It is unlikely that adult daily maintenance requirement exceeds 0.6mmolperkg body weight and could well be below this in many mammals. Newborn, growing, pregnant, or lactating animals have increased requirements. The appropriate sodium intake for humans remains controversial with some cultures managing on less than 1 mmol per day, while Western intakes may be in the range 200-300 mmol per day, more where processed foods are heavily consumed. There has been insufficient awareness among physicians and human nutritionists of just how high such intakes are, compared with requirements in other animals. Granted that humans are bipeds with a stressful lifestyle quite different from those of animals, there is no real evidence that human obligatory losses or sodium requirements are significantly greater. Rather, there is an ingrained tradition of regarding sodium intake as a benign pleasure, involving a harmless and healthy dietary constituent. The main warnings against this view come from the fact that hypertension is virtually unknown in low-salt cultures and that they do not even have an age-related rise in 'normal' blood pressure. Moreover, there are numerous studies that, when rigorously analyzed, indicate that human arterial pressure and salt intake are positively correlated; sufficiently to anticipate reductions in the prevalence of hypertension in response to manageable reductions in dietary sodium. Unfortunately, such reductions are still handicapped by inadequate food labeling and the fact that most sodium is added by the processor rather than the consumer. Humans, other than vegetarians, also have a very low potassium intake compared with other mammals; potassium may ameliorate the hypertensive effects of sodium.
Because obligatory losses of sodium are so low, dietary sodium depletion is hard to induce and sodium deficiency usually results from losses caused by renal, adrenal, or enteric disease; renal disease may cause either retention or loss of sodium. Globally, both in humans and animals, the most common cause of sodium deficits is acute diarrhea. Fortunately, sufficient gut usually remains unaffected for uptake of sodium and water to be stimulated by suitably formulated oral rehydration solutions. These essentially restore ECF volume (and acid-base balance), allowing natural defenses to overcome the underlying cause of the diarrhea. Despite some species variations, such solutions usually work best if their glucose:sodium ratio (in mmoll-1) is close to unity and they are virtually isotonic (i.e., they have a similar osmotic concentration to ECF; hypertonic solutions draw water into the gut). The function of glucose in these solutions is to promote sodium uptake; its nutritional contribution is trivial. Anions such as citrate, acetate, propionate, bicarbonate, and amino acids (e.g., glycine and alanine) may further enhance the uptake of sodium and therefore water. These sodium cotransport mechanisms are very similar to those of the proximal renal tubule. More recently, nutritional oral rehydration solutions that provide calories and glutamine (to sustain the form and function of enteric villi) have been successfully used in calves.
Sodium is thus central to the management of two of the most widespread clinical problems; hypertension (in humans) and diarrhea. Indeed, the World Health Organization (WHO) regards the discovery of oral rehydration, which depends on restoration of enteric sodium uptake, as the main life-saving development in twentieth century medicine. This powerful clinical application rests on a simple physiological observation concerning an elementary but vital dietary constituent.
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