AJCN EB Program 2010
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Related articles in AJCN
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ylihärsilä, H.
Right arrow Articles by Eriksson, J. G
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ylihärsilä, H.
Right arrow Articles by Eriksson, J. G
Agricola
Right arrow Articles by Ylihärsilä, H.
Right arrow Articles by Eriksson, J. G
American Journal of Clinical Nutrition, Vol. 87, No. 6, 1769-1775, June 2008
© 2008 American Society for Nutrition

ORIGINAL RESEARCH COMMUNICATION

Body mass index during childhood and adult body composition in men and women aged 56–70 y1,2,3

Hilkka Ylihärsilä1, Eero Kajantie1, Clive Osmond1, Tom Forsén1, David JP Barker1 and Johan G Eriksson1

1 From the National Public Health Institute, Department of Epidemiology and Health Promotion, Helsinki, Finland (HY, EK, TF, and JGE); the MRC Epidemiology Resource Centre, and Developmental Origins of Adult Health and Disease Centre, University of Southampton, Southampton, United Kingdom (CO and DJPB); and the University of Helsinki, Department of Public Health, Helsinki, Finland (JGE)

See corresponding editorial on page 1587.

2 Supported by the Academy of Finland, British Heart Foundation, Finnish Diabetes Research Foundation, Finnish Foundation for Cardiovascular Research, Finnish Medical Society Duodecim, Finska Läkaresällskapet, Jalmari and Rauha Ahokas Foundation, Juho Vainio Foundation, Päivikki and Sakari Sohlberg Foundation, Signe and Ane Gyllenberg Foundation, and Yrjö Jahnsson Foundation.

3 Address reprint requests and correspondence to H Ylihärsilä, National Public Health Institute, Mannerheimintie 166, 00300 Helsinki, Finland. E-mail: hilkka.yliharsila{at}ktl.fi, or to JG Eriksson, National Public Health Institute, Mannerheimintie 166, 00300 Helsinki, Finland. E-mail: johan.eriksson{at}ktl.fi.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Background: The relation between the change in body mass index (BMI) through childhood and body composition in adult life is important because body composition is known to affect adult health.

Objective: The objective was to examine how the change in BMI throughout childhood is related to adult lean and fat mass.

Design: We examined how the change in BMI in childhood was related to adult body composition in 885 men and 1032 women born during 1934–1944, whose weights and heights during childhood were recorded serially. Adult lean and fat mass were measured by bioelectrical impedance with an 8-polar tactile electrode system.

Results: In these 56–70-y-old men and women, adult lean body mass index (lean mass/height2; in kg/m2) was positively associated with BMI at birth (0.24 and 0.20 higher for each 1-SD increase in BMI at birth, respectively) and with more rapid gain in BMI from birth to 1 y (0.17 and 0.22), 1–2 y (0.21 and 0.20), 2–7 y (0.44 and 0.46), and 7–11 y (0.32 and 0.26) of age. Fat mass index (fat mass/height2) was positively associated with more rapid increases in BMI between 2 and 11 y of age.

Conclusions: Rapid gain in BMI before the age of 2 y increased adult lean body mass without excess fat accumulation, whereas rapid gain in BMI in later childhood, despite the concurrent rise in lean mass, resulted in relatively larger increases in fat mass.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The early life origins of cardiovascular disease and type 2 diabetes have received considerable attention. Although it is now well established that these disorders are predicted by slow rates of intrauterine growth, recent observations have suggested that differences in growth patterns in infancy and childhood are also important predictors (1–4). We recently showed that a slow gain in weight and body mass index (BMI) between birth and 2 y of age was associated with coronary heart disease and its risk factors, including type 2 diabetes (1, 2) and serum lipid profiles (5). The risk of cardiovascular disease and type 2 diabetes was further increased in those individuals who put on weight rapidly during later childhood and adolescence (1–4). The potential public health impact of these observations is considerable, because BMI during infancy and childhood is more amenable to intervention than is the body size of the fetus.

