- Email: [email protected]
Early menarche and adult height: Reprise of the hare and the tortoise?
PEDIATRICS THE JOURNAL OF
May 2001
Volume 138
Number 5
EDITORIALS
Early menarche and adult height: Reprise of the hare and the tortoise? The age at menarche has decreased significantly over the past 150 years, with a more modest lowering over the most recent 4 decades.1 Many explanations have been proffered, but it is likely that there are important interactions among better nutrition, lessened burden of infectious diseases, better environmental conditions, and, more recently, the epidemic of obesity.2 Endocrine causes of obesity are rare (eg, hypothyroidism, Cushing’s syndrome, and growth hormone deficiency) and are associated with small stature. In contrast, children with exogenous obesity are tall-for-age. The report of Biro et al3 in this issue of The Journal provides contemporary standards of longitudinal development for white and black female adolescents in the United States, aged 9 through 19 years, in relation to the timing of pubertal maturation. In addition, the investigators have evaluated the impact of early-, mid-, and late-onset maturation as assessed by age at menarche on height velocity, body mass index [weight (kg)/height2 (m2)], and the regional distribution of body fat. The power of this study is in the very large Reprints not available from author. Correspondence: Alan D. Rogol, MD, PhD, INSMED Pharmaceuticals, Inc, 800 E Leigh St, Richmond, VA 23219.
J Pediatr 2001;138:617-8. Copyright © 2001 by Mosby, Inc. 0022-3476/2001/$35.00 + 0 9/18/114697 doi:10.1067/mpd.2001.114697
number of subjects (almost 2400), the longitudinal nature of the data, and the dual racial and multiple socioeconomic class composition of the cohort. The key finding was that adult height was associated with age at menarche in both races, with the earliest maturers being tallest at younger ages but shortest when adult stature had been attained (see Fig 1 of the published report3). At all ages, the average weight was greatest among the early maturers, although some of the excess weight in the earliest maturers was due to being taller. The body mass index was also greatest in the early maturers, denoting greater relative fatness, as well as greater absolute weight.
See related article, p 636. The lifelong consequences of obesity are related to syndrome X or the metabolic syndrome of obesity, hypertension, cardiovascular disease, and insulin resistance, including type 2 diabetes mellitus and its attendant comorbidities.4 The regional distribution of body fat—visceral versus subcutaneous, axial versus peripheral, and upper body versus lower body—can contribute to the lifelong morbidity; however, no differences between groups or races were noted. The methods used, several skin-fold measurements and the waist/hip ratio, are likely too insensitive to detect important differences that might be found by more
exacting measurement protocols. In other words, the chance for a Type II statistical error might be quite high. A magnetic resonance imaging technique, although impractical for this very large cohort, could distinguish visceral and subcutaneous (abdominal) fat in the same slice, for it is the visceral fat that is apparently better correlated to later cardiovascular risk and syndrome X. The investigators describe the diverse socioeconomic status of the cohort of girls, and one would appreciate an analysis by this parameter, including race. The authors have indicated that such an analysis will appear in a separate article. There is a large amount of data relevant to the issues described above in other places of the report, which state “data not shown.” It would be a great service if this study, initiated and funded by the National Heart, Lung, and Blood Institute, had all of the data available to investigators in an electronic format. This is a very large set of longitudinally gathered data and should be available to those who study adolescent health and those who make health policy for adolescents. The data analysis is, however, mainly cross-sectional. The full power of the longitudinal design should be used. As stated earlier in this commentary, one has a very good idea of the timing of menarche with reference to growth; however, a second biologic anchor, peak height velocity, has not yet been considered. This parameter could 617
EDITORIALS
easily be modeled from the data (eg, the Preece-Baines method5), and a comparison between these welldescribed biologic events could be made. It is my contention that they would be the most tightly correlated of all of the parameters measured because they represent an integrated index of the degree of biologic maturation accounting for genetic, nutritional, psychosocial, and socioeconomic factors. In summary, Biro et al3 have presented a wealth of data to show that early maturing, more rapidly growing girls are the tallest early on (the hare in the race between the hare and the tortoise) but become the smallest as adults because one of the concomitants
618
THE JOURNAL OF PEDIATRICS MAY 2001 of early maturation is greater total body exposure to estrogens, resulting in skeletal maturation. Those who mature the latest are the smallest early on but eventually become the tallest adults (the tortoise “wins” the race). Alan D. Rogol, MD, PhD Professor of Clinical Pediatrics University of Virginia Clinical Professor of Internal Medicine Medical College of Virginia Virginia Commonwealth University Charlottesville, VA 22911-8441
REFERENCES 1. Tanner JM. Growth at adolescence. 2nd ed. Oxford: Blackwell Scientific Publications Limited; 1962. p. 94-155.
2. Chinn S, Rona RJ. Prevalence and trends in overweight and obesity in three cross sectional studies of British children, 1974-94. BMJ 2001; 322:24-6. 3. Biro FM, McMahon RP, StriegelMoore R, Crawford PB, Obarzanek E, Morrison JA, et al. Impact of timing of pubertal maturation on growth in black and white female adolescents: the National Heart, Lung, and Blood Institute Growth and Health Study. J Pediatr 2001;138:636-43. 4. Reaven GM. Role of insulin resistance in human disease (syndrome X): an expanded definition. Annu Rev Med 1993;44:121-31. 5. Preece MA, Baines MJ. A new family of mathematical models describing the human growth curve. Ann Hum Biol 1978;5:1-24.
