children [43], and several cohort studies [44–48] have examined the relation of
childhood obesity to CHD in adulthood. Whereas some children have been followed
prospectively [47, 48], other investigators have identified cohorts in
adulthood who had baseline (historical) data previously collected by schools
[44, 45] or in preparation for military service [46]. In addition, the relation of
BMI at age 18 years, based on the recalled weight of middle-aged adults, to
subsequent CHD has been examined [49, 50].
These long-term studies, many of which span over 50 years, are very difficult
to conduct, and some investigators have been able to re-examine (or
trace) only about one half of eligible subjects [45]. Furthermore, there are many
differences in the design and analysis of these studies, including (1) the classification
of overweight (typically the upper fourth or fifth of the BMI distribution);
(2) sample sizes than range from 508 [47] to 78,000 [46], and (3) mean,
baseline ages that ranged from 8 years [48] to 19 years [44]. In addition, few
studies have data on BMI levels in both childhood and adulthood [45, 47, 49,
50], and in all cases, one of the two estimates is based on self-reported weight,
increasing the possibility of misclassification.
Despite these differences, the results of these studies suggest that
overweight children are at increased risk for CHD in adulthood, with relative
risks (RRs) generally ranging from 1.7 to 2.6. These consistent findings, which
can be contrasted with those of studies of adult obesity, may be due to the long
follow-up periods, as well as to the lack of confounding by preclinical disease
and cigarette smoking. In addition, the strength of the relation of obesity to
CHD decreases with age among adults [51], and it is possible that this interaction
with age extends to adolescents and children. However, it is unclear if
the relation of childhood obesity to adult complications varies by the length of
follow-up, or if there is a J-shaped relation, with the optimal BMI level being
slightly below the median [46, 48]. Although it has been suggested that childhood
obesity is more strongly related to adult CHD among boys than girls [47],
associations with adult carotid IMT are stronger among girls [41].
As is the case adult risk factor levels [24], it is also possible that the
increased risk among overweight children for CHD may be due to adult (rather
than childhood) weight status. The results of the Harvard Growth Study [47]
provide the strongest evidence supporting an independent effect of childhood
obesity, in which adjustment for adult BMI only slightly reduced the relation of
childhood overweight (BMI 75th centile) to CHD morbidity (RRs of 2.8 vs.
2.5) over a 55-year follow-up period among men. These investigators, however,
found that childhood overweight was not related to CHD morbidity or total mortality
among women.
In contrast, other results have emphasized the greater importance
of adult weight status. For example, overweight ( 20% above average weight)
children in Washington County had relatively high rates of vascular disease
in adulthood [45], but the highest rates were seen among thin children who
became overweight in adulthood. Somewhat similar results were reported by
the Nurses Health Study [49], in which the relation of (self-reported) BMI at
age 18 years to subsequent CHD was entirely attributable to the persistence
of obesity throughout life; controlling for adult BMI reduced the RR among
those with a BMI 23.3 kg/m2 at age 18 years from 2.0 to 1.0. It is possible that
weight gain after the cessation of growth, which would largely reflect accumulated
fat mass, may be more pathological than weight gain during growth and
development [1].
Overweight children are at increased risk for adverse levels of CHD risk
factors, atherosclerosis, and CHD in adulthood. Although it is possible that the
adult complications are due to the persistence of obesity throughout life, these
consequences will become increasingly evident due to the recent secular
increases in childhood obesity. In addition, the risks associated with the high BMI
levels currently seen among children may be substantially greater than those
associated with the less severe levels of childhood overweight seen before 1970.
Because of the long follow-up periods needed to study the relation of childhood
obesity to CHD, non-invasive techniques such as B-mode ultrasonography
and electron beam tomography, will likely provide the most useful information
on the relation of childhood obesity to atherosclerosis. The difficulties in preventing
and reversing obesity, along with the frequent nonadherence of adolescents
to lifestyle changes and medical treatment, will complicate treatment and
prevention efforts.
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