However, not all findings have been consistent. Epidemiologic observations in younger populations (6) and randomized trials in extreme groups, such as infants born preterm or small for gestational age (7), have suggested associations with rapid postnatal growth and risk factors of cardiovascular disease. These discrepancies could be explained by different effects of early growth on body composition. Three studies have suggested that high rates of weight or BMI gain in infancy and childhood are associated with an increase in both adult lean mass and adiposity (8–10). However, in the study of young Indian adults the gain in BMI up to 8 y of age was more strongly associated with adult lean mass than with adiposity, whereas the strength of the association with adult adiposity increased steeply between 2 and 8 y and was sustained up to 14 y of age (8).

In the Helsinki birth cohort of men and women born during 1934–1944, we recently showed that birth weight is positively related to adult lean body mass (11). We hypothesized that the gain in SDs for BMI between birth and 2 y of age would promote high adult lean mass, whereas gain in BMI after 2 y of age would lead to a disproportionately high fat mass in relation to lean mass. Here we examined how the change in BMI throughout childhood is related to adult lean and fat mass.


   SUBJECTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
The 1917 participants in this study are a subset of a birth cohort that consists of 4630 men and 4130 women (12). They were born as singletons at Helsinki University Central Hospital between 1934 and 1944, attended child welfare clinics in the city, and lived in Finland in 1971, when a unique personal identification number was allocated to each member of the Finnish population.The majority also went to school in Helsinki. Their birth records include weight and length at birth and gestational age. Records from child welfare clinics and school health care include serial measurements of weight and height (1). On average, the participants had 10 measurements between birth and 2 y of age and 8 measurements between 2 and 11 y.

We used random-number tables to select a subset of people who were still alive and living in Finland. To obtain a sample size in excess of 2000 people, we invited 2902 subjects to attend a clinical examination; 2003 men and women agreed to do so, and 1917 subjects (885 men and 1032 women) who had measurements of body composition were included in the present study. The study was approved by the Ethics Committee of Epidemiology and Public Health of the Hospital District of Helsinki and Uusimaa. Written informed consent was obtained from each subject before any procedures were carried out.

All measurements were performed by a team of 3 trained research nurses between August 2001 and March 2004. Height was measured to the nearest 0.1 cm and weight to 0.1 kg. BMI was calculated as weight in kilograms divided by the square of height in meters. Smoking status and level of physical activity were recorded. We defined those exercising at a level comparable to brisk walking ≥3 times per week as physically active. Social class, based on occupation, was derived from the census data in 1980. Social class in childhood was classified on the basis of the father's occupation, which was recorded in birth, child welfare clinic, and school healthcare records. Families were classified as upper middle class, lower middle class, or manual workers by taking the highest social class recorded and using a classification devised by Statistics Finland.

Body composition was assessed by bioelectrical impedance using the InBody 3.0 eight-polar tactile electrode system, Biospace Co, Ltd, Seoul, Korea (13, 14). The instrument estimates lean body mass and percentage body fat by segmental multifrequency (5, 50, 250, and 500 kHz) analyses separately for each limb and trunk. The resistance measurements were made with the subject standing in light clothing on the 4-foot electrodes on the platform of the analyzer and gripping the 2 palm and thumb electrodes. This method was chosen because of its practicality in large epidemiologic studies (13, 14).

Statistical analyses
We converted each measurement of BMI for each individual to a sex-specific BMI-for-age z score (SD score). The z score is the number of SDs by which an observation differs from the mean for the whole study group. Because the children were not measured exactly on their birthdays, we obtained a z score at each birthday by interpolation if measurements had been made within 2 y of that age. Piecewise linear interpolation was used on the z scale to help accommodate nonlinearity in raw BMI with age. The correlations between BMI z scores in childhood and adult variables were analyzed. Because the number of measurements was smaller at ages 3–5 y than at other ages (866–1318 compared with 1833) and for consistency with our previous studies, data at birth and ages 1, 2, 7, and 11 y were chosen for further analysis. Periods between these ages are long enough to enable our aim to analyze the effects of a change from a growth path predicted by earlier growth.

