• For sulfate, there is no identified indicator of inadequate intake. Requirements for sulfate are met by meeting dietary protein and sulfur amino acid recommendations.

• For water, potassium, and sodium, useful data are lacking for setting requirements for infants, children, adolescents, pregnant and lactating women, and the elderly. As an example, there is a paucity of data on the relationship of dietary sodium and potassium intakes early in life on blood pressure and markers of bone health during adulthood. For water, research studies commonly tested the effects of inadequate intake in men of military age, but not in broad populations.

In free-living persons, accurate measurement of dietary water and electrolytes intake is difficult, as are measurements of total body water and electrolytes. Potential sources of error in self-reported intake data include underreporting of portion sizes and frequency of intake, omission of foods and beverages, and use of food composition tables, which need to be continuously updated and expanded to include new foods and reformulated products.

For several reasons, assessment of sodium intake is problematic. Substantial additions can occur after processing. In fact, many diet collection methods do not collect information on the salt (sodium chloride) added during cooking or eating. More importantly, there is large day-to-day variation in sodium intake. The most accurate method to assess dietary sodium is to measure several timed urinary collections. However, this approach is cumbersome and prone to collection errors. Hence, practical tools to estimate sodium intake are needed.

A substantial body of evidence, including results of clinical trials, has documented that reduced dietary sodium intake and increased potassium intake can lower blood pressure, which itself is a powerful risk factor for cardiovascular disease. Several, but not all, observational studies link increased dietary sodium and reduced potassium intake with subsequent cardiovascular disease. There is also evidence that increased dietary sodium intake and inadequate potassium intake increase urinary calcium excretion and affect calcium balance, but evidence of their effects on subclinical and clini-