As a cause of death and disability, hypertension is second only to smoking in the developed world (World Health Organization, 2002a). The two are of course causally linked. The leading cause of mortality and morbidity in people with the metabolic syndrome is CVD (Lakka etal., 2002). Globally, CVD causes one-third of the world's deaths, i.e. ~15.3 million annually (World Health Organisation, 1999). Within the UK this is the equivalent of 4 out of every 10 deaths (British Heart Foundation Statistics, 2004). A large percentage of the world's populations (South America, Africa, Mid Asia and China) is in transition from a rural to an urbanized economy. Such countries are experiencing large increases in the incidence of chronic adult diseases, including CVD. Several factors are thought to be responsible, including changes in nutrition, diminished physical activity and tobacco use (Reddy, 2002). In India the percentage of CVD-related deaths is expected to rise from 24.2 per cent in 1990 to 41.8 per cent by 2020 (Reddy, 2002). In the past 20 years China also has seen a doubling in death rates from CVD. The incidence of CVD in these two countries is now higher than in all of the economically developed countries added together (World Health Organization, 2002a,b). Globally, type 2 diabetes currently has a prevalence of 84 million and is expected to increase to 228 million by 2025 (Reddy, 2002). Within the USA this represents a 25 per cent increase in prevalence. In India the prevalence by 2025 is expected to treble, to reach 60 million (Reddy, 2002). These trends portend an explosion of atherothrom-botic disease. It is estimated that by 2020 the proportion of global deaths due to chronic disease will reach 57 per cent (approximately half due to CVD, Murray and Lopez, 1996), with enormous increases in cost to society and government.
A recent World Health Organization report described the adoption of a life-course approach to nutrition and prevention of adult disease as being central to any strategy for prevention. The developmental origins of adult disease, the tracking of childhood risk factors into adulthood and evidence that some risk factors act across generations were thought to be crucial considerations (Aboderin etal., 2002). In their review, which discusses this approach, Darnton-Hill, Nishida and James (2004) suggest that the risks of developing a chronic disease accumulate during life and reflect one's cumulative differential lifetime exposures to damaging physical and social factors. It has been suggested also that chronic diseases are likely to have underlying causes that predispose to one another (an example being the close relationship between CVD and type 2 diabetes). The importance of the PARs concept is that it suggests prenatal life and the level of postnatal nutrition as significant risk factors in the accumulation of such risk (see Figures 3.1 and 3.2). The effects of maternal constraint on growth and development cause long-term changes to structure and function, as shown in Table 3.1. In this respect a relative excess of postnatal nutrition in conjunction with such adaptive changes could be seen as the first step in developing adult chronic diseases associated with endothelial dysfunction.
There are several possible avenues of intervention. For ease of discussion these can be grouped on the basis of nutrition, pharmacological therapy and screening strategies.
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