The Evidence in Favour of Reducing Sodium Intake is Less Than Conclusive

sharma-obesity-salt-shaker1Regular readers may well be aware that I spend the first 10 years of my research career studying the effects of salt on blood pressure. Although I am no longer directly involved in sodium research, I continue to follow this issue with keen interest.

Recently, I commented on the  Institute of Medicine’s report that there is little hard evidence on which to base a recommendation to reduce sodium intake to less than 2.3 grams per day to reduce cardiovascular risk.

In today’s post I want to draw readers’ attention to a special issue of the American Journal of Hypertension dedicated to responses and thoughtful commentaries on the Institute of Medicine’s findings.

In one article, David McCarron reminds us that in healthy individuals body sodium is indeed tightly homeostatically controlled, or as he puts it,

“These well-established physiologic pathways provide the biological basis of the fact that actual human sodium intake is set by physiology and not public policy.”

As McCarron points out, any decrease in sodium intake is countered by an increase in hormones like renin, angiotensin, and sympathetic activity, that seek to defend the body’s sodium stores. Interestingly enough, it is exactly these hormones that we block when we treat patients with ACE inhibitors, angiotensin receptor blockers, renin inhibitors, or beta-blockers – all with proven cardiovascular benefits. Stimulating these hormones and systems by restricting salt intake makes no physiological sense – indeed, it is the very opposite of what you may wish to biologically accomplish to reduce cardiovascular risk.

In another article, Salim Yusuf and colleagues point out that despite some studies showing a small blood pressure lowering effect of  sodium restriction,

“…none of these studies addressed the crucial question: Does lowering Na intake reduce CVD? In the absence of reliable randomized controlled trials (RCTs), some clues can be obtained from cohort studies examining the association between Na intake and CVD. Recently, 4 cohort studies with urinary estimates of Na consumption (which are better than dietary estimates) raised concerns that low Na intake (<3g/day) was associated with higher (or no lower) rates of CVD/mortality compared with moderate intake.”

With regard to feasibility and actual consumption, Yusuf and colleagues argue that,

“The average American consumes about 3.5g of Na per day, and this has remained constant for the last 50 years, despite guidelines and population-based efforts to reduce Na intake further. In addition, data from >30 countries have reported a similar level of Na intake. In the United States, only 9% of adults consume <2.3g/day, and just 0.6% consume <1.5g/day. Therefore, the human experience for very low levels of Na consumption is extremely sparse.”


“…in countries such as the United States, there have been marked reductions in CVD rates by about 50% over the last 25 years although Na intake has remained constant. So, Na reduction does not appear to be essential to reducing CVD.”

Yusuf and colleagues also note that there is no known benefit of further lowering their blood pressure in people with normal blood pressure (the vast majority of the population) – if anything, there may be some evidence of harm.

Where I wholeheartedly agree with Yusuf and colleagues, is in their statement that,

“The zeal to recommend extreme reductions in Na intake that are difficult to achieve in the entire population in the United States and other countries with moderate Na intake (e.g., <5 g/day) is a case of ideology replacing good science….As shown repeatedly in the past, well-meaning interventions based on insufficient science can mislead (e.g., hormone therapy, margarines, and total fat intake).”

Or, as the IOM committee chair Brian Strom stated:

“It’s not a question of studies showing benefit being better than those showing harm; there are no studies showing benefit.”

I do not expect for a minute that this state of affairs will in any way deter the anti-salt lobby to ease in their efforts to call for public health campaigns, policies, and other measures to convince people to eat less salt.

Indeed, the same issue of the American Journal of Hypertension features several “pro” articles, essentially rehashing the “epidemiological” case for salt restriction based on the blood pressure surrogate.

Thus, Jenifer Clap and co-authors, use the same age-old blood pressure argument, to make the rather dramatic but unsubstantiated assertion that,

“reducing sodium intake may be second only to controlling tobacco as the most effective intervention to prevent deaths from chronic disease.”

Even more interestingly, also for the “pro” side,  Lawrence Appel and Paul Whelton, fully acknowledge the shortage of conclusive evidence, but then make the surprising statement that,

“Flawed evidence should not derail sound policy.”

Perhaps it is this sort of thinking that does more to muddy the waters than the lack of better evidence.

Personally, I will continue limiting my recommendations to reduce salt intake to those who actually have high blood pressure and, even for them, it may be far easier to simply add a few milligrams of a diuretic to their meds.

Edmonton, AB