Before 1991, very little cholera was reported in Peru. Then, under unusual circumstances, it infected Peru's coastal waters and the fish which are so important to the local diet. The organism responsible for cholera, Vibrio cholerae occurs naturally in the plankton of fresh, brackish, and salt water, attached primarily to copepods in the zooplankton. The coastal waters were unusually warm and untreated sewage supported unusually large zooplankton blooms.
In order to quell the bad publicity regarding the quality of his country's coastal waters, then President Fujimori wished to demonstrate to his citizens that the press reports were exaggerated. He boldly posed for public television cameras eating some locally-prepared ceviche. Within 12 hours, he came down with cholera confirming that pathogens are a biological, rather than a political phenomenon. That cholera outbreak eventually killed 3,500 people.
Fortunately, doctors quickly turned to effective and inexpensive oral rehydration therapy with clean water and salt. If not, the death toll would have been much greater.
Cholera is characterized by prolonged episodes of diarrhea and it is critical to ensure that lost fluids and salts are fully replaced. Common table salt (sodium chloride) is the key electrolyte that has to be replenished along with water.
Now some officials worry that climate change could bring the scourge back to Peru and are making doubly certain to make the population aware of the need to keep themselves fully hydrated and electrolyte-balanced, proving once again that salt is an essential element of life and good health.
To give credit where it's due, Junk Food Science today touched another nerve on a topic seemingly far afield from concerns of the salt industry, but on closer examination, there are alarming parallels.
CBS Evening News reported the story yesterday that an idea generated by a handicapped 16-year old in a high school "There Ought to be a Law" writing contest has been introduced as a bill in the California state legislature. As JFS's Sandy Szwarc explains:
The bill will require all poor women receiving welfare benefits to be tested for narcotics. Those who test positive will be required to undergo treatment or lose their public assistance, including healthcare. The rationale behind the bill is to dispense state healthcare dollars prudently and to protect children from health problems due to women who do drugs while pregnant.
Her concern (and ours) is the "slippery slope" of the argument. In this case, I'd posit, very few would defend the behavior of narcotics use. Certainly every taxpayer also wants government health care costs curtailed. Where do you stop? Which unhealthy actions should be used to deny public welfare benefits (and what benefits? food stamps or Social Security, Medicare, etc.?). Smoking, for example. Should smokers be ineligible for taxpayer-subsidized Medicare hospitalization? What about binge drinkers? Over-eaters (or those not following the Dietary Guidelines)? For some, hard evidence might actually show the behavior caused a burden on taxpayer services, but it could extend to other non-data-driven, politically-correct behaviors such as buying foods not labeled "low salt" or sprinkling salt on your food in a restaurant (surely, we'll still be able to eat as we please at home!). Far fetched? I hope so; I fear not.
It was personally deeply disappointing to read the publication today by my respected, esteemed, even revered think tank, the American Enterprise Instittute (AEI) of a superficial review of the salt and health controversy. Research assistant Sara Wexler properly concluded that FDA regulation of salt was a blind alley, but, instead, she urged "low-sodium campaigners (to) focus their efforts on consumer demand."
This was "think tank lite" at its worst. Both the facts and the analysis were flawed. In fact, the entire article was written to address the wrong problem altogether. This is a worthy subject for a serious AEI analysis, but this wasn't a serious AEI analysis in the proud tradition dating back to Murray Weidenbaum and Chris DeMuth. A sad day.
Where to begin? Let's start with a few facts.
Wexler states the Salt Instittute (and Grocery Manufacturers Association) "have called for voluntary sodium reductions instead of federal regulation." I'll let GMA speak for themselves. The Salt Institute feels that patients should follow their doctors' advice on dietary sodium, but we strongly oppose a general recommendation for sodium reduction. Wexler continues, accurately, to report that the Salt Institute, GMA and the International Food Information Council have concluded that the medical evidence shows "the direct impact of sodium reductin on human health is still unclear." True. That's why we oppose it. Why would we think a "voluntary" program to undertake a major, unjustified health intervention would be appropriate? We don't.
Wexler conflates "blood pressure" and "health risks" regarding dietary sodium. Experts agree salt is related to blood pressure and, indeed, as reported, research at the University of Indiana shows that in a strong majority of people', their blood pressure is unchanged on a low-salt diet while a significant minority actually increase their blood pressure and more has the "desired" fall. But experts do NOT agree that evidence shows that reducing dietary salt actually improves health. In fact, most of the health outcomes studies find no benefit at all and several have found possible risks when people cut back salt. That said, Wexler correctly reports the Salt Institute's support for improving overall dietary quality to improve risks.
