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Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate
fate is used to promote osmotic diarrhea, sulfate absorption is inversely proportional to the extent of the osmotic effect. Sulfate that is not absorbed in the upper gastrointestinal tract passes to the large intestine and colon, where it is either excreted in the feces, reabsorbed, or reduced by anaerobic bacteria to metabolites, such as hydrogen sulfide (Pitcher and Cummings, 1996; Roediger et al., 1997).
Because the majority of body sulfate is obtained from the ingestion of protein-derived methionine and cysteine and because the primary route of sulfate excretion is in the urine, 24-hour urinary sulfate excretion is strongly correlated with 24-hour urinary excretion of urea, the end product of dietary protein metabolism (Greer et al., 1986; Houterman et al., 1997; Sabry et al., 1965). Urinary sulfate excretion has recently been suggested as a measure of sulfur amino acid metabolism in humans (Hamadeh and Hoffer, 2001; Hoffer, 2002).
If one assumes that adults whose dietary protein needs are being met will consume a daily intake of 2 g of methionine and 2 g of cysteine, an equal amount of methionine and cysteine would be oxidized, producing 960 mg of sulfur, or 2.8 g/day of inorganic sulfate. A daily intake of inorganic sulfate as high as 1.3 g/day can be obtained from water and other beverages (0.5 g/L × 2.6 L/day). A quantity of sulfate greater than this amount would likely be produced daily from metabolism of methionine and cysteine in food plus that derived from body protein turnover. An analysis of the sulfate content of various diets using foods purchased at supermarkets suggests a large variation in daily inorganic sulfate intake, ranging from 0.2 to 1.5 g (2.1–15.8 mmol)/day1 (Florin et al., 1991). Metabolism of organic sulfur compounds, such as methionine and cysteine, supplies over half of the sulfate; the remainder is supplied from preformed sulfate in water and foods (see Table 7-1).
Clinical Effects of Inadequate Intake
Extensive work with laboratory animals has shown that growth is stunted when dietary sulfate is purposely eliminated from both the food and water supply and when sulfur amino acids, particularly cysteine, are provided at levels resulting in deficiency signs. Importantly, the addition of sulfate to these deficient diets resulted in
To convert mmol of sulfate to mg of sulfate, multiply mmol by 96.1 (the molecular weight of sulfate).