trients, an intake of sodium or chloride markedly above the AI is not warranted.

Concerns about adverse effects related to sodium intake in children are focused in two areas: first, does a higher level of dietary sodium result in increased blood pressure in children—to the extent that there is a definable increase in risk of cardiovascular disease in children, and second, does increased dietary intake of sodium during childhood track to increased blood pressure during adulthood and thus increased risk for subsequent cardiovascular disease.

The extent to which blood pressure in childhood affects subsequent blood pressure and chronic disease risk in adulthood has been evaluated in a number of studies. Studies that have examined the effects of sodium intake on blood pressure in children include observational studies (Cooper et al., 1983; Geleijnse et al., 1990; Robertson, 1984; Simon et al., 1994; Tucker et al., 1989) and, to a lesser extent, randomized, controlled-design clinical trials (Calabrese and Tuthill, 1985; Cooper et al., 1984; Ellison et al., 1989; Gillum et al., 1981; Howe et al., 1985, 1991; Sinaiko et al., 1993), as well as a study of twins and siblings (Miller and Weinberger, 1986; Miller et al., 1988). A recent review of these studies has been published (Simons-Morton and Obarzanek, 1997).

Many of these studies had methodological limitations, including small sample size, suboptimal blood pressure measurements, and limited experimental contrast. A longitudinal cohort of 233 children (5 to 17 years of age) did not reveal an association between sodium excretion and change in blood pressure over time (Geleijnse et al., 1990). When sodium intake was reduced to less than 1.4 g (60 mmol)/day in 149 nonhypertensive children ages 2.6 to 19.8 years, a small decrease in the average systolic, diastolic, or