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Salt, hypertension, pride and careers
What is the factual basis, and the sequence of events, that made the view that dietary salt intake raises blood pressure, and so the risk of hypertension and cardiovascular disease - so called salt hypothesis - become so deeply rooted in the field of academic medicine that it became the determinant of governmental health policies?
In order to understand what is really happening, we need to throw some light at the scene, and see the actors. At this point in time, we have two big stars there, apparently talking past each other.
One is the National Heart, Lung and Blood Institute (NHLBI, a division of the U.S. National Institutes of Health, or NIH, a major governmental health organization), and National High Blood Pressure Education Program (NHBPEP), as well as a number of associated healh organizations, like CDC (Centers for Disease Control) and IOM (Institute of Medicine). These form the backbone of support for salt hypothesis. And, it is NLHBI that pretty much decide about the official view on the salt health policy, as well as about funding research related to it.
Among the most prominent contemporary researchers supporting salt hypothesis are Drs. Stamler, Cutler, MacGregor, He, Strazzullo, Cappuccio, Elliot and Law (Europe and U.S.).
The other is the Salt Institute, organization founded by salt producers and much of processed food industry. In general, they are opposing the notion that the average U.S. salt consumption poses health threat at the level of population.
Among the researchers who do not find that salt hypothesis is supported by the facts, are Drs. Alderman, Cohen, Swales, McCarron, Hooper, Bartlett, Freedman and Pettiti.
Shouldn't these two sides work together and find a compromise, instead of acting as irreconcilable enemies? Perhaps, in a perfect world but, as devil would have it, they were led to follow different, opposing paths.
The history tells us that the ongoing confrontation between governmental health policy and Salt Institute vs. salt intake and health is merely a continuation of the century-long battle between two opposing views:
!!! one that considers current salt intake levels generally unhealthy with respect to blood pressure, originating in some observations from clinical practice, as well as the fact that it is roughly 2-3 times higher than estimated salt consumption of our primitive predecessors, and
?? one not seeing such conclusion being adequately supported by the facts, which was initially mainly food industry response, and these days includes growing portion of scientific community not associated with food industry.
At this point in time, NIH has decades long history of promoting the danger of present salt intake levels in the U.S., which they consider excessive. Many careers, reputations and feel-good's depend on preserving this view. How this governmental stance came about? Here's the story.
Salt hypothesis story
First clinical observation of the association between salt intake and blood pressure was published in 1904 by Ambard and Brochard, who noticed that the reduction in intake of salt and salty foods often relieves symptoms in six hypertensive patients. Subsequently, the hypothesis of salt promoting hypertension was either supported or challenged by other investigators, with the supporters gradually taking the upper hand.
Low-salt diets were used as a treatment for hypertension as early as 1920s (Allen) and 1940s (Kempner). Their successes were entirely credited to the reduction in salt intake, neglecting that other factors, like reduced caloric intake and higher intake of vegetables (and with it, nutrients like magnesium and potassium), could have as much, or more of an impact.
By the late 1940s, the overwhelming opinion was that salt intake does significantly influence blood pressure. Research data on which this opinion was based generally lacked reliability (Chapmann and Gibbons, 1949), but that, mostly due to low research methodology standards, for the most part remained unrecognized.
Interestingly, the effect of salt on blood pressure was at first attributed to the major component of salt, chloride; it took decades to the scientific community to positively identify the "culprit" as sodium. Recent research, however, indicates that the effect of sodium nearly vanishes in the absence of chloride.
In the late 1940s and early 1950s, it was observed in some studies involving patients with significantly impaired renal function that salt causes predictable rise in blood pressure (Grollman, Kempner), indicating possible physiological origin of the effect. In a series of subsequent trials - mainly rodent experiments - predictable rise in blood pressure could be reproduced
only under extreme conditions.
These were typically including combinations of significant reduction of renal mass, fluid intake restricted to hypertonic saline solution, administration of pharmacological doses of mineralocorticoid hormones, genetic manipulation and/or salt "feeding" comparable to daily human intake of up to a pound of salt, or even more.
The results obtained under these conditions were not relevant to the human salt consumption. Nevertheless, they were generally accepted as a support to the salt hypothesis. The underlying rationale was that current salt consumption is, up to several times higher than that of our primitive predecessors, as well as than salt intake of most remaining indigenous tribes, results in increased fluid retention which, through speculative but unproven mechanisms, increases blood pressure.
