In this large, population-based cohort study of 276,835 children, we found that higher childhood BMI values elevated the risk of having a CHD event in adulthood. Each 1-unit increase in BMI z score, at every age from 7 to 13 years in boys and from 10 to 13 years in girls, significantly increased the risk of an event. The associations became stronger with increasing age during this period of childhood. As children are becoming heavier worldwide, our findings suggest that more children are at risk of having a CHD event in adulthood.
The large size of our study gave us the statistical power to investigate the effects of childhood BMI separately in relation to sex and age. Among boys, we identified significant associations at each age from 7 to 13 years for any event, nonfatal events, and fatal events. A similar pattern was identified among girls. In studies from Finland, childhood BMI at specific ages was not significantly associated with adult CHD in 4630 men20
and 3447 women,21
but this result was probably due to inadequate power. We found that the risk of future CHD associated with childhood BMI increased with the child's age; at 7 years, the risks were small, but by 13 years they had increased considerably in boys and girls. A similar pattern of increase was found in the study of Finnish men.20
As children become older, the BMI distribution widens, and the increase in weight required for a 1-unit increase in BMI z score at 13 years of age is more than double that at 7 years. We speculate that, aside from the fact that body size in late childhood is more proximal in time to adult body size, increases in BMI z scores at these later ages could reflect a greater accumulation of fat, in particular intraabdominal fat, which increases the risk of CHD.22
Comparisons with studies other than the Finnish ones20,21
are challenging, because associations of childhood BMI with CHD according to age and with the same definitions of CHD have rarely been investigated. These methodologic differences probably reflect limitations of the available data sources. Two early studies, one in the United States23
and the other in Sweden,24,25
found indications that heavier children were at greater risk for cardiovascular disease. A British study of 2399 children aged 2 to 14 years reported an association between childhood BMI and death from ischemic heart disease.26
Unlike our study, however, this study did not find significant associations when the data for boys and girls were analyzed separately.26
An investigation of 11,106 Scottish children with a mean age of 4.9 years did not detect an effect of childhood BMI on CHD.27
In our study, the associations were moderate for children at 7 years of age and then increased with age. Thus, it is possible that these associations do not exist for younger children or that the Scottish study lacked sufficient power to detect an effect. A recent meta-analysis did not detect an effect of BMI on future ischemic heart disease, but considerable uncertainty remains because of the wide age range of the subjects (2 to 22 years).28
In accordance with our findings, the results of most of these studies indicate that higher childhood BMI is associated with a greater risk of some aspect of cardiovascular disease in adulthood.
Currently, children are typically classified as being at risk only if their BMI values are above cutoff points such as the 85th or 95th percentile on growth charts. Our results do not support this approach. The linearity of the associations we identified between childhood BMI and adult CHD implies that even a surprisingly small amount of weight gain (illustrated in ) will increase the risk of CHD.
We investigated whether birth weight would modify the associations between childhood BMI and CHD, since it has independent associations with these factors.10,29
No interactions were identified, even in our large data set with sufficient statistical power to detect them if they had been present. We found that, after adjustment for birth weight, the effect of an increase in BMI z score on the risk of CHD in adulthood remained and that this effect was greater than that in models containing only BMI. These results show that childhood BMI, even after the effects of birth weight have been taken into account, is associated with CHD in adulthood. From a public health perspective, focusing on the effect of BMI alone is of greater importance because it is modifiable, whereas birth weight is not.
Our study is based on a unique and very large population-based cohort. The register includes virtually every schoolchild in Copenhagen from 1930 to 1976. Health examinations were performed at all public and private schools, thus eliminating selection bias due to socioeconomic status. Unlike other studies in this area of research, complete follow-up was available for every eligible subject in the study as a result of the efficiency of the National Civil Register. Data on the ethnic background of the schoolchildren are not available, but since less than 3.1% of the population of Copenhagen was of non-European origin in 198030
(the earliest year for which information on ethnic background is available), it can be assumed that nearly all our subjects were white. The population-based nature of our cohort, the complete follow-up, and the ethnic background of the cohort suggest that the results of our study are generalizable to other populations of white descent.
Investigations of the risk factors for CHD have shown that hypertension, dyslipidemia, impaired glucose tolerance, and vascular abnormalities are already present in overweight children.4-8
Higher body weight in childhood is associated with the presence of these risk factors in children,4,31
and this association suggests a plausible mechanism linking higher childhood BMI with an increased risk of adult CHD. It is also possible that childhood BMI is associated with CHD as a result of its relation with adult BMI. Correlations between childhood and adult BMI exist; however, they vary in magnitude, and not every heavy child becomes a heavy adult, nor was every heavy adult a heavy child.11,32,33
We do not have information on adult body size for our subjects. Nonetheless, the ability to identify boys and girls who are at risk because of their childhood BMI, whatever their BMI may be when they become adults, is important for the prevention of future CHD. An analysis of the relation between adolescent BMI and adult CHD found that the effects were independent of adult BMI, although this study was conducted on subjects older than those in our study.34
The subjects of our study were born from the 1930s onward and therefore include children born before and during the emergence of the obesity epidemic.35-37
We found that the association between childhood BMI and adult CHD was the same irrespective of which birth cohort the children came from. Several studies have demonstrated that socioeconomic status in childhood is inversely associated with the risk of CHD, but these associations often diminish when adult socioeconomic status is taken into account.38,39
Information about socioeconomic status was not available for our cohort. In a study of childhood BMI and adult heart disease, the associations remained virtually unchanged when adjustments were made for childhood and adult socioeconomic status.26
Of course, it cannot be ruled out that socioeconomic status, through its associations with different behavioral and psychosocial risk factors, has a direct effect on CHD independent of childhood body weight. However, because childhood obesity is already associated with distinct biologic risk factors for CHD,4
it is likely that the associations we observed are based on biologic effects of the children's BMI. Moreover, the population-based nature of our sample (which included all socioeconomic-status groups) and the dramatic societal, environmental, and medical changes that occurred throughout the time period under study make it unlikely that differences in socioeconomic status explain the effects of childhood BMI that we observed. We indirectly adjusted for these factors by stratifying the analyses according to birth cohort, and the association was surprisingly stable across birth cohorts, a result suggesting that the mechanism of the association is probably biologic in nature.
Contemporary children are heavier than their counterparts from the past. In the United States, there is no sign that the increases in childhood overweight and obesity are slowing down,2
and the situation is similar in Denmark.40
The linear association we identified between childhood BMI and adult CHD suggests that more children than ever before are facing increased risks of CHD in adulthood. To put these results in perspective, we calculated the children's probability of having a future CHD event. The example of a 13-year-old boy who weighs 11.2 kg more than average — which results in a 33% increase in the probability of his having a CHD event before the age of 60 — illustrates the deleterious effect of childhood obesity on future health. The BMI values of average and larger-than-average boys in this prediction correspond to the 41st and 88th percentiles, respectively, of the BMI-for-age references of the CDC; thus, these predictions are based on boys who fit within the range of body size of contemporary children.41
Similar predictions were obtained for girls. Nonetheless, since the magnitude of the risk was moderate for 7-year-olds and increased dramatically by the age of 13, these results suggest the possibility of intervention during this period of childhood to reduce the risk of future CHD.
In this study, we determined that higher BMI values in childhood are associated with a greater risk of CHD in adulthood. Furthermore, these risks increase with increasing age of the children. Cutoff points at which the risk dramatically increased were not identified; the risk increased across the spectrum of BMI values. Because more children are becoming heavier at progressively younger ages, our results suggest that a focus should be placed on helping children to attain and maintain appropriate weight to prevent future adverse health consequences.