This week’s news that researchers had apparently debunked the link between dietary salt intake and heart disease was surprising to say the least, but for all that it was lapped up enthusiastically by the media. Some headline writers revelled in the newness of the findings: “Scientists shake up what we know about salt” announced CBS News; “New salt study stirs up controversy” said The Independent. Many outlets remained hesitant about dispensing with prior wisdoms: “Eating less salt may not help heart health” cautioned US News & World Report; “Is sodium actually good?” wondered Shape Magazine. However, as always, other news reports were quite happy to shift the paradigm straight away, providing verdicts that turned previous wisdom on its head. “Salt is GOOD for you” announced the Daily Mail. “Low-salt diet kills” warned the Canada Free Press. “Pass the potato chips” cheered The Globe and Mail. So what’s the story with this research then? Should we now start munching on salt rocks straight out of the shaker? Or should we take these new findings with a pinch of, well, you know…?
The study described in these media reports appears in the current issue of JAMA: Journal of the American Medical Association. The team of European researchers, led by a group from Belgium, studied data drawn from a prospective population study of 3,681 adults who were followed for around eight years. They measured salt intake by analyzing urine samples taken individually from each person in the sample, and drew information about heart disease outcomes from official medical records. Their results suggested that persons with the lowest dietary salt levels were four times more likely to die from cardiovascular disease (CVD) than those with the highest salt levels, during the follow-up period. The effects remained statistically significant even when other relevant measures of heart disease risk were included in the analyses. Referring to their measure of dietary salt as “sodium excretion”, the researchers concluded that “Lower sodium excretion was associated with higher CVD mortality”. As research reporting goes, this is a very clear-cut claim indeed.
However, the reason these results are surprising is that they fly in the face of conventional — and evidence-based — wisdom. Previous large-scale studies have reported strong effects for salt intake in precipitating elevations in blood pressure (which is known to increase heart disease risk), and effects for salt-reduction diets in successfully lowering blood pressure. Other prospective studies have linked dietary salt to the development of heart disease and stroke, to cardiovascular disease, and to cardiovascular events. It is important to note that such conclusions are based on the accumulation of very many separate studies conducted in different places and at different times, with calculations of risk based on aggregated computations across a cumulatively enormous dataset.
On the other hand, the new JAMA study is limited by several methodological restrictions. The main problem is that the overall scale of the study is – in relative terms – very small indeed. While following 3,681 people for 8 years sounds like a lot of work, it does not offer enough scope to examine comparative deaths from heart disease. This is primarily because the average age of participants at baseline was just 40 years. Within the study timeframe for people of this age group, the expected base-rate in deaths from heart disease would be extremely tiny, even if high levels of cardiovascular disease risk factors were present in the sample (for example, even if all the participants were smokers). Simply put, the expected frequency of heart disease death in such a group will be too small to support confident comparisons across sub-groups.
As it turned out, out of all 3,681 participants, only 84 (i.e., around 2%) ended up dying from heart disease during the study period. To put these figures into perspective, we can note that 135 participants died from other causes during this time. The problem is compounded by the fact that the study focused on heart disease death (mortality) rather than heart disease occurrence (morbidity). Essentially, only the 84 participants who died (from heart disease) are actually shedding light on the research question. That is to say, 98% of the participants – all of whom provided urine samples and were followed for nearly a decade – did not really contribute information towards the main study hypothesis at all. To be frank, while it looks as though this research examined thousands of participants, it was essentially a study of 84 people.
Another major problem with the study is that the researchers examined salt intake on one occasion only, namely across a 24-hour period at the outset of the 8 years during which participants were followed. Therefore, when the researchers make assertions about the effects of “sodium excretions”, what they mean is “sodium excretions on one day nearly a decade ago”. Such a measure is entirely contingent on what participants ate the day before. This isn’t a measure of dietary salt intake at all, because it cannot be said to be representative of participants’ regular dietary habits across their daily lives in general. Furthermore, it takes no account of changes in participants’ dietary habits during the study period of 8 years. People change their diets as they grow older. And given the high-profile public health information encouraging people to reduce their salt intake, dietary salt intake is one the aspects of diets that people will change the most.
