The Human Penchant for Deranged Salt Balance
Consequences and Study of Deranged Salt Intake
“Habitual high salt intake is one of the quantitatively important, preventable mass exposures causing the unfavorable population-wide pattern that is a major risk factor for epidemic cardiovascular disease,” and “…CVD is the world’s leading cause of death and excess dietary sodium has convincingly been shown to be a serious public health hazard…” (The Lancet 2011; Stamler 1997). In contradiction, in a human experiment, blood pressure (BP) was not found to increase with sodium load, unlike animal experiments, and recent evidence highlights a protective role of salt intake in cardiovascular disease (Alderman and Cohen 2012; Dong et al. 2010; Taylor et al. 2011; Todd et al. 2012).
The consensus that dietary sodium is toxic, and the contention that it is not, fuel an important debate that, astonishingly, ignores its root cause—why humans eat salt in the first place. What high salt intake causes is well researched, what causes high salt intake is not known at all (Beauchamp 1987; Leshem 2009a; Mattes 1997). There have been very many and extensive studies on tens of thousands of people over at least 4 decades elucidating and refining the connection between sodium intake and pathology, and there has been considerable public investment in health promotion and legislation to reduce sodium dietary content and intake (Boscoe et al. 2006; Cohen et al. 2006; Institute of Medicine (US) Committee on Strategies to Reduce Sodium Intake 2010; Dietary Guidelines for Americans 2010; He and MacGregor 2010; Millett et al. 2012; Stamler 1997). Despite this tremendous investment, in the same period only three review articles have addressed human sodium appetite. They concluded that “we know of no reason for intake of salt in humans” (Beauchamp 1987), that “the basis for the high, apparently need-free, sodium chloride ingestion … has not been established” (Mattes 1997), and that “humans do not have a sodium appetite as we know it in animals, leaving us with a rather limited understanding of why humans ingest so much salt” (Leshem 2009a).
Hence, essentially, the efforts to manage sodium consumption, by the individual, the physician, and government, are not evidence-based. In contrast, we have a solid base of knowledge from animal experiments about the controls of salt intake as a biological homeostatic system—we can halt salt intake when it is crucially required, and we can boost it when it is not, both acutely and for the duration of the animal’s life. However, the animal system has primarily evolved to prevent and repair sodium deficit—not to cope with persistent and chronic excess. Analogous arguments have been applied to the obesity epidemic as a failure to regulate ingestion with homeostatic controls evolved to contend with famine rather than feast; however, there is an important difference between salt and food with crucial implications for control—the results of excess caloric intake are visible and persistently troubling even if its long-term implications are not, whereas those of excess sodium are not. In susceptible individuals, its primary pathology is hypertension, for which we have no senses, no defenses, and no warnings. Thus, among hypertensives worldwide, 6–97% are unaware or uncontrolled (Dreisbach 2011). These are no trivial figures; hypertensives may include 67% of U.S. adults aged 60 years and over (Ostchega et al. 2007).
The study of the causes and determinants of salt appetite will assist in addressing its behavioral regulation, largely sodium overconsumption, but also the increasingly recognized problems of hyponatremia and fluid regulation, neonatally, in exertion, in disease, in mental anguish, and in senescence (Almond et al. 2005; Boscoe et al. 2006; He and MacGregor 2010; Johnson and Grippo 2006; Koleganova et al. 2011; Malaga et al. 2005; Moritz 2008; O’Donnell et al. 2011; Shirazki et al. 2007; Stein et al. 2006; Stolarz-Skrzypek et al. 2011).
Deranged Intake of Salt
Some experts point to the benefits of a daily sodium intake of 0.9 mmol (21 mg sodium, 0.53 g salt; Mancilha-Carvalho et al. 2003), some go 5-fold higher to 5 mmol (115 mg, 0.29 g) for healthy adults living in a temperate climate, but in consideration of the wide variation in (U.S.) physical activity and climatic exposure, increase that 4-fold to a safe minimum of 21.7 mmol (500 mg, 1.27 g), tripled to 65 mmol (1500 mg, 3.8 g), not because this is the actual sodium requirement, but because it ensures that the overall diet provides an adequate intake of other important nutrients, as well as to cover possible excessive sodium loss (Dietary Reference Intakes 2005). This is increased by a further 50% to 100 mmol (2300 mg, 5.85 g) by health authorities (e.g., the U.S.) as an achievable interim reduction goal (Dietary Guidelines for Americans 2010; The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure 2004).
However, 12- to 50-year-old American men consume 196 mmol (4500 mg, 11.5 g) and American women a third less, which averages to the similar intake of people all over the world at 162.4 ± 22.4 mmol (3735 mg, 9.5 g; Bernstein and Willett 2010; Brown et al. 2009; McCarron et al. 2009). This is 2–200 times the requirement estimates, a difference showing the human penchant for deranged salt balance. This derangement is repeated daily, and for perspective, ponder our ponderosity were our caloric intake similarly apportioned. We have no inkling as to the reasons for this derangement. It has been sparsely researched, and where so, the conclusion has been unanimous—there is no known reason for the deranged intake of salt (Beauchamp 1987; Leshem 2009a; Mattes 1997).
An alternative approach suggests that this may be no derangement, but an imperative— that although the requirement estimates, based on human physiology, may be adequate for physiological function, there are additional benefits to the persistently higher intake of salt in humans. Such benefits can make salt tasty by conditioning, that is, if salt does us good, it will come to taste good. Taste will therefore regulate its intake, not physiological necessity. On the contrary, physiology is harnessed to cope with this overload, and clearly at a price in bodily resources and health. According to this rationale, and it is presently the best available, to understand the human penchant for deranged salt balance all that remains is to discover how salt benefits us. In an interesting departure from the reduction proposals, it has recently been argued that, in fact, the current level of intake is the healthiest in terms of cardiovascular mortality—sodium intakes above and below the range of 2.5–6.0 g/day (6.4–15.3 g/day salt) are associated with increased risk (Alderman and Cohen 2012). However, the long-term benefits of sodium cannot condition sodium preference in the healthy individual—although over generations such increased fitness might.
Extant Notions about Why We Have Deranged Intake
We review extant notions about the causes of our salt intake, as a derived derangement of animal salt appetite, the suggestion that much of our salt intake is insensible by virtue of sodium being veiled in industrialized foods, that we are instilled with a love of salt at an early age, or that we are addicted to salt. We end with a review of the single established determinant of salt intake—perinatal sodium loss.
Let us contemplate the nature of the human predilection for salt. We have four, possibly five, basic taste sensors in our mouths. In concert, they inform us of the infinite variety of tastes we enjoy. Yet, of these few sensors, one is dedicated entirely and specifically to respond to sodium, the charged atom that gives salt its unique taste.
Micah Leshem. (2014). The human penchant for deranged salt balance. In: Neurobiology of body fluid homeostasis (transduction and integration). Eds: De Luca L, Menani JV, Johnson AK. Taylor & Francis Group. Series: Frontiers in Neuroscience Boca Raton (FL): CRC Press; 2014. Chapter 1.