As discussed previously, blood pressure, on average, is directly related to dietary sodium intake. However, evidence from a variety of studies, including observational studies and clinical trials, has demonstrated heterogeneity in the blood pressure responses to sodium intake. Those individuals with the greatest reductions in blood pressure in response to decreased sodium intake are termed “salt sensitive” (Kawasaki et al, 1978; Miller et al., 1983; Morris et al., 1999; Sullivan et al., 1980; Weinberger, 1996) (see Box 6-1). Some studies have documented that salt sensitivity is reproducible over time (Weinberger and Fineberg et al., 1991) and that salt sensitivity as assessed by two different techniques is highly correlated (Weinberger et al., 1993a).

A variety of factors influence the blood pressure response to changes in sodium intake. Some factors, particular dietary factors, are modifiable, while other factors are fixed, such as genetic factors. Several factors are acquired, such as advanced age and chronic medical conditions, specifically, hypertension, diabetes, and chronic kidney disease.

Salt-sensitive hypertensive individuals are at an increased risk for cardiovascular events (Morimoto et al., 1997). Salt sensitivity, even in those who are nonhypertensive, also increases the risk of incident hypertension and cardiovascular death (Weinberger et al., 2001). At present, an agreed upon definition and practical tools to measure salt sensitivity in individuals are unavailable. Hence even though individuals who are considered salt sensitive should benefit from a level of sodium intake below the UL of 2.3 g (100 mmol)/ day, there is no practical strategy to identify such individuals, except perhaps by identifying specific subgroups of the population with a high prevalence of salt sensitivity (i.e., older-aged individuals, African Americans, and individuals with hypertension, diabetes, or chronic kidney disease).