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(Hypertension. 2005;45:1083.)
© 2005 American Heart Association, Inc.
Original Articles |
From the Longitudinal Studies Unit, School of Population Health, University of Queensland, Brisbane, Australia, (A.A.M.); Department of Social Medicine, University of Bristol, United Kingdom (D.A.L.); Child Development and Rehabilitation Services, Mater Childrens Hospital, Brisbane, Australia (M.J.O.); Longitudinal Studies Unit, School of Population Health, University of Queensland, Brisbane, Australia (G.M.W.); Longitudinal Studies Unit, School of Population Health, University of Queensland, Brisbane, Australia (J.M.N.).
Reprint requests to Abdullah Al Mamun, Longitudinal Studies Unit, School of Population Health, Public Health Building, Herston Rd, Herston, QLD 4006, Australia. E-mail mamun{at}sph.uq.eud.au
| Abstract |
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Key Words: blood pressure obesity
| Introduction |
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3-fold in most industrialized countries over the last 10 to 20 years, and these trends are likely to have major public health consequences.16 Recent data link the rise in levels of childhood obesity and overweight status to secular trends of increasing blood pressure in childhood and adolescence over the same time period.2 However, little is known about the effect of weight gain among children in the general population (as opposed to the extreme obese in clinical populations) on blood pressure. The aim of this study was to compare mean blood pressure at age 14 between 4 groups of individuals based on measures of their body mass index (BMI) at ages 5 and 14: (1) those who had normal weight at both ages (reference group); (2) those who had normal weight at 5 but were overweight at 14; (3) those who were overweight at 5 but normal weight at 14; and (4) those who were overweight at both ages.
| Methods |
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Outcome Measurements
Blood pressure was assessed at ages 5 and 14, with 2 readings taken 5 minutes apart using the OMRAN HEM-703C automatic blood pressure device. We used the reading given by the machine, with the average being taken of the 2 readings with the child seated and at rest. Cuff sizes appropriate to the childs arm circumference were used (either
32 cm or
33 cm). The average of 2 blood pressure measures was used in all analyses.
Measurements of Exposure and Covariates
The average of 2 measures of the childs weight lightly clothed with a scale accurate to 0.2 kg was used in all analyses. Height was measured using a portable stadiometer, which was accurate to 0.1 cm. Overweight status or obesity was defined according to standard definitions derived from international surveys by Cole et al.9 Thus, using the standard definition, in this study, a 5-year-old child was defined as overweight or obese, if his/her BMI was >17.42 kg/m2 for a male and 17.15 kg/m2 for a female. Similarly, overweight or obese was defined at age 14 if BMI exceeded 22.62 kg/m2 for a male and 23.34 kg/m2 for females. These values are equivalent to exceeding 25 kg/m2 in adulthood.9 There were too few participants in the obese categories for meaningful analyses; therefore, we classified children as either overweight or obese (equal to or above the overweight threshold) or normal weight (below the overweight threshold).
The covariates considered were the childs exact age in days at which their BMI was assessed, sex, blood pressure at age 5, family income (in Australian dollars; low <$15 599; medium $15 600 to $31 148; high $31 149 or more), maternal education (did not complete secondary school, completed secondary school, completed further/higher education), maternal age at birth, parity (3 categories: 1, 2, and 3, or more), birth weight (nearest gram), weight gain at first 6 months after birth, pubertal development10 at age 14 (4 categories: stages 1, 2, 3, and 4), childhood intelligence11,12 (cases defined as 10% cutoffs) and behavioral pattern13 (cases defined as 10% cutoffs), self-reported chronic morbidity in the last 12 months (yes/no), and maternal BMI (calculated from the measured height and self-reported prepregnancy weight), which are all plausibly associated with the exposure and outcome and may therefore confound any association.
