Salt Sensitivity

Evidence presented to the committee in its data-gathering workshop (see Appendix C) and reviewed in IOM (2005) reinforces that reducing sodium intake can have widely varying effects among individuals. Nevertheless, the term “salt sensitive” has been used to describe those who experience the greatest reduction in blood pressure in response to decreased sodium intake. Conversely, “salt-resistant” individuals experience little change in blood pressure, even with dramatic changes in sodium intake (Weinberger, 1996). Interindividual heterogeneity in blood pressure in response to dietary sodium is described in IOM (2005, pp. 286-291), and includes findings from Obarzanek and colleagues (2003). This study examined blood pressure differences between two points: when sodium intake was similar and when sodium intake was decreased. A wide statistically normal distribution in measured blood pressure was seen among individuals at both intake levels. The standard deviation of the distribution change, however, was similar for both distributions, suggesting that the variability in blood pressure responses to reduced sodium intake likely occurred in response to factors unrelated to sodium intake. Biological variation in the physiological response to dietary sodium, mediated through the renin-angiotensin-aldosterone system (RAAS), has been postulated as a possible mechanism (Chamarthi et al., 2010).

Genetic Variation and Salt Sensitivity

Evidence examining a relationship between genetic variations and salt sensitivity and risk of high blood pressure suggests that such variations may be specific to certain population subgroups. Beeks et al. (2004) conducted a systematic review of reports across population groups on genetic factors associated with salt sensitivity. The review identified several candidate polymorphisms from among the studies reviewed. However, due to methodological differences, variations in the way salt sensitivity was defined, and a limited number of studies examining a given polymorphism, definitive conclusions could not be drawn. Other studies examining polymorphisms within specific population subgroups have identified genetic variants associated with racial/ethnic groups and risk of high blood pressure or hypertension, as illustrated in the following studies. These studies also show that multiple pathways are involved in blood pressure response to expression of gene variants.

Miyaki et al. (2005) used a food frequency questionnaire to estimate

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