Sir-Claudio Napoli and colleagues’ (Oct 9, p 1234)1 observation that children from hypercholesterolaemic 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 atheroenic genes; the difference in streak frequency may be due to any hereditary or environmental 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 adulthood with any certainty. In Webber and colleagues’ observational study, half the hypercholesterolaemic 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 efficient 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 manipulation 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.
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 childhood: fate of early 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 lipoproteins from childhood to adulthood. The Bogalusa Heart Study. Am J Epidemiol 1991;133:884-99.
5. Ravnskov U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. J Clin Epidemiol 1998; 51:443-60.