Commentary on Childhood Origin of Coronary Heart Disease.

Post-mortem studies of children killed in road accidents show signs of early degenerative changes in their arteries (Sanders, 1987). Post-mortem examination of Korean War casualties showed 77% of USA servicemen had some degree of atherosclerosis, with some 15% having considerable coronary narrowing (Enos, 1953). USA casualties in Vietnam showed 45% with some degree of atherosclerosis (McNamara, 1971).

The Coronary Prevention Group has stated that “the physiological conditions that predispose to adult CHD can occur during childhood: children can have raised blood pressure, raised cholesterol levels or be overweight.” In addition – middle-aged atherosclerosis is related to the extent of fatty streaking in childhood, whilst other population studies have shown that levels of blood cholesterol in youth correlate with adult ,levels of cholesterol and incidence of CHD (American Health Foundation, 1983).

It is accepted that atherosclerosis starts in childhood, see Figure 12.1, is also associated with a diet high in saturated fat and low in polyunsaturates, and is therefore a paediatric problem (Widhalm, 1988; Sanders, 1987). Major changes occur in childhood for CHD risk with major changes in BP, TC and HDL levels (Berenson, 1983; Lauer, 1988; Hofman, 1989; Mauer, 1991). There is still uncertainty surrounding the identification of hyperlipidaemia, hypertension, obesity in children yet by the age of ten many have already developed overt signs of predisposing factors of ten. The challenge becomes one of defining risk status more precisely Lancet, 1991b).

If serum lipids track over time then high risk profile adolescents would become high risk adults – in fact such tracking over time has been been shown to be the case (Stein, 1981) with other longitudinal studies defining the tracking of elevated lipids into adult life (Lancet, 1991b; Lauer, 1988). The Cincinnati Study (cited in Stein, 1981) showed, on the average, adolescents with high range cholesterol levels (e.g 4.65 mmol/l) approximate adult levels (e.g. 6.2 mmol/1). An Ohio Study showed 20% of 3-18 year olds above total cholesterol 4.8 mmol/1 (Garcia, 1989).

The Heartbeat Wales Clinical Survey (1985) showed children 12-19 years had mean cholesterol levels of 4.42 mmol/1 (boys) and 4.67 (girls). (Heartbeat Wales, 1985).  In a Northern Ireland survey some 20-25% of young adults aged 18-21 had blood cholesterol levels above the WHO recommended optimum of 5.2 mmol/1 (Brown, 1989). For people under 20 years every cholesterol value higher than 5.2 mmol/1 (200mg/dl) must be considered elevated (Widhalm, 1988). Baseline HDL levels have been shown to be lowest in boys of poor physical fitness, declines in physical fitness associated with decreases in HDL levels (Hofman, 1989).

Numerous epidemiological surveys of children show “…differences  in cholesterol and triglyceride levels appear early in childhood among cultures, among race-sex groups within cultures, and among socioeconomic groups within cultures.” (Stein, 1981). Figure 12.2 compared adult and childhood ‘ideal’, ‘present’ and ‘feasible’ mean TC according to the WHO (1990).

It has been estimated that children who are heterozygous for the inherited condition of familial hypercholesterolaemia (FH) have a mean serum cholesterol level of 7.75 mmol/1 (Kwiterowich, 1974). FH confers susceptibility to premature coronary disease and underlies about 4% of heart attacks (AMI) during middle-age (Coronary Prevention Group, 1988). The condition can be identified in childhood – with a frequency of about 1:500 individuals. Elevated lipids are found in less common inherited hyperlipidaemic conditions e.g., familial combined hyperlipidaemia (FCH).

Evidence shows that it is worthwhile to screen children (as well as  a necessity in terms of preventive cardiology) but also to track them (if possible) over a period of years – especially those found with lipid levels above 5.17 mmol/1 if not a possible optimum level of 4.65 mmol/1. There is considerable variability in childhood blood pressure with BP in adolescents being far more labile than adults, nonetheless ‘normal’ values have been established in relation to sex and age in children Purcell, 1985).

In the UK 1/100 children have mild persistent essential hypertension, 1/ 500 have evidence of severe secondary hypertension (Chantler, 1983). Hypertension in children is regarded as factual when a persistent BP of 130/90 mm Hg is present – by such criteria 1 or 2% of children are seen as hypertensive (Catzel, 1984). Studies have also shown that tracking of children with elevated BP still show high levels in later years (Purcell, 1985). It is suggested that “all British children should have their blood pressure measured by the school nurse at five and eleven years.” (Chantler, 1985).

Blood pressure distribution curves for child populations show a gradual increase in both systolic and diastolic values from infancy through adolescence.” (Stein, 1981). Height and body mass are significant BP and and obesity determinants (Purcell, 1985), and that that blood pressure patterns “may therefore be established from an early age, which would be consistent with reports that emphasise the importance of childhood in the origins of cardiovascular disease.” (Whincup, 1988).

There is a tendency for children with raised blood pressure to become hypertensive as adults. (Coronary Prevention Group, 1988).  There is a strong familial element in CHD susceptibility the extent of which is mediated by other major risk factors (Tunstall-Pedoe, 1982a). CHD is a multifaceted disease where heredity and familial aggregation play an important role (Bloor, 1972), especially “…in the development of premature coronary heart disease.” (Deutscher, 1970).

Family studies show “…serum cholesterol levels are correlated between parents, offspring and siblings while the levels of spouses are not.” (Coronary Prevention Group, 1988). Children whose parents suffer heart attacks before fifty have “…significantly increased cholesterol levels relative to control children born to parents without early myocardial infarction.” (Stein. 1981). Table 12.1 is an example showing family history and CHD from the Kilkenny Health Project. Noteworthy is the predominance of females for strong and positive correlations of CHD within families for deciles 35-64 years – relatives who were/are fathers uncles, brothers, sons. There occur significant correlations between parents and children for total cholesterol, triglyceride and high density lipoprotein (Morrison, 1980). For TC, PBP and BMI it has been shown that “Fathers and daughters exhibit aggregation on a greater number of these factors than fathers and sons.” (Feldman, 1973).

Familial aggregation must not be seen only in terms of inherited traits. Familial aggregation must be understood in terms of communicated and shared dietary habits, smoking and other shared lifestyle factors (Deutscher, 1966). Familial aggregation includes common environments as well as shared genetic susceptibility. Cholesterol levels are a family characteristic (Strunge, 1976) with low, but positive, correlations between children’s TC values and those of their parents. Moreover, “Daughters of men with high levels of cholesterol, uric acid, skinfold and ponderal index also had high levels of these variables.” (Feldman, 1973). In addition, familial aggregation is far more common in young women with CHD (Wenger, 1985).

Familial aggregations exist for blood pressure with known “positive aggregation of blood pressure exist(ing) between parent and child and between siblings.” (Wilson, 1974). The aggregation of BP’s “…of parent and child appeared more marked if the relationship involved mother and child.” (Wilson, 1974). It is believed BP patterns may be “established from an early age, which would be consistent with reports that emphasise the importance of childhood in the origins of cardiovascular disease.” (Whincup, 1988). Furthermore, BP aggregation is “…always positive, and in most instances significant, for relationships involving siblings only.” (Wilson, 1974).

References to follow.

Originally Appendix 182 to my MPhil thesis entitled “Population Variation for Risk Factors for Ischaemic Heart Disease.” CNAA. Oxford Polytechnic/Oxford Brookes University, 1987-1992.


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