Association between general and central adiposity in childhood, and change in these, with cardiovascular risk factors in adolescence: prospective cohort studyBMJ 2010; 341 doi: http://dx.doi.org/10.1136/bmj.c6224 (Published 26 November 2010) Cite this as: BMJ 2010;341:c6224
- Debbie A Lawlor, professor of epidemiology12,
- Li Benfield, research associate12,
- Jennifer Logue, clinical lecturer in metabolic medicine3,
- Kate Tilling, reader in statistics2,
- Laura D Howe, research associate12,
- Abigail Fraser, research fellow12,
- Lynne Cherry, research staff3,
- Pauline Watt, research staff3,
- Andrew R Ness, professor of epidemiology4,
- George Davey Smith, professor of epidemiology12,
- Naveed Sattar, professor of metabolic medicine3
- 1MRC Centre for Causal Analyses in Translational Epidemiology, University of Bristol, Bristol BS8 2BN, UK
- 2School of Social and Community Medicine, University of Bristol, Bristol
- 3Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow
- 4Department of Oral and Dental Science, University of Bristol, Bristol
- Correspondence to: D Lawlor
- Accepted 14 September 2010
Objectives To examine the prospective associations between body mass index (BMI), waist circumference, and fat mass in childhood and cardiovascular risk factors at age 15-16.
Design Prospective cohort study.
Setting Avon Longitudinal Study of Parents and Children.
Participants 5235 children aged 9-12 at start of study.
Main exposures BMI, waist circumference, and fat mass determined by dual energy x ray absorptiometry, assessed at age 9-12 and at age 15-16.
Main outcome measures Systolic and diastolic blood pressure and concentrations of fasting glucose, insulin, triglycerides, low density lipoprotein cholesterol, and high density lipoprotein cholesterol assessed at age 15-16.
Results In girls a 1 SD greater BMI at age 9-12 was associated with cardiovascular risk factors at age 15-16 in fully adjusted models: odds ratio 1.23 (95% confidence interval 1.10 to 1.38) for high systolic blood pressure (≥130 mm Hg); 1.19 (1.03 to 1.38) for high concentration of low density lipoprotein cholesterol (≥2.79 mmol/l); 1.43 (1.06 to 1.92) for high concentration of triglycerides (≥1.7 mmol/l); 1.25 (1.08 to 1.46) for low concentration of high density lipoprotein cholesterol (<1.03 mmol/l); and 1.45 (1.22 to 1.73) for high concentration of insulin (≥16.95 IU/l). Equivalent results in boys were 1.24 (1.13 to 1.37) for systolic blood pressure; 1.30 (1.07 to 1.59) for low density lipoprotein cholesterol; 1.96 (1.51 to 2.55) for triglycerides; 1.39 (1.22 to 1.57) for high density lipoprotein cholesterol, and 1.84 (1.56 to 2.17) for insulin. BMI was associated with high fasting glucose (≥5.6 mmol/l) only in boys (1.18, 1.03 to 1.36). With these binary outcomes there was statistical evidence that associations differed between girls and boys for fasting glucose (P=0.03) and insulin (P<0.001). When risk factors were examined as continuous outcomes there was evidence for stronger associations of BMI with more adverse levels in boys than girls for fasting insulin, glucose, and triglyceride concentrations (all interaction P≤0.03). BMI, waist circumference, and fat mass were all strongly correlated with each other (r=0.89-0.94), and associations of the three with cardiovascular outcomes were of similar magnitude with statistical evidence of consistency in associations (all P>0.2 for heterogeneity). When waist circumference or fat mass or both were added to models including BMI they did not increase the variation in cardiovascular risk factors already explained by BMI and confounders alone. Girls who were overweight/obese at age 9-12 but were normal weight by 15-16 had similar odds of adverse levels of risk factors to those who were normal weight at both ages. In boys odds of high systolic blood pressure, high concentrations of triglycerides and insulin, and low concentrations of high density lipoprotein cholesterol remained higher in this group compared with those who were normal weight at both ages but were lower than in those who remained overweight/obese at both ages.
Conclusions Measurements of waist circumference or directly assessed fat mass in childhood do not seem to be associated with cardiovascular risk factors in adolescence any more strongly than BMI. Girls who favourably alter their overweight status between childhood and adolescence have cardiovascular risk profiles broadly similar to those who were normal weight at both time points, but boys who change from overweight to normal show risk factor profiles intermediate between those seen in boys who are normal weight at both ages or overweight at both ages.
We thank all the families who took part in this study, the midwives for their help in recruiting them, and the whole ALSPAC team, which includes interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists, and nurses.
Contributors: DAL proposed the study objectives, obtained funds for the fasting blood assays, wrote the statistical protocol, undertook analyses, and wrote the first draft of the paper. LB helped with data cleaning and revised later drafts of the paper. JL contributed to developing the study objectives and revised later drafts of the paper. KT contributed to the statistical protocol and revised later drafts of the paper. LDH contributed to the statistical protocol and revised later drafts of the paper. AF contributed to developing the study objectives and revised later drafts of the paper. LC and PW completed assays on fasting blood samples and revised later drafts of the paper. ARN obtained funds for the DXA scans and other anthropometric data, contributed to developing the study objectives, and revised later drafts of the paper. GDS is scientific director of ALSPAC and has obtained core funding for this study over the past six years, contributed to developing the study objectives, and revised later drafts of the paper. NS supervised the laboratory assays on the fasting blood samples, contributed to developing the study objectives, and revised later drafts of the paper. DAL is guarantor.
Funding: This study was funded by a grant from US National Institutes of Health (NIH) and the National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK077659). The Medical Research Council (MRC), the Wellcome Trust, and the University of Bristol provide core funding support for ALSPAC. The MRC (G0600705) and the University of Bristol provide core funding for the MRC Centre of Causal Analyses in Translational Epidemiology. AF is funded by a UK Medical Research Council research fellowship. The views expressed in this paper are those of the authors and not necessarily those of any funding body or others whose support is acknowledged. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: All authors have completed the Unified Competing Interest form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare: no support from any institution for the submitted work; no financial relationships with any institutions that might have an interest in the submitted work in the previous 3 years; no other relationships or activities that could appear to have influenced the submitted work.
Ethical approval: This study was approved by the ALSPAC law and ethics committee (IRB 00003312) and the local research ethics committee.
Data sharing: All scientists are able and encouraged to use ALSPAC data. Requests for data to conduct research are made via the ALSPAC executive on a form that is available from the study website: www.bristol.ac.uk/alspac/ (please click on the “scientific community” button for this information). Most requests are accepted and anonymised datasets provided. Where a request is made to conduct research that overlaps with another scientist the executive try to facilitate collaboration between the groups if possible. ALSPAC is a large prospective cohort study with repeat collections of data on parents and children over a 17 year period. There is no single protocol document but full details of the study and each period of data collection are available at the study website: www.bristol.ac.uk/alspac/ (please click on the “scientific Community” button for this information).
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