Statistical Analyses
A series of multiple linear regression was used to determine the mean difference in systolic and diastolic blood pressure between the different weight change categories, taking into account potential confounding factors. In the first model, age (continuous variable), sex, and blood pressure at age 5 were included as confounders. In the second model, family income, maternal education, parity (all 3 level categorical variables), and maternal age at birth (continuous variable) were added. In the third model, birth weight (in kilograms) and weight gain at first month after birth was added. In the fourth model, puberty stage (4 level categorical) was added. And in the fifth model, maternal BMI (continuous) was added.
To assess whether nonresponse biased our results, we used logistic regression (response versus nonresponse as outcome) to determine weights for each individual using the inverse probability of response. Response and nonresponse category was defined on the basis of the measured systolic and diastolic blood pressure at 5- and 14-year follow-ups. A child whose blood pressure was measured at 5- and 14-year follow-ups belongs to response category, and the child whose blood pressure was measured at 5 but not at 14 belongs to nonresponse category. The inverse probability of response for each individual was estimated, adjusting for the factors that predict nonresponse. Nonresponse was mainly predicted by mothers age at birth, family income, maternal education, and ethnic groups of the parents. The individual weighting factor was used as a sample weighting adjustment into the main analyses. All analyses were undertaken using Stata version 8.0 (Stata Inc.).
| Results |
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35 kg. Diastolic blood pressure increased marginally, but systolic blood pressure increased by
9 mm Hg.
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Of the 2794 participants, 469 (17%) were overweight or obese at age 5. Of these overweight children, 63% (296) were still overweight at age 14, and the remaining 37% (173) made the transition to normal BMI. Of those children who were not overweight at age 5, 17% (405) had become overweight at age 14. For the children who changed from being overweight at age 5 to being normal weight at age 14, their BMI increased between the 2 age points by 2.44 (95% confidence interval [CI], 2.11, 2.56) on average, which compares to increases of 3.34 (95% CI, 3.21, 3.38) for the group who were normal at both ages, 8.86 (95% CI, 8.54, 8.99) for the group who were normal at 5 but overweight or obese at 14, and 8.15 (95% CI, 7.56, 8.39) for the group who were overweight at both ages. Thus, the mean BMI increase between the 2 age points in the group that moved down from being overweight at age 5 to being normal weight at 14 was 0.90 kg/m2 lower than that for the group staying normal at both ages, and 5.71 kg/m2 lower than those who remained overweight at ages.
Figure 1 shows the sex- and age-adjusted mean systolic and diastolic blood pressure at age 14 for each of the 4 categories of weight change. This demonstrates that the mean systolic and diastolic blood pressure was similar among children who were normal weight at both ages and those who were overweight at age 5 but normal weight at 14. Mean systolic and diastolic blood pressure was greatest among those who were overweight at age 14, irrespective of whether they were normal or overweight at age 5.
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Table 2 shows mean differences in systolic and diastolic blood pressure, comparing each group of weight change between 5 and 14 to the reference group of normal weigh at both ages. Those children who were overweight at age 5 but had normal weight at age 14 had the same mean blood pressure at age 14 as those who were normal weight at both ages, whereas the children who remained overweight from 5 to 14 had systolic blood pressures that were on average 4.07 mm Hg [CI, 2.56, 5.57] (model 3) higher than the children who were normal at both ages and diastolic blood pressures that were on average 6.12 mm Hg [CI, 5.04,7.20] higher. The association remained consistent with further adjustments with puberty (model 4), maternal BMI (model 5), and other factors, such as child behavioral problems and chronic morbidity (results are not shown for other factors because incorporation of more factors increases missing values and reduces the sample population).
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Figure 2 shows the mean difference (95% CI) of systolic and diastolic blood pressure by fifths of weight gain from age 5 to 14, with the third quintile of weight gain as the reference category. Results are presented for fully adjusted model 5. It shows that children who gain more weight have higher blood pressure than children who belong to the third quintile. Similarly, those who gain less weight (first and second quintiles) have lower blood pressure than those in the reference (third quintile) weight gain category. When we repeated the analyses using weights for factors that predicted nonresponse, the results did not differ from those presented here.
