Relationship of urinary sodium and sodium-to-potassium ratio to blood pressure in older adults in Australia

Raised blood pressure (BP) is one of the most common and preventable risk factors for cardiovascular disease. It has been estimated that 33% of the Australian adult population have established hypertension,1 and that hypertension contributes 42% of the cardiovascular disease burden in Australia.2 There is compelling evidence across countries that total dietary sodium intake and sodium-to-potassium ratio (assessed by 24-hour urine collection, which provides an objective measure of total dietary sodium intake) are associated with an age-related rise in BP.3 Few studies have demonstrated an effect within populations with relatively high sodium intakes.4,5 Urinary potassium, reflecting dietary intake, has been shown to have an independent inverse association with BP.6 A large prospective study and a randomised controlled trial have shown that high urinary sodium or a high urinary sodium-to-potassium ratio increases the risk of cardiovascular events and mortality7-9 independently of the effects on BP.

There are limited data on sodium intake in Australia assessed using 24-hour urine collection. In 1995, a small population-based sample indicated mean urinary sodium excretion of 170 mmol/day (9.8 g salt/day) for 87 men and 118 mmol/day (6.8 g salt/day) for 107 women,10 and small convenience samples have reported excretion of 105–210 mmol/day (6–12 g salt/day).11-16

We assessed 24-hour urinary sodium and potassium excretion and examined the relationship to BP in a cross-section of middle-aged and older Australian adults participating in the Melbourne Collaborative Cohort Study (MCCS), a large prospective study investigating the role of lifestyle factors in the development of common chronic diseases.

This is one of the few within-population studies4,5 and the first study in Australian adults to demonstrate a positive association between urinary sodium or sodium-to-potassium ratio and SBP. Our findings provide supporting evidence that the current high intake of sodium in older adults in Australia is related to higher BP. This has been difficult to demonstrate within populations because the urinary sodium–BP relationship within a community is affected by regression dilution bias, as daily sodium excretion can vary considerably within individuals and BP varies throughout the day.21 The association may be evident in this study because this population was older and ethnically diverse. Most participants were consuming excessive amounts of sodium, which appears to be making a significant contribution to elevated BP and increased rates of hypertension. In this population with a high-sodium diet that would be common in the Western world, we found that a reduction in sodium intake of 100 mmol/day (6 g salt/day) was associated with a 2.3 mmHg reduction in SBP.

This finding is consistent with the Intersalt international cross-population study,3 which estimated that a 100 mmol/day lower sodium intake was associated with a 2.2 mmHg lower SBP. Sodium-to-potassium ratio has also been previously related to BP regulation,8,22 and we observed that a 1 unit decrease in the sodium-to-potassium ratio was associated with a reduction in SBP of 1.8 mmHg. A population-wide fall in SBP of 2 mmHg has been predicted to lower stroke mortality by 10% and ischaemic heart disease and other vascular diseases by 7%.23

Epidemiological and observational studies are likely to underestimate the association between urinary sodium and BP; randomised controlled trials have demonstrated greater falls in BP for a given reduction in sodium.24 The strength of the positive associations between sodium and the sodium-to-potassium ratio and SBP may have been underestimated in our study. BP measurements and urine collections were performed on average nearly 3 years apart. It is possible that there may have been small improvements in dietary habits, as participants were taking part in an intensive exercise to measure their food intake over this period, which would have tended to reduce any sodium–BP association. In this cohort, participants with pre-existing cardiovascular disease were more likely to have reported a healthier diet than others in the cohort.25 However, overall, most participants were consuming excessive amounts of sodium, with only 21% of the sample at or below the upper recommended limit of 100 mmol/day. After adjusting for age and sex, the odds of hypertension in participants in the two highest quintiles of urinary sodium (≥ 160 mmol or ≥ 9.2 g salt/day) were twice the odds in those in the lowest quintile. This is concerning because the majority of these participants were aware of their high BP but were still consuming large amounts of salt.

The major strength of our study is that sodium excretion from 24-hour urine collection was used to estimate sodium intake in a relatively large, ethnically diverse sample of adult Australians. The fully adjusted model indicated that the covariates, including country of birth, explained 20% of the variation in SBP. Although the stratified sampling was based on age and country of birth, all participants lived in the Melbourne metropolitan area, which may limit the generalisability of these findings.

Lowering the sodium intake of populations has been predicted to shift the population distribution curve of BP towards more optimal levels. Reducing dietary salt by 3 g per day has been projected to reduce mortality by 3%–11% for adults aged 35–64 years and to have cardiovascular benefits similar to population-wide reductions in tobacco use, obesity, and cholesterol levels.26 However, it is very difficult for individuals to effectively reduce dietary sodium intake, as over three-quarters of total intake is from sodium present in purchased foods.27 The most effective strategy to achieve a significant reduction in population-wide salt intake would be to reduce the salt added to staple processed foods.

With health organisations around the world advocating reduction of salt intake, more targeted government and industry support is required to reduce the sodium content of processed foods, together with educational strategies to advise consumers to limit discretionary salt consumption.28 Such public health initiatives could effectively lower sodium intake and reduce the incidence of hypertension.