Cut out the salt

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Cutting back your salt intake is an effective way to reduce systolic and diastolic blood pressure and decrease your risk of dying from cardiovascular disease. The current guidelines suggest that we should reduce our dietary sodium intake to 2.4g daily and there are moves afoot to reduce this goal even further. This is what we tell our patients and the evidence is unequivocal. Isn’t it?

Well… no. Multiple studies have shown that cutting salt intake reduces blood pressure. Putting patients on a DASH diet leads to lower blood pressure and two recent cochrane reviews of salt restriction in diabetics and non-diabetics found a significant effect on blood pressure which was especially marked in those with pre-existing hypertension. However, all of these studies were short-term and any effect on cardiovascular morbidity was extrapolated from the effect on the blood pressure. In a similar vein, Matt previously posted about a study published in the NEJM last year which found enormous potential financial benefits that would be derived from a population-wide reduction in salt intake. However, again, this was entirely based on the assumption that the reduction in blood pressure achieved by decreasing salt intake would translate directly into an equivalent reduction in cardiovascular morbidity.
In contrast, a study of the NHANES II data published in 2006 suggested an inverse relationship between salt intake and overall mortality. This study was criticized because salt intake was measured through diet recall, which is notoriously inaccurate. That said, this can be said of many of the intervention trials relating to salt intake as most do not use the gold-standard of 24 hour sodium excretion.
A paper was recently published in Diabetes Care that examined the relationship between dietary salt intake, as measured by 24 hour excretion, and mortality in diabetics over 10 years. 638 patients were included and over the study period, there were 175 deaths, 75% from cardiovascular disease. After adjusting for baseline risk factors, there was a 28% reduction in mortality for every 100mmol increase in sodium excretion. Why would less salt be bad for diabetics? There are a number of theories. A low-salt diet can lead to an increase in the activation of RAAS and this is postulated to be more problematic in diabetics, given the undoubted benefits of RAAS blockade in these patients. However, diuretics have a similar effect on renin and aldosterone levels and yet are associated with a reduction on mortality. Salt reduction has also been associated with increased LDL and insulin resistance in normal individuals. It has to be said that this was not an intervention trial. Baseline blood pressure was the same in all 3 groups and it is impossible to say what the effect of salt reduction might be in the individual groups. It is well known that men have a higher salt intake than women, which is related to their higher caloric intake and the high salt group in this study had a disproportionate number of men. Perhaps the lower salt intake was related to poor nutrition. Maybe the patients with lower salt consumption were advised to reduce their intake because of a perceived higher cardiac risk. It is impossible to say for certain.
So does this mean we can tell our patients to eat whatever they want? No, I don’t think so. It is unlikely that we will ever see a large randomized trial of salt intake in the same way that we won’t see a randomized trial of smoking v. not smoking. We know that lowering blood pressure decreases cardiovascular risk and we know that reducing salt intake decreases blood pressure. Reassuringly, a large meta-analysis was published in the BMJ in 2009 which found that a high salt diet was associated with a relative risk of 1.23 for stroke and 1.14 for cardiovascular disease.
Still, having reviewed this topic, it was surprising to me that there was such a relative paucity of evidence for an intervention that I recommend every day. I’m not going to change that recommendation based on one study, but it is good to have your assumptions challenged every once and a while.


  1. For a weigh-in on both sides of the issue:

    In general the preponderance of evidence supports salt lowering strategy well below the "typical" US diet, but one should not lose sleep over it if HTN is adequately controlled.

    The recent sodium bicarbonate studies for CKD involved doses around 2g/day, translating to 500 mg or so net sodium. Compared to the typical or even "reduced"-sodium daily diet, this change is quite modest. Therefore, the relative lack of the expected dire consequences from "so much sodium" should perhaps not have been such a surprise.

  2. I was a salt sceptic due to the modest reductions in blood pressure with pretty significant dietary modifications. It seemed not worth the effort for the payoff. Cook's TOHP follow up study in the BMJ turned me.

    Take a look at Cook's long-term follow-up of two prospective studies (TOHP I and II) on sodium restriction. They found, by dietary recall, that patient originally randomized to low salt diets continued to make low salt choices after the study ended and they also foiund that those patients randomized to low salt diets had 30% lower incidence of cardiovascular events in the next 10-15 years, irrespective of sex, ethnic origin, age, body mass, and blood pressure.

    Because of the randomizedish nature, long follow-up and use of hard end-points I find this to be the most compelling data on low salt diets.

  3. The "salt wars" continue. Interesting side-note on the Mahajan et. al. study on sodium bicarbonate therapy for early hypertensive nephropathy–3rd "sodium chloride" arm had slightly lower BP than even the placebo. Perhaps salt vilified too much. All things in moderation.

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