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      Pubertal Timing and Growth Influences Cardiometabolic Risk Factors in Adult Males and Females

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          Abstract

          OBJECTIVE

          Early pubertal onset in females is associated with increased risk for adult obesity and cardiovascular disease, but whether this relationship is independent of preceding childhood growth events is unclear. Furthermore, the association between male puberty and adult disease remains unknown. To clarify the link between puberty and adult health, we evaluated the relationship between pubertal timing and risk factors for type 2 diabetes and cardiovascular disease in both males and females from a large, prospective, and randomly ascertained birth cohort from Northern Finland.

          RESEARCH DESIGN AND METHODS

          Pubertal timing was estimated based on pubertal height growth in 5,058 subjects (2,417 males and 2,641 females), and the relationship between puberty and body weight, glucose and lipid homeostasis, and blood pressure at age 31 years was evaluated with linear regression modeling.

          RESULTS

          Earlier pubertal timing associated with higher adult BMI, fasting insulin, diastolic blood pressure, and decreased HDL cholesterol in both sexes ( P < 0.002) and with higher total serum cholesterol, LDL cholesterol, and triglycerides in males. The association with BMI and diastolic blood pressure remained statistically significant in both sexes, as did the association with insulin levels and HDL cholesterol concentrations in males after adjusting for covariates reflecting both fetal and childhood growth including childhood BMI.

          CONCLUSIONS

          We demonstrate independent association between earlier pubertal timing and adult metabolic syndrome-related derangements both in males and females. The connection emphasizes that the mechanisms advancing puberty may also contribute to adult metabolic disorders.

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          Most cited references15

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          Early age at menarche associated with cardiovascular disease and mortality.

          The relationship between age at menarche and cardiovascular disease remains unclear. Two recent studies found an inverse association between age at menarche and all-cause mortality. The aim of this study was to examine the relationship between age at menarche and cardiovascular disease risk factors, events, and mortality. A population-based prospective study involving 15,807 women, aged 40-79 yr in 1993-1997 and followed up to March 2007 for cardiovascular disease events (median follow-up 10.6 yr) and February 2008 for mortality (median follow-up 12.0 yr) was used. Odds ratios for cardiovascular disease risk factors and hazard ratios for incident cardiovascular disease and mortality were calculated. There were 3888 incident cardiovascular disease events (1323 coronary heart disease, 602 stroke, and 1963 other) and 1903 deaths (640 cardiovascular disease, 782 cancer, and 481 other) during follow-up. Compared with other women, those who had early menarche (<12 yr) had higher risks of hypertension [1.13 (1.02-1.24)], incident cardiovascular disease [1.17 (1.07-1.27)], incident coronary heart disease [1.23 (1.06-1.43)], all-cause mortality [1.22 (1.07-1.39)], cardiovascular disease mortality [1.28 (1.02-1.62)], and cancer mortality [1.25 (1.03-1.51)], adjusted for age, physical activity, smoking, alcohol, educational level, occupational social class, oral contraceptive use, hormone replacement therapy, parity, body mass index, and waist circumference. Early age at menarche (before age 12 yr) was associated with increased risk of cardiovascular disease events, cardiovascular disease mortality, and overall mortality in women, and this association appeared to be only partly mediated by increased adiposity.
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            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.
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              The adolescent growth spurt of boys and girls of the Harpenden growth study.

              Logistic curves have been fitted to the growth during puberty of the 55 boys and 35 girls of the Harpenden Growth Study who were measured every three months during puberty and thereafter until growth ceased. Very good fits were obtained for stature, sitting height, subischial leg length, biacromial and bi-iliac diameters from approximately six months after the beginning of the adolescent spurt. This beginning, called "take-off", was determined graphically as the point of minimum velocity. The total height gained from take-off point to cessation of growth averaged 28 cm in boys and 25 cm in girls with standard deviations of about 4 cm. The adult sex difference in height was due much more to the later take-off in boys than to a greater male adolescent spurt. A sex difference in the spurt occurred in sitting height but not in leg length. Mean-constant curves for the four measurements are presented. In each measurement size at take-off and total adolescent gain were nearly independent, the average correlation coefficient being --0-2. The correlations between adolescent gains in different measurements averaged only 0-47, and between peak velocities of different measurements only 0-27. This implies considerable shape change at adolescence. In contrast the average correlation between ages at which the peak velocities were reached was 0-87. Ages at take-off, at peak velocity, and at menarche were independent of mature size, though correlated with percentage of adult size reached at the ages in question, a measure of somatic maturity. Relationships with the development of breasts, pubic hair and genitalia were examined; ages at take-off and at peak velocity correlated to the extent of 0-6 to 0-8 with ages of B2 and PH2 but both these parameters and also peak velocities were uncorrelated with the rapidity with which sex characters developed.
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                Author and article information

                Journal
                Diabetes Care
                Diabetes Care
                diacare
                dcare
                Diabetes Care
                Diabetes Care
                American Diabetes Association
                0149-5992
                1935-5548
                April 2012
                13 March 2012
                : 35
                : 4
                : 850-856
                Affiliations
                [1] 1Institute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland
                [2] 2Department of Public Health, University of Helsinki, Helsinki, Finland
                [3] 3Department of Epidemiology and Biostatistics, Imperial College, London, U.K.
                [4] 4Department of Medical Statistics, London School of Hygiene and Tropical Medicine, London, U.K.
                [5] 5National Institute for Health and Welfare, Helsinki, Finland
                [6] 6Department of Obstetrics and Gynaecology, University of Oulu, Oulu, Finland
                [7] 7Finnish Institute of Occupational Health, Oulu, Finland
                [8] 8Institute of Health Sciences, University of Oulu, Oulu, Finland
                [9] 9Biocenter Oulu, University of Oulu, Oulu, Finland
                [10] 10Broad Institute of Massachusetts Institute of Technology and Harvard, Boston, Massachusetts
                [11] 11Wellcome Trust Sanger Institute, Cambridge, U.K.
                [12] 12Department of Medical Genetics, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland
                Author notes
                Corresponding author: Elisabeth Widén, elisabeth.widen@ 123456helsinki.fi .
                Article
                1365
                10.2337/dc11-1365
                3308310
                22338106
                dfd6964d-d1d9-4cd1-ac12-2a5aa3c156c6
                © 2012 by the American Diabetes Association.

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

                History
                : 20 July 2011
                : 21 December 2011
                Categories
                Original Research
                Cardiovascular and Metabolic Risk

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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