Postnatal change in BMI between chosen ages was calculated by saving the residuals from linear regression models of BMI z scores at each successive age versus BMI z scores at all earlier ages. These residuals, which we refer to as conditional z score, are mutually uncorrelated by construction and enable the effects of change in BMI during different growth periods to be distinguished (15). Multivariate linear regression was used to examine the effects of BMI at birth and change in BMI after birth during the 4 aforementioned periods of growth on adult body composition. Analyses were adjusted for age, which affects lean and fat body components (16). Obviously, body size indicates the absolute amounts of both lean and fat mass. We therefore used height-normalized index, as has been recommended [lean and fat mass were divided by height squared, lean mass index (LMI) and fat mass index (FMI)] (17, 18). Further adjustments with lifestyle factors were performed. One extremely obese man with a BMI of 68 was excluded from the analyses. Significance was defined as P < 0.05. The statistical software used was SPSS for WINDOWS (version 13.0; SPSS Inc, Chicago, IL).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Characteristics of the study subjects in childhood and adulthood are shown in Table 1Go. According to current World Health Organization (WHO) growth charts (19), the mean BMI at birth corresponded to the 52nd and 50th percentiles in boys and in girls, respectively; 2.7% and 3.7% of newborn boys and girls, respectively, were at or above the 95th percentile. The mean BMI at age 2 y corresponded to the 68th percentile in boys and to the 71st percentile in girls according to WHO growth charts. At age 2 y, 8.7% or 7.9% of boys and 12.3% or 11.3% of girls were at or above the 95th percentile according to WHO or at or above the BMI cutoff point corresponding to a BMI of 25 at age 18 y according to the International Obesity Task Force (20), respectively. Only the latter growth charts include the age of 11 y. At this age no one was above the BMI corresponding BMI of 30, the limit for obesity, and 0.9% of boys and 3.8% of girls were overweight (at or above the BMI corresponding to a BMI of 25 at age 18 y by the IOTF; 19).


View this table:
[in this window]
[in a new window]

  		TABLE 1. Characteristics of the 1917 men and women aged 56–70 y who underwent bioimpedance analysis1

 
During the first 2 y after birth 43% of boys and 45% of girls followed the same BMI percentile (gain or loss in BMI z score ≤0.67 SD), whereas 27% and 28% of boys and girls, respectively, crossed upward. Between ages 2 and 11 y, 49% of boys and 46% of girls remained at the same BMI percentile, whereas 24% of them had crossed upward.

Adult body composition and change in BMI in infancy and childhood
The relation between childhood BMI and BMI in adulthood is shown in Figure 1Go. In both sexes, a higher adult BMI was predicted by a higher BMI throughout childhood. Similarly, a higher BMI during childhood predicted a higher LMI in adulthood. We therefore used conditional, mutually uncorrelated measures to examine to what extent the change in BMI in different periods of growth was related to adult LMI. This measure tells whether the change in BMI between 2 ages is greater or less than would be expected from BMIs at earlier ages, rapid gain meaning crossing from an original growth percentile to a higher one. Independently of each other, a higher BMI at birth and a more rapid gain in BMI during each period analyzed were associated with a higher LMI in adulthood (Table 2Go and Table 3Go). For example, a 1-SD increase in conditional BMI between birth and 1 y of age was related to a 0.17-kg/m2 and 0.22-kg/m2 increase in adult LMI in men and women, respectively. The effects of different periods of growth were similar in men and women.


Figure 1
View larger version (24K):
[in this window]
[in a new window]

  		FIGURE 1.. Cross-sectional Pearson's correlation coefficients of adult BMI, lean mass index, and fat mass index with BMI at each birthday between 0–2 and 6–11 y, with the points connected for ease of reading. Values are adjusted for adult age and shown for men and women separately; dashed lines connect the 95% confidence limits.