It can also be noted that the researchers did not include measures of exercise in their statistical model. This is important because people who exercise more consume more food, and therefore more salt, but are less likely to develop heart disease. This alone could account for any apparent link between high salt intake and low cardiovascular disease.
In summary, despite the news coverage, the JAMA study is insufficient to support many of the conclusions presented as media headlines over the last few days. This is because much reporting failed to account for the pre-existing scientific context. In essence, the JAMA study is an outlier within a much larger literature that predominantly pulls the consensus in the opposite direction. Thorough media reporting of such findings should really acknowledge this overall state of play (as was successfully achieved in some cases, such as in the New York Times and LA Times).
Whatever about the lessons for media reporting of new science, it is certainly clear that the JAMA study fails to change the basis for conventional health advice surrounding sodium levels: dietary salt intake remains a significant risk factor for heart disease for all adults, healthy or otherwise.
Brian Hughes is an academic psychologist and university professor in Galway, Ireland, specialising in stress, health, and the application of psychology to social issues. He writes widely on the psychology of empiricism and of empirically disputable claims, especially as they pertain to science, health, medicine, and politics.
Brilliant! How did this study get published at all is my question? In the era of exhaustive, P.C. ethics boards, somehow this cuts the mustard methodologically? Amazing.
Not only is science reporting in public health dreadful, actual science in public health is dreadful too. Gary Taubes wrote an excellent article about the history of “Salt Science” in 1998.
You need access to sciencemag to view the article in full.
I’m not sure salt intake is a significant risk factor for heart disease for all adults, healthy or otherwise. The Cochrane report you linked to in the text explains in the discussion that their meta-analysis shows a reduction in blood pressure on a “modest” salt reduction diet in hypertensives to be 5/3 mmHg and in normotensives of 2/1 mmHg.
Considering normal blood pressure is 120/80 and stage 1 Hypertension is 140/90, a reduction of 5/3 or 2/1 seems hardly worth it. Especially when you then consider this impact on people with stage 2 or stage 3 hypertension – 170/105 and up to 210/120 respectively.
Wow, a study that goes against what every doc has told their patient so it must be garbage? Has any study looked at salt and healthy people? NO, now that we have, maybe we can stop telling every person in America that salt is bad for them if they are healthy and active. Here in Arizona, there are far too many people who suffer from a lack of salt than too much (because they sweat a lot and need to replace it).
The Cochrane report you linked to (salt reduction diets) in the text concludes
“In individuals with normal blood pressure the median reduction in urinary sodium was 74 mmol/24h (4.4 g/day of
salt), the mean reduction in blood pressure was -2.03 mmHg (95% CI: -2.56 to -1.50) for systolic and -0.99 mmHg (-1.40 to -0.57)
So, as noted above, negligible, and certainly not justifying the current campaign.
The fact that this is a meta analysis, authored by G A MacGregor, the Chairman of a charity? called CASH (Consensus Action on Salt and Health) doesn’t help.
Thanks for that. You make two excellent points. The personal reduction SBP of -2 mmHg is almost negligible at the individual level; and the fact that the analysis was linked with a lobby group should indeed be borne in mind.
That said, while a decrease of -2 mmHg would mean little to an individual, according to epidemiologists such a decrease would not be trivial at the population level. If everyone in the population (normotensive and hypertensive) experienced such a decrease, then quite a sizeable effect would be seen on population rates of heart disease, stroke, etc. This is essentially the basis for advising people to reduce their intake of caffeine, salt, etc. (see, for example, http://www.psychosomaticmedicine.org/content/66/1/63.abstract).
This is more a public health issue than a personal health one. But the recommendation to reduce salt intake is still important in that context, even if the reduction is only 2 mmHg.