The units of salt are confusing

The main thing that I learned - or rather was reminded of - was that the units of salt are confusing and unintuitive. This is annoying because if I were contemplating changing my diet to reduce my risk of cardiovascular disease then I would want to know two things:

1. how much less salt do I need to eat?
   
2. how much will this reduce my risk of stroke and heart attack?

We can answer both questions, but unfortunately it can be hard to extract this information from a literature that flits between grams NaCl, grams Na and mmoles. We need first to know how to interconvert these units (100 mmol Na = 2.3 g Na = 6g NaCl), and how to put them into some sort of meaningful context.

How much salt do we eat?

Most dietary salt is consumed “hidden” in processed foods that are perhaps not immediately perceived as salty (bread, pizza, sandwiches, processed meats, soups…). A Big Mac contains ~1000 mg Na⁺; a shop-bought sandwhich contains ~666 mg Na⁺; a packet of crisps contains ~500 mg Na⁺.

So wouldn’t it be better if we talked about salt in terms of “shop-bought-sandwich-equivalents” rather than g or mmol? In these terms, the recommended daily intake of Na⁺ (less than 5 g NaCl / 2 g Na⁺ / 86 mmol) equates to around ~3 sandwich-equivalents. The global average daily intake is significantly higher than that at ~7 sandwich-equivalents.

Similarly, we could use the banana-equivalent as a unit of potassium intake. Bananas are usually cited as a high-K food although of course there is nothing particularly special about bananas; K⁺ content is high for most fruit, veg, seafood and dairy. A baked potato (skin on) = 1000 mg; a banana or glass of orange juice = 500 mg. Therefore the recommended daily intake of K⁺ (more than 3.5 g K⁺ / 90 mmmol) equates to at least 7 banana-equivalents.

Effect sizes

But what about the second question: how much of an effect will Na⁺ reduction (or K⁺ supplementation) have on cardiovascular risk? That is a bit of a how-long-is-a-piece-of-string question because there is a continuous relationship between Na⁺ / K⁺ intake and blood pressure. However, we can perform a back-of-an-envelope calculation, using what we know about the dose-response relationship between Na⁺ and blood pressure, to work out roughly how big a dietary change we would need to make in order to make a sizeable (say 10%) reduction in the relative risk of cardiovascular disease.

In randomised controlled trials of salt reduction, every 50 mM reduction in daily Na⁺ intake causes a 2.0 – 2.5 mmHg drop in ABP. In our sandwich-equivalent units: one sandwich (c. 25 mM) equates to a drop in of ~1 mmHg systolic. For potassium supplementation, the benefit in RCTs is around 3 mmHg for every 50 mmol daily supplementation; so that one banana (12.5 mM) equates to a ~0.75 mmHg drop in blood pressure. Therefore, if we were able to cut out around two processed sandwiches from our diet every day and replace these with three bananas, we can expect to realise a ~4 mmHg drop in arterial blood pressure. This effect size is significiant; it is broadly similar to that seen for a lone anti-hypertensive medication and should cause a ~10% relative reduction in the risk of CVS disease. (Provided, of course, that these dietary changes are sustained over the long term - which is easier said than done; see below.)

Some individuals stand to gain more from this sort of dietary change, because their blood pressure will be more sensitive to dietary salt. This is likely to be the case for individuals who are older, non-white, hypertensive and who have diabetes mellitus or kidney disease.

Making dietary changes is hard

In general then, one can achieve the twin benefits of sodium reduction and potassium supplementation by switching from processed foods to a fresh, mainly plant-based diet. However, this is a difficult thing to do because we have a strong inherent salt preference, because most people are exposed to a diet in which sodium is present in an abundance that far outweighs physiological need and because making this sort of dietary change requires time, effort, knowledge and money. (In our article we mention the 2013 JAMA paper looking at concordance with a ‘DASH diet’ in different socioeconomic groups. Uptake of a low-Na, high-K DASH diet was highest in those groups with higher income and educational attainment.) For these reasons, we argue there is a strong case for making interventions at a population-wide / societal level.

However, we can offer some hope to individuals wishing to cut their salt intake. Although transitioning to a low-salt diet is initially tough, there is evidence that salt-taste thresholds reset over a period of months, so that low-salt food no longer tastes bland and high-salt food becomes less palatable. Having previously experienced this after abruptly reducing dietary salt intake, I was intrigued to discover that this phenomenon was characterised in the 1980s.

Salt content of medicines

In hospital, it is alarmingly easy to deliver sodium chloride in vast excess to usual daily intake - let alone minimal physiological requirements. One 500 ml bag of 0.9% NaCl contains 77 mmol (1.8 g Na), which is just over 2.5 of our sandwhich-equivalents and close to the 2.0 g Na WHO recommended daily intake. For a table showing the electrolyte content of various medications and IV fluids, see chapter 3 of Nephromaths.)

Salt restriction and kidney stones

Salt restriction is probably helpful in individuals prone to kidney stones (the literature is much smaller than for salt and blood pressure). It can be helpful to remember the likely tubular mechanism. Na⁺ and Ca²⁺ transport in the proximal tubule are coupled through the effects of Na⁺ and water reabsorption on the transluminal [Ca²⁺] gradient and through solvent drag. This explains why hypercalcaemia can be aggravated by volume depletion (high proximal Na⁺ uptake drives Ca²⁺ reabsorption) and why high salt intake can predispose to kidney stones (suppressed proximal Na⁺ uptake limits Ca²⁺ reabsorption).

How potassium supplementation lowers blood pressure

K⁺ supplementation reduces blood pressure and K-rich salt substitutes reduce cardiovascular disease in cluster-randomised RCTs. But what is the mechanism? This is usually explained as dietary K⁺ inhibiting NCC activity - i.e. inducing a thiazide-like effect. (And there is some evidence for a direct vasodilatory effect.) This makes teleological sense if we view NCC as a master gatekeeper of the distal nephron, setting the balance of electroneutral and electrogenic Na⁺ reabsorption to maintain K⁺ homeostasis. However, exactly how NCC inhibition translates into lower blood pressure is a little murky, in the same way that the mechanism through which thiazides lower blood pressure in the long term is debated.