 

View this table:
[in this window]
[in a new window]

  		TABLE 2. Body mass, lean mass, and fat mass indexes at age 56–70 y in men according to tertiles of BMI at birth and change in BMI up to the age of 11 y1

 

View this table:
[in this window]
[in a new window]

  		TABLE 3. Body mass, lean mass, and fat mass indexes at age 56–70 y in women according to tertiles of BMI at birth and change in BMI up to the age of 11 y

 
The FMI in adulthood was predicted by a higher BMI later in childhood (Figure 1Go). Accordingly, a higher FMI was predicted by a higher gain in BMI between 2 and 7 y and between 7 and 11 y, but not by BMI at birth or change in BMI between birth and 2 y (Tables 2Go and 3Go). Percentage body fat showed similar associations. Birth weight and rate of weight gain in childhood predicted adult LMI and FMI in the same way as did childhood BMI.

Adult body composition in relation to age and lifestyle factors
In a simultaneous regression with age, physical activity level, smoking status, and social class in childhood and in adulthood, LMI was lower by higher age in men (β = –0.06 kg/m2/y; 95% CI: –0.11, –0.02; P < 0.006). In women, LMI was lower by higher social class in adulthood (P = 0.003). Higher FMI was predicted by physical inactivity (P < 0.0001), by lower social class in adulthood (P = 0.03 in men and 0.0005 in women), in men by nonsmoking (P = 0.02) and lower social class in childhood (P = 0.0003), and in women by higher age (P = 0.004). Adjustment for these variables did not change the relations between childhood growth and adult body composition.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
We found that the timing and magnitude of gain in SDs for BMI during childhood had a significant impact on the adult body fat and lean compartments in 56–70-y-old men and women. High BMI at birth and rapid gain in z scores for BMI in infancy and in early and late childhood up to the age 11 y were independently related to higher adult lean body mass. Higher adult body fat mass was predicted only by a rapid increase in BMI beginning after 2 y of age.

Comparison with previous studies
Fetuses and children are suggested to follow their genetically set growth trajectory (21). Prenatally restricted growth for nutritional or other reasons would not reset this trajectory, but would be followed after birth by compensatory accelerated growth aimed at reaching the original growth path. This is illustrated by studies showing that 25% of all infants and {approx}90% of infants born small for gestational age show postnatal catch-up growth in weight, height, and BMI (22–24), usually evident by 6 mo of age. Overall, only 50% of all infants follow the same weight or length centile position from birth (23). Our results are comparable with the following: 46% of boys and 47% of girls followed the same BMI percentile during the first year after birth.

All 3 studies, which assessed the effects of childhood growth rate on body components in later life, have associated both early and later rapid growth positively with adult lean mass consistently with our findings (8–10). However, in contrast with our study, early growth predicted adult fat mass. A study of 17-y-oldSwedish men and women reported that rapid weight gain during the first 6 mo after birth, as well as between 3 and 6 y of age, predicted higher fat mass and percentage body fat in addition to fat-free mass (9). A study in young adults in India showed, however, that higher BMI at birth and rapid gain in BMI during infancy and childhood up to 8 y of age were associated more strongly with higher adult lean mass than with adiposity (8). Correspondingly, in 18-y-old Brazilian men, the increments in both lean and fat mass were related to weight gain during all assessed periods (0–1, 1–2, 2–4, and 4–15 y), but the ratio of fat to lean mass was associated with weight gain during later childhood, from 4 y onward (10). To what extent younger age, slenderness, different methods, nutritional status of the population, or ethnic background of the subjects in these studies explain their dissimilar results is unknown.

We emphasize that, despite the rapid gain in BMI between 2 and 11 y of age that was related to adult adiposity, only a small minority of our subjects were overweight as children. According to the contemporary International Obesity Task Force BMI references (20), at age 11 y, only 1–4% exceeded the limit for overweight; no one was obese. We also stress that the adult adiposity–related rise from the earlier BMI percentile to a higher one between the ages 2 and 7 y may have happened at any age during this period. We did not split this period to shorter ones because the limited number of measurements between 2 and 7 y might have introduced error.