Wexler points out there is "confusion" on the issue, but she states that "(t)he biggest problem for industry groups seems to be the lack of adequate demonstrative studies." That's just wrong. First of all, the problem isn't an "industry" problem, it's a "health" problem. The prospect of imposing billions of dollars of additonal cost on American food consumers is not the issue here (though legitimate), the question is whether evidence shows that the proposed major re-engineering of the American food supply has any scientific justification and whether the intended benefit will be sacrificed to unintended consequences. The "confusion" isn't with the evidence. The confusion is caused by those who persist on ignoring the evidence of a lack of a health benefit and suggesting that the "industry" should fund the research to document the government's policy. As an aside, HHS has stonewalled release of key data at every step and fought an attempt by the Salt Institute and the US Chamber of Commerce to force transparency in the process.
Wexler implies FDA's regulation awaits a determination of "(w)hether or not sodium can be linked to high blood pressure." We certainly hope not. And all Americans should hope that FDA should not consider regulations in this area until it can show that 1) reducing salt will improve health and 2) regulating the amount of sodium in individual foods will reduce overall dietary sodium intakes sufficient to achieve a health benefit. Neither has been shown. That's why the US Preventive Services Task Force has concluded there is a lack of evidence for a general salt reduction recommendation.
Wexler seems to consider salt to be just another nutrient, like fat, carbs and sugars, ignoring the fact that it is an essential nutrient necessary for life. As such, the body has redundant systems to ensure an appetite for salt, as discussed as recently as this month's Experimental Physiology and discussed in our blog by both Mort and me . What this suggests is that "consumer demand" will never be the answer.
We won't get the right answer until we start asking the right question: Will a low-sodium diet improve health? We may need to go no further. HHS should fund the controlled trial of this question that will answer this serious question.
Wexler's once-over-lightly piece is fluff. We expected more from AEI.
Less than 20 percent of U.S. adults with high blood pressure eat foods that align with government guidelines for controlling hypertension, a recent study found .
This outcome is no great surprise. The American Heart Association (AHA), the American Medical Association (AMA) and the National Heart Lung and Blood Institute (NHLBI) have all deliberately mislead the public by spinning the results of the DASH-Sodium trial to indicate that most of the blood pressure benefits were the result of salt reduction. It is hard to say if this myth-information was the work of specific individuals within these organizations or the organizations themselves. What is critical, however, is that these organizations have not lived up to their responsibilities and barely promoted the importance of the DASH- or Mediterranean-type diet in reducing cardiovascular disease. Instead, they have adopted the magic-bullet, single nutrient approach and almost exclusively promoted salt reduction as the dietary approach to improve cardiovascular health. That is why so few U.S. adults now follow the DASH diet.
It is time that the credibility of these organizations comes under far greater public scrutiny. The recent disasters of hormone replacement therapy and the disasterous strategy to aggressively drive down blood sugar in diabetes patients are clear examples of our medical establishments doing harm with ill-considered policies and information.
The following graph encapsulates the results of the DASH-Sodium trial:
It is immediately apparent that moving from a regular U.S. diet (blue line) to a DASH-type diet (red line) has a far greater impact on blood pressure than lowering salt consumption. On the regular diet, dropping from the current level of sodium consumption to the recommended daily level of 2,300mg Sodium/day dropped the systolic pressure by an average of 2.1 mm Hg (mercury). However, changing from a regular U.S. diet to the DASH diet, without any changes to sodium consumption, reduced the systolic blood pressure by 5.9 mm Hg, almost three times the drop resulting from the sodium reduction! There is no equivalency here. The move to a DASH diet far exceeds the benefits of salt reduction - there is no comparison. This clearly explains why Mediterranean people enjoy an excellent cardiovascular status despite their high salt consumption, as mentioned in a previous article . With a DASH diet, the impact of sodium on the blood pressure of hypertensives is minimal (and is of no significance to normotensive people - the majority in the population). On top of that, the DASH- or Mediterranean-type diet has myriad other health benefits aside from reducing blood pressure.
Yet, the AHA, the AMA and NHLBI always spin the data to place the majority of the benefits on salt reduction first and then the DASH diet, almost as an afterthought. In lock step, the Center for Science in the Public Interest (CSPI) repeats this in much the same manner.
What a pity that people take their advice!
No wonder we see headlines like, "Not many follow anti-hypertension diet " or "Fewer hypertensives adhering to DASH diet " or "Most With High Blood Pressure Do Not Follow Recommended Diet ". AHA, the AMA and NHLBI must all share in this predictable consequence of myth-direction.
