No salt, low salt, salt free, heart-healthy salt substitution–any added salt will hurt your constitution. It reads like some bizarre, Seussian tale. Excepting that we’ve heard it not from the good Dr. Geisel but from the medical community and public health advocates everywhere. We watch as celebrity chefs take the salt elimination cooking challenge to prepare an “improved healthy” cuisine. Self-anointed “experts” cadge, coax, and cajole us to decrease our salt, or, more specifically, sodium intake. If that doesn’t work then the specter of heart attacks and strokes is unleashed upon us, along with a dash of fire and brimstone for good measure. It is, after all, clearly in our best personal and the greater public interest.
The hypothesis is sound and the supporting data is impeccable, right?
The theory goes as follows: Salt acts to make us retain fluid. When we retain more fluid it increases our blood pressure (albeit temporarily). Increased blood pressure is hypertension. Hypertension is a risk factor for cardiovascular disease like heart attacks and stroke. Heart attacks and strokes are bad. Therefore, hypertension is bad. Thus, sodium must be bad; A causes B which causes C, therefore A causes C. Get rid of A and you get rid of C—simple basic arithmetic, no? Reduce sodium intake and you will reduce blood pressure and thus reduce the incidence of stroke and heart attack. Reducing sodium intake is good—simple, effective, and undeniably the prevailing conventional wisdom these days.
Except… one thing is missing.
The conclusive data—or any data-that definitively shows that cutting back on dietary sodium reduces mortality or significantly reduces cardiovascular morbidity. For over half a century, starting in the 1960s, there has been a vehement and salty exchange just out of public earshot involving respected scientists on both sides of this line. But with the advent of an aggressive public policy to reduce dietary sodium intake for presumed public health benefit and studies emerging suggesting negative consequences of a low-sodium diet, the clamor of dissension is heating up.
Public policy on salt dates back to 1977 when Senator George McGovern released Dietary Goals for the United States, a report that introduced the first national salt targets. This was set at three grams per day. The aforementioned theory of salt inducing hypertension quickly became science fact or urban legend, depending on your take of the data. A report from the surgeon general issued over a decade later highlighted this disparity. It acknowledged that the policy to restrict salt consumption had been implemented in the absence of studies that proved a low salt diet might prevent increases in blood pressure. Throughout the ‘80s the definitive answer remained elusive.
The Framingham Heart Study, a seminal trial following a cohort of Americans from Framingham, Massachusetts, since 1948, has yielded many landmark insights into cardiovascular risk, morbidity, and mortality. But the study failed to find any correlation between sodium and blood pressure (PDF). Another study in 1985 of over 8,000 men of Japanese descent found no relationship between sodium consumption and stroke. Halfway around the globe, over 7,000 Scottish men were studied, with the conclusion that “association between sodium and blood pressure is extremely weak.” In 1990, the director of nutrition at the Food and Drug Administration remarked in an Associated Press article that “there is no conclusive evidence that salt consumption causes hypertension; it’s only a hypothesis.”
Despite this lack of closure, in 2008, under Michael Bloomberg, “the New York City Department of Health and Mental Hygiene coordinated the launch of the national salt reduction initiative, a public-private partnership of more than 85 state and local health authorities and national health organizations that has set voluntary targets to lower salt levels in packaged and restaurant food,” according to the official New York City website (PDF). Two years later, in 2010, the Institute of Medicine recommended methods of sodium reduction in a report. The group had been asked to develop strategies for sodium reduction, not to evaluate whether sodium reduction was of any benefit, though that may have been the more important question. The Institute’s action plan was based on the presupposition that increased salt consumption caused significant harm. Based on this report, the director of the Centers for Disease Control and Prevention, Thomas Frieden, along with other professional organizations, including the American Heart Association, have moved forward with national campaigns like the Million Hearts initiative aimed at reducing sodium consumption. Programs like this, paid in part with tax dollars, aim to reduce sodium consumption by 20 percent despite any solid evidence for the return on investment.
In 2011, some experts involved in a rigorous scientific review of the studies done on salt remarked that it “is surprising that many countries have uncritically adopted sodium restriction, which probably is the largest delusion in the history of preventive medicine.” Despite this call for caution, “public health recommendations at global, national, and local levels have been nearly unanimous in asserting that the evidence is incontrovertible that salt consumption should be reduced (PDF).”
At the crux of the argument are two fundamental questions:
• Do low-sodium diets prevent hypertension?
• Would a population level decrease in salt consumption save lives (PDF)?
Answering these questions requires an evidence-based approach. Those who feel the current level of evidence is sufficient argue that more data collection will require too much time and money, costing us lives. However, it should be noted that over the last 45 years, while sodium intake has gone up, death from heart disease has continued to decline. Key tools for the successful implementation of evidence-based approaches include meta-analyses to identify effects that may not be apparent in individual smaller studies and the use of randomized clinical trials (RCTs) to help eliminate bias.
The first meta-analysis involving salt was performed in 1986. It found that lowering sodium intake may reduce blood pressure, particularly in people with pre-existing hypertension, but that the effect was extremely small. Subsequent meta-analyses delivered similar results.
Advocates for salt reduction believe that “guidance is based on the best available evidence,” as Sir Michael Rawlins, chair of the National Institute for Health and Clinical Excellence in the United Kingdom, notes. “The evidence may not, however, be very good and is rarely complete.”
