ABSTRACT
It is well recognised that atherosclerosis begins early in life, even though clinical manifestations of this disease do not normally appear until well into adulthood. It was thus originally believed that atherosclerosis was a normal and hence inevitable phenomenon of aging. As infectious diseases became better controlled in the early part of this century, due to better sanitation and the efforts of public health, it became apparent that there was a rising incidence of coronary heart disease and cerebrovascular disease (Murray and Lopez, 1997). This was particularly evident in industrialised societies after World War II. Case-control studies suggested that coronary artery disease (CAD) was associated with increased serum cholesterol levels and hypertension (Steiner and Domaski, 1943; Master et al., 1939). Also of significance was the epidemiological work of Ancel Keys, showing that saturated fat intake and serum cholesterol levels were strongly related to standardised rates of coronary disease in different countries (Keys, 1980). The strength and consistency of these associations suggested a causal relationship, however, this could only be demonstrated conclusively by measuring appropriate parameters in healthy individuals, following the incidence of CAD in these individuals over a long period of time, and then relating incidence of CAD to the measured parameters (a longitudinal population study). Such a study was initiated by the United States Public Health Service Division of Chronic Diseases in 1948. The town of Framingham in Massachusetts
was chosen to serve as a site for recruiting an appropriate study population. The Framingham Heart Study was thus launched, and this study is now in its fourth decade of investigation (Dawber, 1980).
