Bad science slams salt
Again this year, salt was slammed by both the USDA and the Center for Science in the Public Interest in reports that had all of the trappings of legitimate science, but little — if any — substance.
By David Feder, R.D., Managing Editor | 05/31/2005
For reasons unclear, salt continues to suffer sensationalist treatment in the media while fending off degreed experts who ignore the science to decry this most common of seasonings. Food processors will have to decide how, if at all, to react to this latest lab-coat-inspired fad. Is it worth making major overhauls to well-accepted product lines? Do you risk dumping millions of dollars of flavorless, unloved low- and no-salt foods into bargain bins at a loss?
It’s hard to find a nutrition professional who has not counseled healthy people to decrease their intake of sodium. In addition to the USDA, the American Heart Assn., the National Heart, Lung, and Blood Institute (NHLBI) and the National High Blood Pressure Education Program — a coalition of health organizations and federal groups — plus a dozen others all insist healthy people can reduce their risk of heart disease or stroke by eating less than 2,400 mg of sodium, quite a cut from the 4,000 to 6,000 mg we currently ingest on a daily basis.
Nutrition policies of whole countries have sanctioned the call for salt reduction. Yet oddly, the scientific backing for healthy individuals to decrease salt in their diets simply isn’t there. What’s behind this stampede by otherwise responsible scientists to ignore the evidence of their own research? After several decades, there’s still no answer to that question.Where the myth began
The effect of dietary sodium on hypertension was first studied clinically in the 1940s, when the Kempner Diet was developed to treat high blood pressure through reduced sodium intake. The favored method of noninvasive hypertension treatment, it was a standard that went a long way to entrench the notion that salt causes high blood pressure. Two major variables were ignored: The Kempner diet was used to treat people who were already ill, and the diet was also low-calorie, low-fat and high-potassium (salt’s metabolic “opposite”). But the paradigm was set.
The connection made sense from a chemistry standpoint, since blood pressure is related to electrolyte regulation in the kidneys. As levels of sodium rise and fall, so too can blood pressure as the body retains water to maintain equilibrium. (Note: This is a very basic description. Dozens of metabolic reactions, biochemical exchanges and other factors work in bodily ballet to keep all systems go.) A flood of studies on how this regulatory mechanism affects people with hypertension ensued.
In the 1970s and 1980s, epidemiological studies across the board yielded results that were conflicting, if not completely polarized. For example, studies of Japanese populations with high salt intake saw higher incidences of hypertension. But follow-up studies of specific groups within those populations found no connection. Attempts to scale down the research for a clearer picture resulted in wildly differing results.
And therein lies the problem: The majority of lab research into the sodium-hypertension (and other disease states) connection involved animal models or unhealthy human subjects. Discounting the animal studies, which usually involved abnormally high amounts of sodium (in some cases hundreds of times normal intake) or animals specially bred to react to salt, human research failed to firmly justify restricting sodium in the diets of healthy persons.
Persons with kidney failure figured prominently in many of these studies, and so the effect of dietary sodium on people with damaged “regulators” ended up being applied across the board to people without damaged regulators. (The evidence is not that strong for the folks with the damaged regulators — not everyone with hypertension is salt-sensitive.)
|Despite the new wave of critics on the salt-restriction bandwagon, there are signs consumers will not give up their favorite seasoning. |
The fact is, healthy kidneys will increase excretion of sodium and other electrolytes, while conserving others, if there is an increase in blood pressure. That’s what they’re supposed to do.
In fact, too little sodium can also wreak havoc on the body, negatively impacting hormone balance, insulin levels and nerve conduction.
When studies began to investigate the effects of dietary sodium on healthy individuals, the evidence failed to support the reduction of salt in the diet. The studies showing increases in blood pressure related to high salt intake did not show the effect to persist over time, and did not show the effect to be significant from a clinical standpoint.
In a response to the ballyhooed report by CSPI accusing salt of being a “forgotten killer,” Richard Hanneman, president of the Salt Institute (www.saltinstitute.org
), Alexandria, Va., called for a full-blown, comprehensive clinical trial. “(The) only evidence we have,” he writes, “is from observational studies. There are no clinical trials at all. And worldwide, there have been only a dozen observational studies reported. Eleven of the 12 show just the opposite of what [CSPI] is saying. None of these 11 studies shows improved rates of heart attacks or strokes on low-salt diets; three, in fact, show just the opposite – [patients on] low-salt diets have higher risks of heart attacks. Many of the other 11 studies are quite large studies and none of them could find a population benefit in reducing dietary sodium.”
Intersalt, an international study of electrolyte excretion and blood pressure, attempted to firmly establish, once and for all, a positive link between sodium intake and hypertension in large and concerted analysis of more than 10,000 men and women across 52 different clinical centers worldwide. When the results turned out to contradict the connection, all hell broke loose in the salt wars as scientists involved on both sides of the dispute culled and reanalyzed the data.