Lancet
2000;355:69.
Prevention
of atherosclerosis in children
Sir-Claudio
Napoli and colleagues' (Oct 9, p 1234)1 observation that children
from hyper-
cholesterolaemic mothers had more fatty streaks than children from
normocholesterolaemic
mothers is interesting, but their interpretation of the finding does not agree
with present
knowledge, or common sense. If the fatty streaks were early atherosclerotic
lesions, why
were they more common in the fetuses than in the children?
Fatty
streaks are found worldwide in almost all children, equally often in countries
where
atherosclerosis is rare, as in countries where it is frequent.2 The
development of raised
lesions later in life in some individuals must therefore be due to factors other
than the mere
presence of fatty streaks. Even if we assume that fatty streaks are the
forerunners of raised
lesions, there is no evidence for blaming a high maternal cholesterol
concentration or athero-
genic genes; the difference in streak frequency may be due to any hereditary or
environ-
mental factor associated with high cholesterol concentrations.
To
use Napoli and colleagues' findings as an argument for cholesterol concentration
lowering
in childhood, as did Berenson and Srinivasan in their commentary,3
seems unfounded. As
Napoli and colleagues emphasise, cholesterol concentration was normal and
similar in both
groups, and the fatty streaks cannot therefore have been caused by high
concentrations in the
child. Even if the fatty streaks had been caused by high concentrations, the
predictive value of
cholesterol screening is low because concentrations in childhood cannot be
tracked to adult-
hood with any certainty. In Webber and colleagues' observational study, half the
hyperchole-
sterolaemic children had normal values after 12 years.4
But
let us assume that a screening programme could identify children at high risk
only and that
a lowering of cholesterol would reduce that risk; the question remains of what
to do, because
diet is poor as a cholesterol-lowering treatment, particularly in children. Even
if diet were effi-
cient as a cholesterollowering treatment, there is no evidence that diet
prevents cardiovascular
morbidity or mortality. This effect was shown in a systematic review of eight
ecological, 41
cross- sectional, 25 cohort, six case- control studies, and a meta-analysis of
nine controlled
randomised dietary trials.5 Instead of the prevention of
cardiovascular disease, dietary manipu-
lation of healthy children may rather create families of unhappy hypochondriacs,
obsessed with
their blood chemistry and the composition of their diet.
The
only way to lower cholesterol concentrations effectively is by drugs. There is
no evidence,
however, that a possible benefit from cholesterol lowering from a young age may
balance possible
side effects from long-term drug use, because luckily, such trials have never
been done. I doubt
that any parents, with all the facts and assumptions, would allow their child to
be screened.
Uffe
Ravnskov
References
1.
Napoli C, Glass CK, Witztum JL,Deutsch R, D'Armiento FP, Palinski W. Influence
of maternal
hypercholesterolaemia during pregnancy on progression of early atherosclerotic
lesions in child-
hood: fate ofearly lesions in children (FELIC) study. Lancet 1999; 354: 1234-41.
2.
Strong JP, Eggen DA, Oalmann MC, Richards ML, Tracy RE. Pathology and
epidemiology
of atherosclerosis. J Am Diet Assoc 1973; 62: 262-68.
3. Berenson GS, Srinivasan SR. Prevention
of atherosclerosis in childhood. Lancet 1999;
354:1223-24.
4.
Webber LS, Srinivasan SR, Wattigney WA, Berenson GS. Tracking of serum lipids
and lipo-
proteins from childhood to adulthood. The Bogalusa Heart Study. Am J Epidemiol
1991;
133:884-99.