childhood to adulthood: in the Muscatine Study 2,446 subjects were initially
examined at ages 8–18 years and were re-examined as young adults at ages 20–25
or 26–30 years. Measurements of cholesterol, height, weight, and triceps skinfold
thickness were obtained during childhood. Lipids, lipoprotein fractions, as well as
lifestyle, medication, alcohol, and tobacco use were determined during the adult
examination. Elevated levels of cholesterol during childhood were associated with
elevation of lipids and lipoproteins in adult life. On average, of children found to
have cholesterol levels greater than or equal to the 90th percentile for their age and
gender, on a single measurement 43% remained above the 90th percentile, 62%
remained above the 75th percentile, and 81% remained above the 50th percentile.
The authors conclude that obesity acquired in adolescence and the young adult
years has deleterious effects upon adult cholesterol levels and lipoprotein fractions.
Similar long-term effects of childhood obesity regarding lipids and
lipoproteins are reported from the Bogalusa Heart Study [11]: this longitudinal
cohort was constructed from two cross-sectional surveys in a community-based
population over an 8-year period: 1,606 children and young adults aged 5–23
years participated in the first survey. Subjects with levels of insulin consistently
in the highest quartile showed significantly (p 0.001) higher levels of body
mass index ( 9 kg/m2), triglycerides ( 58 mg/dl), LDL-cholesterol
( 11 mg/dl), and VLDL-cholesterol ( 8 mg/dl), and significantly (p 0.001)
lower levels of HDL-cholesterol ( 4 mg/dl). 739 young adults aged 20–31
years were followed up. As adults, individuals with consistently elevated insulin
had 36-fold increased (p 0.05) prevalence of obesity and a 3-fold increased
rate of dyslipidemia. Moreover, there was a clustering of various components
of syndrome X, which intensified as BMI increased in a subset of children studied
longitudinally in the population [12].
Long-Term Consequences of Altered Lipids
There are numerous reports on the short- and mid-term consequences of
obesity in children and adolescents, but of special interest are not only acute
metabolic changes in lipid profiles but also the long-term effect on cardiovascular
morbidity and mortality. During the past few years a small number of
studies investigated the long-term effects of childhood obesity. Moreover, few
studies demonstrated that altered lipids and lipoproteins even in adolescence and
early adulthood have directly consequences on carotid intimal-medial thickness
and other subclinical cardiovascular disease.
Several prospective and retrospective studies with varying sample size and
follow-up intervals, as well as a few studies with baseline information on obesity
during childhood or adolescence and adult health outcomes several years later
exist [32–37]. The main findings of all studies are similar: overweight in adolescence,
particularly in men, is associated with an increased morbidity and mortality
from CVD, atherosclerosis and colorectal cancer. All-cause mortality is
highest for those with the highest percentage of body fat as adolescent men, but
not for the group of adolescent women. There is good evidence to suggest that
this increased morbidity and mortality from CVD and atherosclerosis at least in
part can be explained by the metabolic changes of lipids and lipoproteins.
The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study
collected arteries, blood, and other tissue from approximately 3,000 persons aged
15–34 years dying of external causes and autopsied in forensic laboratories [14].
In all persons measurements of gross atherosclerotic lesions in the right coronary
artery, American Heart Association (AHA) lesion grade in the left anterior
descending coronary artery (LAD) as well as serum lipid concentrations, intimal
thickness of renal arteries (for hypertension), and adiposity by body mass index
(BMI) together with thickness of the panniculus adiposus were available. In
young men the BMI was associated with both fatty streaks and raised lesions in
the RCA and with AHA grade and stenosis in the LAD. The effect of obesity –
defined as a BMI 30kg/m 2 – on right coronary artery raised lesions was greater
in young men with a thick panniculus adiposus. As found in several other studies
before, obesity was associated with non-HDL-cholesterol and (inversely) HDLcholesterol
concentrations (fig. 1). However, in young women BMI was not associated
with coronary atherosclerosis although there was trend among those with
a thick panniculus adiposus. The results of the study demonstrate that obesity is
associated with accelerated coronary atherosclerosis in adolescent and young
adult men. The conclusions of the PDAY study are consistent with results of longterm
follow-up studies, which show that obesity in youth not only predicts obesity
in adulthood, but also predicts CHD morbidity and mortality. Moreover, the
results of the study indicate that obesity in adolescents and young adults accelerates
the progression of atherosclerosis decades before clinical manifestations
appear. One of the promoting factors for accelerated atherosclerosis probably is
changes in lipid metabolism caused by excessive body fat.
Similar conclusions were drawn from The Muscatine Study [38]. Carotid
intimal-medial thickness was measured in young and middle-aged adults in 346
men and 379 women aged 33–42 years who were representative of a cohort
followed since childhood and who live in Muscatine, Iowa. Aim of the study
was to determine the relationship of intimal-medial thickness with risk factors
measured in childhood, at the time of studying, and as a ‘load’ from childhood
to adulthood. Carotid ultrasound studies were performed and the mean of the
measurements of maximal carotid IMT at several locations was determined for
each subject. On the basis of multivariable analysis, the significant current
predictors of IMT were age and LDL-cholesterol in both sexes. Total cholesterol
was a significant childhood predictor in both sexes, while childhood body
mass index was significant only in women. For men, LDL-cholesterol, HDLcholesterol,
and diastolic blood pressure were predictive of carotid IMT in a
risk factor load model, whereas in women, LDL-cholesterol, body mass index,
and triglycerides were predictive. Higher carotid intimal-medial thickness
in young and middle-aged adults was associated with childhood and current
cardiovascular risk factors.
From several similar studies there is growing evidence that obesity and dyslipidemia
in children and adolescents is associated with a considerable risk for
increased morbidity and mortality from atherosclerosis in adulthood [39–42].
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