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mately 50 million and is estimated to be 65 million in 1999–2000 (Cutler et al., 2008). Blood pressure levels among children and adolescents also increased between 1988 and 2000 (Muntner et al., 2004).

Although increases in the prevalence of hypertension in both adults and children were partially explained by increases in body mass index (BMI)—an indirect measure of body fat—over the corresponding periods of comparison, adjusting for increasing BMI levels cannot completely explain the increasing prevalences (Cutler et al., 2008; Muntner et al., 2004). This suggests that, separate from the issue of obesity, the overconsumption of calories (and the concomitant overconsumption of sodium) is problematic. Moreover, while the measurement of short-term absolute risk for hypertension is determined by incidence rates, the long-term risk for hypertension can be reported by using the lifetime risk statistic, defined as the probability of developing hypertension during the remaining years of life (NHLBI, 2004). The lifetime risk of hypertension is approximately 86–90 percent for women and 81–83 percent for men after adjusting for competing mortality (Vasan et al., 2002).

In assessing the nature of the public health problem associated with elevated blood pressure levels, it is also important to consider its major consequences—heart disease, stroke, and kidney disease. Heart disease is the largest cause of death in the United States (26 percent of deaths in 2006), and stroke is the third-largest underlying cause of death (5.7 percent of deaths in 2006) (Xu et al., 2009). Furthermore, available data from cross-sectional studies in hypertensive individuals have consistently documented a progressive, direct relationship between sodium intake and left ventricular mass (a powerful predictor of stroke and other forms of cardiovascular disease). Sodium may have a direct effect apart from an indirect effect mediated through blood pressure (IOM, 2005). While one controlled trial (Jula and Karanko, 1994) suggests that the association between sodium intake and left ventricular mass is causal, additional trials are needed (IOM, 2005).

Given the direct causal relationship between sodium intake, blood pressure, and associated cardiovascular disease risk, several analyses of cost effectiveness have assessed the health effects and costs of population-wide reductions in salt intake of the U.S. population. Danaei et al. (2009) concluded that smoking and high blood pressure are the risk factors responsible for the greatest number of deaths in the United States, with high blood pressure responsible for 395,000 deaths annually. They estimated that population-wide reductions in sodium intake could prevent more than 100,000 deaths annually (Danaei et al., 2009). High dietary sodium intake, compared to the other dietary risk factors examined (i.e., low omega-3 fatty acids, high trans fatty acids, alcohol use, low intake of fruits and vegetables, low polyunsaturated fatty acids as an indicator of high saturated

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