Our subjects may not be representative of the population born in Helsinki. The data are restricted to subjects who were born in the University Hospital, attended voluntary child welfare clinics, went to school in Helsinki, did not emigrate, and were still alive and willing to participate in the year 2003. However, we believe that our results, based on internal comparisons within the cohort, are unlikely to differ between those who attended and those who did not. Another concern is that our study has a limited applicability to contemporary cohorts in the Western world. These men and women were children around the World War II and some of them may have suffered from food shortages. In addition, there is evidence that children from historical cohorts may have different fatness for a given BMI compared with contemporary children (25).

Early growth and adult health: public health relevance
Alteration in body composition may be one of the mechanisms behind the association between early growth trajectories and the adult metabolic syndrome and related traits. In the present study, rapid gain in BMI before the age of 2 y promoted gain in lean mass but not in fat mass; early poor gain in BMI might predispose to deficiency in lean mass. Because lean mass consists primarily of muscle tissue, which is a major site for insulin-mediated glucose metabolism, this deficiency in lean mass may further predispose to reduced insulin sensitivity, an early and central feature of the metabolic syndrome. On the other hand, after the age of 2 y, rapid gain in BMI was related to a higher increase in fat mass in relation to lean mass. During recent years, adipose tissue has been recognized as a metabolically active tissue that secretes several agents that regulate processes involved in carbohydrate and fat metabolism (26). Increased fat mass per se, particularly in subjects with low compensatory lean mass, may thus induce insulin resistance, which promotes the development of type 2 diabetes and cardiovascular disease. Indeed, in studies assessing the relations between early growth and adult health, a period of poor fetal or infant growth preceding later rapid gain in weight or BMI seems to predict adverse adult health outcomes, including glucose intolerance and coronary heart disease (1, 2, 4, 12). According to a recent review, studies from countries undergoing the nutritional transition are consistent in showing that growth failure in early childhood and development of overweight in later childhood are associated with several cardiometabolic risk factors in early adulthood (27).

The pathway to adult cardiovascular diseases and type 2 diabetes in the Helsinki Birth Cohort Study is different from that leading to obesity. Children who later gained weight to exceed a BMI of 30 in adult life had above-average and increasing z scores for BMI at all ages from birth to 12 y of age (28). Several contemporary studies have shown a similar association between rapid weight gain in infancy and later risk of obesity, as assessed mainly by BMI (23, 29–32). However, studies assessing obesity on the basis of BMI should be interpreted with caution because BMI does not distinguish between lean and fat mass. In the present study, rapid weight or BMI gain in infancy, as well as in later childhood, predicted higher adult lean mass, which contributes to higher BMI and thus increases the likelihood of exceeding the obesity cutoff. In addition, a recent study showed that increases in BMI percentile in children aged 8–18 y reflected uniform increases in fat-free mass across the range of BMI percentiles, whereas percentage body fat tended to increase dramatically only at higher BMI percentiles (33). That study also suggested that, even in the overweight range, BMI may reflect different degrees of fatness in boys versus girls and in younger versus older children.

In conclusion, the results of this study suggest that rapid gain in BMI before the age of 2 y promotes an increase in lean mass and later rapid gain in BMI, which results in an increase in fat mass in relation to lean mass. These findings provide further insight into the mechanisms that underlie the link between low birth weight or thinness at birth, childhood growth patterns, and adult health outcomes.


