al., 1997) has documented that sodium reduction had no apparent benefit in lowering blood pressure or preventing pregnancy-induced hypertension or its complications. Neither was there any evidence of adverse effects on obstetrical outcomes from sodium reduction in these studies. In the three clinical trials, the mean urinary sodium excretion values in the control and reduced sodium groups were approximately 130 mmol (2.9 g)/day versus 60 mmol (1.4 g)/day (Steegers et al., 1991b), 124 mmol (2.8 g)/day versus 84 mmol (1.9 g)/day (Knuist et al., 1998), and 142 mmol (3.3 g)/day versus 61 mmol (1.4 g)/day (van der Maten et al., 1997). Hence, available evidence indicates that reducing sodium intake has little impact on preventing hypertensive disorders of pregnancy or their complications.

Overall, there is inadequate evidence to support a different upper intake level for sodium intake in pregnant women from that of nonpregnant women as a means to prevent hypertensive disorders of pregnancy. Also, there are inadequate data to justify a different UL for lactating women. Therefore, the ULs for sodium for pregnant and for lactating women are the same as for nonpregnant women. Similarly, there is no data to indicate that chloride is handled differently during pregnancy or lactation; thus the ULs for chloride remain the same as for the nonpregnant and nonlactating states.