These proponents for salt reduction also assume that there is no consequence to a low-sodium diet. This may not hold true; some amount of sodium is necessary for life. A low-sodium diet has some known negative effects. Significantly decreasing the salt in one’s diet increases renin secretion by kidney. Renin is associated with the development of hypertension and can contribute to the development of cardiovascular morbidities and mortality. Decreasing salt intake also increases aldosterone secretion by the adrenal gland, sympathetic nerve activity, and insulin resistance (the condition associated with Type 2 diabetes).
This is not all theoretical, either. In 2011, a study performed by the European Project on Genes in Hypertension (EPOGH) investigators sought to confirm that a reduction in salt intake would reduce the number of cardiovascular events. They followed over 3,500 participants for almost eight years. Surprisingly, those who ate less salt had the highest risk of dying; those who ate the most salt had the lowest mortality rate.
An even larger study was conducted that same year by a group at Canada’s McMaster University and published in The Journal of the American Medical Association. Over 30,000 people were tracked for about four years. The researchers examined low sodium intake (less than 2.3 grams), moderate intake (2.3 to seven grams), and high (more than seven grams). The moderate sodium intake group (which reflects the daily consumption of the average American at 3.4 grams) had the lowest risk of cardiovascular morbidity and mortality. A low level of sodium intake was associated with an increased risk of cardiovascular death and increased risk of hospitalization for heart failure. In addition, the low-sodium group had a 2.5 percent increase in their cholesterol and a seven percent increase in their triglyceride levels—changes not seen in the other groups.
Yet another meta-analysis examining 167 smaller studies drew similar conclusions. The study author, Niels Graudal of Copenhagen University Hospital in Denmark, concluded that “I can’t really see, if you look at the total evidence, that there is any reason to believe there is a net benefit of decreasing sodium intake in the general population.”
Finally, let’s consider two Cochrane reports, which generally consist of meta-analyses and RCTs and are considered a gold standard in delivering reviews of available data. The first, released in 2011, focused on people without hypertension. It found “no strong evidence” that sodium reduction reduced all-cause mortality. The second review, released the same year, also examined people without hypertension. The report concluded that all available evidence did not permit a determination as to whether a low-salt diet improved or worsened health. However, the authors concluded that “after more than 150 RCTs and 13 population studies without an obvious signal in favor of sodium reduction, another position could be to accept that such a signal may not exist.”
What we are learning is that the key may not lie in any absolute amounts, but in the ratio between sodium and potassium—the goal being to achieve a ratio ≤ 1. An alternative to the hypothesis that any health benefit is a result of sodium reduction is considering that any positive findings may arise because of increased potassium consumption. Sodium and potassium, which is often a component of salt substitutes, fresh fruit, vegetables, legumes, salmon, and chicken, exist in the body in a natural balance. Processing, however, affects the sodium to potassium ratio.
A 100-gram (about 3 1/2 ounces) serving of fresh pork, for example, contains roughly 60mg of sodium and about 340mg of potassium. But if you industrially process that into the average deli ham you end up with 920mg of sodium and only 240mg of potassium.
A study out of Sweden examined 10 previous trials looking at data from almost 270,000 people. They found that the higher the potassium intake, the less the risk of stroke. Another study, part of the third National Health and Nutritional Examination Survey(NHANES III), examined more than 12,000 people and found, over a 15-year period, that the group with the highest cardiovascular risk had a very high ratio of sodium to potassium in their diets.
This continues to be an area of intense inquiry.
WHAT DO WE KNOW?
We know that treating hypertension with medical therapy saves lives and reduces cardiovascular disease and complications. We know we need salt to live; 70 percent of our body is made up of salt water. We also know that, in the body, sodium exists in a balance with potassium. Potassium is another element necessary for proper functioning and is especially important from a cardiovascular perspective. We know that for most normotensive people sodium intake can vary tremendously from day to day without significant problems; even quintupling the amount of sodium ingested does not affect blood pressure adversely. The longest-lived people on Earth (and by some accounts the healthiest) are the Japanese, who routinely consume two to three times as much salt as the average American (whose salt consumption has been stable over the last three decades). We know that the effect of dietary sodium restriction, if any, on blood pressure appears extremely modest. And we know that significant sodium reduction has other potentially negative health consequences.
We do not know if salt reduction will result in a health benefit. We do not know the consequences of reducing the salt content of food. In the 1970s a campaign was initiated to reduce fat consumption among Americans. It has worked, and the percentage of fat in the American diet, even saturated fat, has continued to decline. But people ate more, which explains why obesity and diabetes are on the rise. Any manipulation of a system, whether by addition or subtraction, invokes to some extent The Law of Unintended Consequences—with possibly negative outcomes. Hormone replacement therapy (HRT) for post-menopausal women was based on the extrapolation of the desirable effects these hormones had on blood pressure and cholesterol levels (sound familiar?). It is no longer routinely prescribed due to the increased risks of heart attacks, breast cancer, and strokes associated with this therapy.
We cannot simply blame bad policy, especially if it is truly born of good intentions (and scientific ignorance) at the time of implementation. Policy, like science, is the purview of humankind and thus subject to our inherent flaws and growing pains. But to implement overarching public policy when good science raises serious concerns is to engage in public folly.