   ACKNOWLEDGMENTS
 
The responsibilities of the authors were as follows—DJPB and JGE: conception of the study and obtaining funding; HY, EK, TF, and JGE: conduct of the study; TF, EK, and CO: data set preparation; CO: statistical expertise; and HY: data analysis, interpretation, and writing of the manuscript with review and input from EK, CO, DJPB, and JGE. All authors were responsible for the study design. None of the authors had a conflict of interest.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Barker DJ, Osmond C, Forsén TJ, Kajantie E, Eriksson JG. Trajectories of growth among children who have coronary events as adults. N Engl J Med 2005;353:1802–9.[Abstract/Free Full Text]
  2. Eriksson JG, Osmond C, Kajantie E, Forsén TJ, Barker DJ. Patterns of growth among children who later develop type 2 diabetes or its risk factors. Diabetologia 2006;49:2853–8.[Medline]
  3. Eriksson JG, Forsén TJ, Osmond C, Barker DJ. Pathways of infant and childhood growth that lead to type 2 diabetes. Diabetes Care 2003;26:3006–10.[Abstract/Free Full Text]
  4. Bhargava SK, Sachdev HS, Fall CH, et al. Relation of serial changes in childhood body-mass index to impaired glucose tolerance in young adulthood. N Engl J Med 2004;350:865–75.[Abstract/Free Full Text]
  5. Kajantie E, Barker DJ, Osmond C, Forsén T, Eriksson JG. Growth before 2 years of age and serum lipids 60 years later: the Helsinki Birth Cohort study. Int J Epidemiol 2008;37(2):280–9.[Abstract/Free Full Text]
  6. Ong KK, Petry CJ, Emmett PM, et al. Insulin sensitivity and secretion in normal children related to size at birth, postnatal growth, and plasma insulin-like growth factor-I levels. Diabetologia 2004;47:1064–70.[Medline]
  7. Singhal A, Cole TJ, Fewtrell M, Deanfield J, Lucas A. Is slower early growth beneficial for long-term cardiovascular health? Circulation 2004;109:1108–13.[Abstract/Free Full Text]
  8. Sachdev HS, Fall CH, Osmond C, et al. Anthropometric indicators of body composition in young adults: relation to size at birth and serial measurements of body mass index in childhood in the New Delhi birth cohort. Am J Clin Nutr 2005;82:456–66.[Abstract/Free Full Text]
  9. Ekelund U, Ong K, Linne Y, et al. Upward weight percentile crossing in infancy and early childhood independently predicts fat mass in young adults: the Stockholm Weight Development Study (SWEDES). Am J Clin Nutr 2006;83:324–30.[Abstract/Free Full Text]
  10. Victora CG, Sibbritt D, Horta BL, Lima RC, Cole T, Wells J. Weight gain in childhood and body composition at 18 years of age in Brazilian males. Acta Paediatr 2007;96:296–300.[Medline]
  11. Ylihärsilä H, Kajantie E, Osmond C, Forsén T, Barker DJ, Eriksson JG. Birth size, adult body composition and muscle strength in later life. Int J Obes (Lond) 2007;31:1392–9.[Medline]
  12. Eriksson JG, Forsén T, Tuomilehto J, Osmond C, Barker DJ. Early growth and coronary heart disease in later life: longitudinal study. BMJ 2001;322:949–53.[Abstract/Free Full Text]
  13. Bedogni G, Malavolti M, Severi S, et al. Accuracy of an eight-point tactile-electrode impedance method in the assessment of total body water. Eur J Clin Nutr 2002;56:1143–8.[Medline]
  14. Malavolti M, Mussi C, Poli M, et al. Cross-calibration of eight-polar bioelectrical impedance analysis versus dual-energy X-ray absorptiometry for the assessment of total and appendicular body composition in healthy subjects aged 21–82 years. Ann Hum Biol 2003;30:380–91.[Medline]
  15. Gale CR, O'Callaghan FJ, Bredow M, Martyn CN. The influence of head growth in fetal life, infancy, and childhood on intelligence at the ages of 4 and 8 years. Pediatrics 2006;118:1486–92.[Abstract/Free Full Text]