May 2001
Volume 138
Number 5
EDITORIALS
Early menarche and adult height: Reprise of the hare and the tortoise? The age at menarche has decreased significantly over the past 150 years, with a more modest lowering over the most recent 4 decades.1 Many explanations have been proffered, but it is likely that there are important interactions among better nutrition, lessened burden of infectious diseases, better environmental conditions, and, more recently, the epidemic of obesity.2 Endocrine causes of obesity are rare (eg, hypothyroidism, Cushing’s syndrome, and growth hormone deficiency) and are associated with small stature. In contrast, children with exogenous obesity are tall-for-age. The report of Biro et al3 in this issue of The Journal provides contemporary standards of longitudinal development for white and black female adolescents in the United States, aged 9 through 19 years, in relation to the timing of pubertal maturation. In addition, the investigators have evaluated the impact of early-, mid-, and late-onset maturation as assessed by age at menarche on height velocity, body mass index [weight (kg)/height2 (m2)], and the regional distribution of body fat. The power of this study is in the very large Reprints not available from author. Correspondence: Alan D. Rogol, MD, PhD, INSMED Pharmaceuticals, Inc, 800 E Leigh St, Richmond, VA 23219.
J Pediatr 2001;138:617-8. Copyright © 2001 by Mosby, Inc. 0022-3476/2001/$35.00 + 0 9/18/114697 doi:10.1067/mpd.2001.114697
number of subjects (almost 2400), the longitudinal nature of the data, and the dual racial and multiple socioeconomic class composition of the cohort. The key finding was that adult height was associated with age at menarche in both races, with the earliest maturers being tallest at younger ages but shortest when adult stature had been attained (see Fig 1 of the published report3). At all ages, the average weight was greatest among the early maturers, although some of the excess weight in the earliest maturers was due to being taller. The body mass index was also greatest in the early maturers, denoting greater relative fatness, as well as greater absolute weight.
See related article, p 636. The lifelong consequences of obesity are related to syndrome X or the metabolic syndrome of obesity, hypertension, cardiovascular disease, and insulin resistance, including type 2 diabetes mellitus and its attendant comorbidities.4 The regional distribution of body fat—visceral versus subcutaneous, axial versus peripheral, and upper body versus lower body—can contribute to the lifelong morbidity; however, no differences between groups or races were noted. The methods used, several skin-fold measurements and the waist/hip ratio, are likely too insensitive to detect important differences that might be found by more
exacting measurement protocols. In other words, the chance for a Type II statistical error might be quite high. A magnetic resonance imaging technique, although impractical for this very large cohort, could distinguish visceral and subcutaneous (abdominal) fat in the same slice, for it is the visceral fat that is apparently better correlated to later cardiovascular risk and syndrome X. The investigators describe the diverse socioeconomic status of the cohort of girls, and one would appreciate an analysis by this parameter, including race. The authors have indicated that such an analysis will appear in a separate article. There is a large amount of data relevant to the issues described above in other places of the report, which state “data not shown.” It would be a great service if this study, initiated and funded by the National Heart, Lung, and Blood Institute, had all of the data available to investigators in an electronic format. This is a very large set of longitudinally gathered data and should be available to those who study adolescent health and those who make health policy for adolescents. The data analysis is, however, mainly cross-sectional. The full power of the longitudinal design should be used. As stated earlier in this commentary, one has a very good idea of the timing of menarche with reference to growth; however, a second biologic anchor, peak height velocity, has not yet been considered. This parameter could 617
EDITORIALS
easily be modeled from the data (eg, the Preece-Baines method5), and a comparison between these welldescribed biologic events could be made. It is my contention that they would be the most tightly correlated of all of the parameters measured because they represent an integrated index of the degree of biologic maturation accounting for genetic, nutritional, psychosocial, and socioeconomic factors. In summary, Biro et al3 have presented a wealth of data to show that early maturing, more rapidly growing girls are the tallest early on (the hare in the race between the hare and the tortoise) but become the smallest as adults because one of the concomitants
618
THE JOURNAL OF PEDIATRICS MAY 2001 of early maturation is greater total body exposure to estrogens, resulting in skeletal maturation. Those who mature the latest are the smallest early on but eventually become the tallest adults (the tortoise “wins” the race). Alan D. Rogol, MD, PhD Professor of Clinical Pediatrics University of Virginia Clinical Professor of Internal Medicine Medical College of Virginia Virginia Commonwealth University Charlottesville, VA 22911-8441
REFERENCES 1. Tanner JM. Growth at adolescence. 2nd ed. Oxford: Blackwell Scientific Publications Limited; 1962. p. 94-155.
2. Chinn S, Rona RJ. Prevalence and trends in overweight and obesity in three cross sectional studies of British children, 1974-94. BMJ 2001; 322:24-6. 3. Biro FM, McMahon RP, StriegelMoore R, Crawford PB, Obarzanek E, Morrison JA, et al. Impact of timing of pubertal maturation on growth in black and white female adolescents: the National Heart, Lung, and Blood Institute Growth and Health Study. J Pediatr 2001;138:636-43. 4. Reaven GM. Role of insulin resistance in human disease (syndrome X): an expanded definition. Annu Rev Med 1993;44:121-31. 5. Preece MA, Baines MJ. A new family of mathematical models describing the human growth curve. Ann Hum Biol 1978;5:1-24.