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More than half a century has passed since the idea that the lower blood pressure (BP) associated with lower sodium intake justifies reduced intake for all. Authoritative bodies have subsequently endorsed this view with increasingly ambitious reduction goals. The US Department of Agriculture and US Department of Health and Human Services currently recommend <1.5 g sodium/day for virtually half the population, with <2.3 g1 levels for the remainder. While in much of the world, including the UK and the USA, mean sodium intake approximates 3.5 g/day.2 However, emerging evidence has led to increased uncertainty that, despite BP effects, there is insufficient evidence to support these recommendations.3
Aburto and colleagues have updated their previous meta-analysis of the relationship between sodium intake and BP with morbidity and mortality outcomes. An analysis of 36 trials confirmed previous findings of sodium related BP reduction.
Lower sodium intake was associated with decreases in BP in adults as well as children. For adults, when sodium intake was <2g/day versus ≥2 g/day, systolic BP was reduced by 3.47 mm Hg (0.76–6.18) and diastolic BP by 1.81 mm Hg (0.54–3.08). In children, lower sodium intake significantly reduced systolic (0.84 mm Hg, 0.25–1.43) and diastolic BP (0.87 mm Hg, 0.14–1.60). For cardiovascular disease (CVD) and mortality outcomes, the results were mixed. Analysing 14 observational studies and seven experimental studies, they found that higher sodium in adults was significantly associated with an increase risk of stroke (risk ratio 1.24, 95% CI 1.08 to 1.43), stroke mortality (1.63, 1.27 to 2.10) and coronary heart disease mortality (1.32, 1.13 to 1.53). However, there was no significant association between sodium intake and all-cause mortality, all CVD, or all coronary heart disease events. The significant association with fatal coronary heart disease events was reported based on three observational studies, two from very high-sodium populations and one from an overweight subset. No associations were seen on lower sodium intake with changes in blood lipids, catecholamine levels or renal function in adults.
This systematic review further fuels the sodium controversy. A prior analysis of 26 observational studies investigating dietary sodium intake and CVD mortality suggested that the relation to health outcomes was not linear, but rather J-shaped with a broad ‘safe zone’ (about 2.5–5 g/day).3 As with other essential nutrients, there is evidence of increased morbidity and mortality above and below a safe middle range. Moreover, randomised trials among heart failure patients, which were not included in the present study, found those randomised to 1.8 g/day had higher mortality and morbidity compared with those allocated to 2.8 g/day. At the same time, a trial, comparing sodium intake (5.3 vs 3.8 g/day) of military retirees, found substantially higher mortality among the higher sodium group. Assuming that the sodium intervention accounted for the observed health effect despite fundamental confounding by a simultaneous increase in potassium intake, then both experimental studies are consistent with a ‘safe zone’ with increased risk above or below that zone. However, these trials do not provide evidence that is actionable for the general population; there is no assurance that repetition of either the heart failure studies, or the Taiwan study, in different populations, would produce either similar or different results.
The Institute of Medicine (IOM) has issued a comprehensive assessment of health outcomes associated with dietary sodium intake.4 The content and conclusions of this compelling report have scrambled the scientific landscape. The committee concluded that there was insufficient evidence (for or against) to support a general recommendation to reduce sodium to <2.3 g/day. The committee registered support for sodium reduction from high levels, while cautioning that intake below 2.3 g/day might cause harm for some. They had not been tasked to define the ‘safe zone’ for sodium intake; however, the report implicitly recognises that such must exist. Randomised trials with CVD event outcomes comparing low and high intake to middle levels will be needed to more precisely identify dimensions of the ‘safe zone’.
Here, as often in the past, steady accretion of scientific evidence has clarified uncertainty. In the case of sodium, evidence that has often appeared in conflict is now seen to be resolved by a single coherent hypothesis. A J-shape linking sodium intake to health outcomes accommodates virtually all the available evidence. The early hope that the BP effect of sodium reduction would guarantee a health benefit for all is no longer tenable. The multiple physiological effects of sodium reduction mandate that the consequences of sodium reduction be assessed by studies that measure morbidity and mortality. The substantial data already available indicates that sodium reduction might well benefit those at the very high end of sodium intakes, whereas if pushed too far, may be harmful. The IOM report has not yet identified the dimensions of the ‘safe zone’. Hopefully, the range will turn out to be easily accommodated by most people.
Competing interests None.