The "official" medical opinion on the subject of salt intake and hypertension seemed to be sealed in favor of salt hypothesis after the publication of a study showing linear positive relationship between salt intake and rates of hypertension in a small group of selected populations (1960 paper by Dahl).
Dahl's use of statistical association between salt intake and hypertension rates is hauntingly similar to Dr. Ansel Keys graphic presentation of such association between fat intake and cardiovascular disease death rates. Both concepts lacked relevant, material evidence from the very beginning - with Keys apparently tailoring the data to his purpose - yet spurred decades-long anti-salt and anti-(saturated)fat, anti-cholesterol sentiments, that became firmly imbedded in the national health policies.
Looking at these two plots, we are looking at two deliberate deceptions: in "proving" his hypothesis, Keys leaves out data clearly implying non-linear relationship and the existence of major confounding factors, while Dahl wouldn't even mention well known to him fact that Japanese, despite their higher average salt intake, had (and still have) the lowest CHD mortality rates, and highest life expectancy.
While it is certain that the success of Keys' evil-(saturated)fat-cholesterol concept was helped by the interest of pharmaceutical industry, which didn't miss the opportunity to open this huge market (first approved cholesterol-lowering drug, Atromid-S, was released in 1967), Dahl's evil-salt concept seem to be owing its progress mainly to the power of personal opinion, which led to the formation of an influential, belligerent advocating force in the medical circles, particularly within the segment in charge of the official health policy.
The fact that pharmaceutical industry generally sides with the supporters of this concept as well may have simply be doing what is best for the business. It is fairly certain that the industry knew that the concept lacks material evidence, thus backing it wouldn't hurt the business (as some other alternatives to addressing the hypertension problem could).
Along these lines, during the two decades following Dahl's 1960 paper, his opinion worked its way up to become the determinant of the official U.S. health policy on dietary salt intake. From the early 1970s,
current salt intake was de facto officially proclaimed public enemy.
The extent of governmental involvement is reflected in the 1977 publication by the U.S. Senate (Dietary Goals for the United States) and 1979 Surgeon Generals report, both promoting low-sodium diet.
At that point, the only piece of evidence relating to the actual human experience was that severe reduction in sodium intake was usually followed with decreased blood pressure in hypertensive patients with renal disease. Yet, the official policy proclaimed that any daily salt intake above 6g - a figure based on the estimates of salt intake of our primitive predecessors - is danger to health, significantly raising the risk of heart disease and stroke.
It hasn't changed since.
As this brief overview of the salt hypothesis' evolution indicates, the root of the problem is that it became predominant medical and policy doctrine
before it was sufficiently backed by reliable scientific data.
At the time it was first questioned by new research during the 1980s, it already had formidable support in the medical and governmental circles, with the mountain of pride, influence and career interest at stake.
On the other side, processed food industry is well aware how important is this taste-enhancing nutrient for their sales. They don't want to jeopardize that by reducing salt content of their products to the extent of making them unpalatable. And they have pretty valid counter-arguments as to
why substantial reduction in salt intake is unnecessary,
and could be be even dangerous.
Both sides are very influential, and that unavoidably shapes up the research, and its presentation. In addition to the complexity of human metabolism, this is why after decades of investigating the salt-hypertension link, there is no consensus on its effect on health in sight. This also means that many studies on this subject not only have objective limitations, but as well a
certain degree of bias in their design and interpretation.
In other words, they should be taken with - what else? - a grain of salt...
The power of personal belief was often evident as a major factor, particularly on the academic/governmental side, which did postulate the concept of salt toxicity at the present level of consumption and needed to come up with an actual, definite proof. Overriding scientific spirit, this made it look for the "right" evidence, "right" data interpretation, or "help it" come about, since the actual research data coming in was
overwhelmingly unsupportive of the concept.
With that in mind, let's take a look at two specific studies, both claimed by the salt hypothesis camp to be backing their cause. Although only snapshots in the continuum of the debate, these two studies can be seen as pivotal points connecting two different eras of research. As such, these two studies are illustrative of their differences and similarities.
One of the two is Dahl's 1960 paper, and the other is the largest yet observational study on the subject of salt and hypertension, Intersalt, published in 1988.