  16. Gallagher D, Ruts E, Visser M, et al. Weight stability masks sarcopenia in elderly men and women. Am J Physiol Endocrinol Metab 2000;279:E366–75.[Abstract/Free Full Text]
  17. Wells JC. A critique of the expression of paediatric body composition data. Arch Dis Child 2001;85:67–72.[Abstract/Free Full Text]
  18. VanItallie TB, Yang MU, Heymsfield SB, Funk RC, Boileau RA. Height-normalized indices of the body's fat-free mass and fat mass: potentially useful indicators of nutritional status. Am J Clin Nutr 1990;52:953–9.[Abstract/Free Full Text]
  19. World Health Organization. The WHO Child Growth Standards. Internet: http://www.who.int/childgrowth/standards/en/ (accessed May 2007).
  20. Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. Establishing a standard definition for child overweight and obesity worldwide: international survey. BMJ 2000;320:1240–3.[Abstract/Free Full Text]
  21. Tanner J. Growth as a target-seeking function: catch-up and catch-down growth in man. 2nd ed. New York, NY: Plenum Press, 1986.
  22. Karlberg J, Albertsson-Wikland K. Growth in full-term small-for-gestational-age infants: from birth to final height. Pediatr Res 1995;38:733–9.[Medline]
  23. Ong KK, Ahmed ML, Emmett PM, Preece MA, Dunger DB. Association between postnatal catch-up growth and obesity in childhood: prospective cohort study. BMJ 2000;320:967–71.[Abstract/Free Full Text]
  24. Ezzahir N, Alberti C, Deghmoun S, et al. Time course of catch-up in adiposity influences adult anthropometry in individuals who were born small for gestational age. Pediatr Res 2005;58:243–7.[Medline]
  25. Wells JC, Coward WA, Cole TJ, Davies PS. The contribution of fat and fat-free tissue to body mass index in contemporary children and the reference child. Int J Obes Relat Metab Disord 2002;26:1323–8.[Medline]
  26. Rosen ED, Spiegelman BM. Adipocytes as regulators of energy balance and glucose homeostasis. Nature 2006;444:847–53.[Medline]
  27. Stein AD, Thompson AM, Waters A. Childhood growth and chronic disease: evidence from countries undergoing the nutrition transition. Matern Child Nutr 2005;1:177–84.[Medline]
  28. Eriksson J, Forsén T, Osmond C, Barker D. Obesity from cradle to grave. Int J Obes Relat Metab Disord 2003;27:722–7.[Medline]
  29. Dietz WH. Critical periods in childhood for the development of obesity. Am J Clin Nutr 1994;59:955–9.[Abstract/Free Full Text]
  30. Stettler N, Zemel BS, Kumanyika S, Stallings VA. Infant weight gain and childhood overweight status in a multicenter, cohort study. Pediatrics 2002;109:194–9.[Abstract/Free Full Text]
  31. Baird J, Fisher D, Lucas P, Kleijnen J, Roberts H, Law C. Being big or growing fast: systematic review of size and growth in infancy and later obesity. BMJ 2005;331:929.[Abstract/Free Full Text]
  32. Monteiro PO, Victora CG. Rapid growth in infancy and childhood and obesity in later life—a systematic review. Obes Rev 2005;6:143–54.[Medline]
  33. Demerath EW, Schubert CM, Maynard LM, et al. Do changes in body mass index percentile reflect changes in body composition in children? Data from the Fels Longitudinal Study. Pediatrics 2006;117:e487–95.[Abstract/Free Full Text]
Received for publication December 13, 2007. Accepted for publication January 4, 2008.


Related articles in AJCN:

The first months of life: a critical period for development of obesity
Matthew W Gillman
AJCN 2008 87: 1587-1589. [Full Text]  




This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Related articles in AJCN
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ylihärsilä, H.
Right arrow Articles by Eriksson, J. G
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ylihärsilä, H.
Right arrow Articles by Eriksson, J. G
Agricola
Right arrow Articles by Ylihärsilä, H.
Right arrow Articles by Eriksson, J. G

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS