlation and best agreement with DXA %BF in identifying children with excess fat (+1 s.d.).

SummaryThe evidence for the existence of testicular dysgenesis syndrome (TDS) is presented in this review. Several epidemiological studies have shown that conditions like cryptorchidism, impaired spermatogenesis, hypospadias and testicular cancer can be associated as risk factors for each other. Thus, the risk of testis cancer is significantly increased in men with cryptorchidism and/or infertility. Several recent studies point towards early dysgenesis of the foetal testis as the biological link between these disorders. Dysgenesis has been demonstrated in biopsies of the contralateral testis of men with testis cancer and in infertile men. The histological evidence includes immature seminiferous tubules with undifferentiated Sertoli cells, microliths and Sertoli-cell only tubules. Dysgenetic testes often have an irregular ultrasound pattern, where microliths may also be visible. Our current hypothesis is that maternal exposure to endocrine disrupting chemicals may contribute to the pathogenesis of TDS. Animal experiments have shown that all TDS symptoms, except testicular cancer, can be induced by foetal exposure to anti-androgenic chemicals. However, the cause of TDS in humans remains to be determined.