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| Discussion |
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Study Strengths and Limitations
The most important strength of our study is the repeated measures of BMI and blood pressure in childhood/adolescence. The most important limitation is that of loss to follow-up. Data on blood pressure and BMI at ages 5 and 14 were only available on 39% of the original cohort, and those without these data were more likely to be from poorer family backgrounds.8 Although this is a substantial attrition, our results would only be biased if the associations we have presented here were either nonexistent or in the opposite direction among those who were not examined at ages 5 and 14 compared with those who were included in these analyses. That is to say that among the nonresponders, there was no effect on blood pressure among those who gained less weight or had blood pressure increases in this group. We compared our estimates of overweight or obese status at ages 5 and 14 with the 1995 Australian National Nutritional Survey (NNS) for similar age category. Results are comparable. At age 5, prevalence of overweight status or obesity was 17% in MUSP and 15% in NNS. At age 14, it was 25% versus 23%. The small difference could be because of regional variations. Another limitation is that we do not know how those children who gained less weight managed to do so. A related issue is that we do not know whether the link between slower weight gain and improved blood pressure outcome was the direct result of the weight loss or if it occurred because the means by which weight was gained slowly (most likely dietary and physical activity) also had a direct effect on blood pressure. We only had data on parental BMI at the time of the mothers pregnancy and not at the childs 5- and 14-year follow-ups. It would have been valuable to have had parental BMI data for these follow-up periods so that we could have assessed the extent to which childhood change in BMI status reflected parental changes.
Comparisons With Other Studies and Implications
Our results are consistent with studies of smaller samples of children from clinical populations with extreme obesity in whom weight reduction has been shown to improve blood pressure and other atherogenic risk factors.14,15 Our results add to these studies by showing that slower weight gain in the general population of children is likely to reverse the recently reported increases in blood pressure associated with the obesity epidemic.2 Because the effects we have found are independent of a range of important confounding factors, our findings suggest that programs that successfully result in slower weight gain in childhood may have important beneficial effects on subsequent blood pressure.
Perspectives
This study showed the natural history of changes in blood pressure with the changes in weight or BMI status from 5 to 14 years of age. Although prevention of childhood overweight status or obesity is important, and this study provides additional evidence to support that stance, this study also provides valuable evidence suggesting that change from overweight to obese status to normal BMI results in important reductions in blood pressure. This is important because it suggests that being overweight or obese at 1 time point in childhood does not result in irreversible damage with respect to blood pressure.
Future research should focus on 2 important extensions of the work presented here. First, we need to understand the important determinants of change from overweight/obese status to normal BMI and, in particular, the determinants of this change that are related to blood pressure change. Randomized trials of interventions to treat obesity in childhood should aim, and have sufficient power, to examine other outcomes in addition to weight loss. Specifically, they should aim to examine cardiovascular disease risk factor end points, including blood pressure, fasting lipids, and fasting glucose. Secondly, future research should examine the relationship between different childhood and early-life BMI trajectories and adult cardiovascular disease risk. Blood pressure tracks from childhood into adulthood and these tracking coefficients increase with increasing age.16 Thus, the blood pressure distribution at age 14 will be strongly related to this distribution in adulthood. Adult blood pressure is strongly related to cardiovascular disease outcomes. As a consequence, our results suggest, but do not definitively prove, that changes from overweight/obese status to normal BMI during childhood will have beneficial effects in terms of adult cardiovascular disease risk. With the evolution of a number of birth cohorts, including long-term follow-up of the MUSP study, it will be possible to determine whether the effects we report here do extend into effects on adult cardiovascular disease risk.
| Acknowledgments |
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Received December 12, 2004; first decision January 5, 2005; accepted April 6, 2005.
| References |
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This article has been cited by other articles:
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