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In determining what constitutes “normal” sodium intake for humans, the disciplines of medicine and public health long ago fell prey to the “emperor’s new clothes” syndrome; For decades a theoretical case has been built on assumptions that sodium intake has been increasing over time, is at levels far in excess of physiological needs, is a major cause of cardiovascular disease, and is modifiable by public policy.1 Just as the emperor found out about his clothes, these suppositions do not reflect reality. A frequent claim by the advocates of lower sodium intake is that the current average intake of 3,400 mg/d far exceeds the US guidelines.1,2 That is true, as 2,300 mg/d is the current recommendation for healthy adults aged <50 years, and 1,500 mg/d is recommended for those at risk of cardiovascular disease and/or aged ≥50 years. The advocates’ claim is only relevant, however, if i) the current guidelines are based on reproducible evidence of benefit in terms of health outcomes, ii) the current 3,400 mg/d average sodium intake is an aberration of physiology, and iii) it is physiologically possible for freeliving individuals to achieve the recommended levels of dietary sodium on a consistent basis. On each count the scientific evidence is unequivocal: the current guidelines are physiologically irrelevant. Thus, the mantra of the advocates that current sodium intakes are excessive is also irrelevant and, thus, misguided in its intent to frame public policy on sodium intake; at the core of the science that refutes the advocates’ claim is 8 decades of neuroscience research that has defined the neural networks involved in regulating sodium intake in vertebrates.3 These primal networks are interfaced with peripheral signals that inform the brain of the adequacy of organ perfusion (i.e., intravascular volume status). The renin angiotensin system and its generation of angiotensin II and aldosterone are the primary stimuli activating the neural networks that control sodium intake.3 These well-established physiologic pathways provide the biological basis of the fact that actual human sodium intake is set by physiology and not public policy. It is true, and obviously so, that when sodium intake is measured by the best techniques (24-hour urinary sodium excretion), there is a reproducible average intake with a “normal” distribution for the population.4–6 That average—3,600 mg/d, with a range of 2,600–5,000 mg/d—is a mean intake that has been recorded consistently over 5 decades, across 45 countries, and in multiple ethnic groups.6 It has also been verified by a number of National Institutes of Health–sponsored, controlled trials intended to decrease sodium intake and numerous governmental surveys monitoring sodium intake over time.4–6 As with hemoglobin, fasting blood glucose, and many other physiologically set parameters, sodium intake as a critical determinant of intravascular volume regulation is set within a normal range in healthy individuals. This range of sodium intake appears fundamental to survival because intravascular volume is dependent on sodium and water. Although angiotensin II and other critical hormonal responses that modulate vasoconstriction can maintain organ perfusion as a rescue response to inadequate volume, there is little debate in terms of cardiovascular pathophysiology that dependence on vasoconstriction as opposed to volume maintenance for organ perfusion is associated with adverse health outcomes. That reality was elegantly established, although not commented upon, in a 1972 New England Journal of Medicine report that documented 2 important physiologic principles.7 First, as 24-hour urinary sodium excretion decreased, there was a logarithmic increase in plasma renin activity (PRA), and, second, in persons whose PRA was most increased, there was an increase in cardiovascular disease morbidity and mortality. What was not commented on, but recently noted by us,6 was that the point at which the confidence interval of the PRA parabolic curve was intersected by the asymptote of the curve represented the lowest level of 24-hour urinary sodium excretion associated with maximal suppression of PRA (Figure 1). This observation demonstrates the physiologic coordination between sodium intake and the regulation of PRA and subsequent generation of angiotensin II. As noted above, the stimulation of angiotensin II and aldosterone release by low sodium intake is the proximate and most powerful input to the neural circuits to provoke an increase in dietary sodium appetite.3 Based on this physiologic regulatory loop between peripheral sensors of sodium adequacy and the regulation of sodium appetite, it follows that sodium intake in humans should be expressed by a classic normal distribution. That distribution, as with all essential nutrients, is characterized by a bell-shaped curve,6,8 as we recently reported (Figure 2). The distribution is defined at both the lower and upper ends by a relatively strict cutoff. We observed that <1% of the free-living general population consumed <2,600 mg/d of dietary sodium or >5,000 mg/d, consistent with physiologic regulation within a defined and limited range. This scientifically Correspondence: David A. McCarron (dmccarron@mccarrongroup.com).

Physiology, Not Policy, Drives Sodium Intake