NY Times op ed contributor Gary Taubes weighed in on the recent Vytorin flap , registering insights with equal applicability to the ongoing salt controversy. Said Taubes of lessons to be learned from the cholesterol trial:
(The authors') interpretation is based on a longstanding conceptual error embedded in the very language we use to discuss heart disease. It confuses the cholesterol carried in the bloodstream with the particles, known as lipoproteins, that shuttle that cholesterol around. There is little doubt that certain of these lipoproteins pose dangers, but whether cholesterol itself is a critical factor is a question that the Vytorin trial has most definitely raised. It's a question that needs to be acknowledged and addressed if we're going to make any more headway in preventing heart disease. ...
The truth is, we've always had reason to question the idea that cholesterol is an agent of disease. Indeed, what the Framingham researchers meant in 1977 when they described LDL cholesterol as a "marginal risk factor" is that a large proportion of people who suffer heart attacks have relatively low LDL cholesterol.
So how did we come to believe strongly that LDL cholesterol is so bad for us? It was partly due to the observation that eating saturated fat raises LDL cholesterol, and we've assumed that saturated fat is bad for us. This logic is circular, though: saturated fat is bad because it raises LDL cholesterol, and LDL cholesterol is bad because it is the thing that saturated fat raises. In clinical trials, researchers have been unable to generate compelling evidence that saturated fat in the diet causes heart disease. ...
One obvious way to test the LDL cholesterol hypothesis is to find therapies that lower it by different means and see if they, too, prevent heart attacks. This is essentially what the Vytorin trial did and why its results argue against the hypothesis. ...
Because medical authorities have always approached the cholesterol hypothesis as a public health issue, rather than as a scientific one, we're repeatedly reminded that it shouldn't be questioned. Heart attacks kill hundreds of thousands of Americans every year, statin therapy can save lives, and skepticism might be perceived as a reason to delay action. So let's just trust our assumptions, get people to change their diets and put high-risk people on statins and other cholesterol-lowering drugs.
Science, however, suggests a different approach: test the hypothesis rigorously and see if it survives. If the evidence continues to challenge the role of cholesterol, then rethink it, without preconceptions, and consider what these other pathways in cardiovascular disease are implying about cause and prevention. A different hypothesis may turn out to fit the facts better, and one day help prevent considerably more deaths.
To reiterate the lesson: rather than accept that high blood pressure is a problem that demands such urgent action that we sacrifice the discipline of conducting a health outcomes trial of the intervention, we should, as Taubes argues, "the hypothesis rigorously and see if it survives." If the evidence continues to challenge the role of (salt), then rethink it, without preconceptions, and consider what these other pathways in cardiovascular disease are implying about cause and prevention. A different hypothesis may turn out to fit the facts better, and one day help prevent considerably more deaths." Good plan.
Health outcomes matter. We were reminded yet again this week that entirely-plausible, widely-accepted, even vociferously-advocated interventions still need to be supported by rigorous scientific data. Headlines in the Washington Post screamed: "Deaths Halt Part of Diabetes Study. Scientists Fear Heart Attacks, Strokes Were Tied to Treatment. "
The headlines were similar to those when the feds halted part of the ALLHAT trial of anti-hypertension drugs because, while lowering blood pressure, they weren't reducing heart attacks or strokes. The headlines mirrored those when the government embarrased itself advocating Hormone Replacement Therapy (HRT) for post-menopausal women only to find it was killing them. After all, scientists had offered untested assurances that the interventions "can't hurt anyone."
Soon, the same headlines may be written to apply to advice to lower dietary salt.
Public health leaders are so anxious to overcome serious and perplexing health problems that they lose their discipline. They set aside standards of evidence-based medicine that demand scientific support before approving an intervention. Everyone wants heroes. Certainly the researchers want success. So do the intervention sponsors, whether a pharmaceutical company or an activist lobby group like, in this case, the American Diabetes Association. So do the media; overcoming a dread health threat is important news. All of us, frankly, want these interventions to work. But we cannot ignore the discipline of the scientific process in our enthusiasm and zeal. And we need to temper our noisy presumptions, the arrogance that we know all the answers and now have only to force implementation of strategies never fully tested, with a profound humility. Pride goeth before the fall.
So this week's news was that adverse findings "stunned and disappointed experts." Rob Stein reported in the Post story:
Aggressively driving blood sugar levels as close to normal as possible in high-risk diabetes patients appears to increase the risk of dying from a heart attack or stroke ...
The findings are the second major blow to widespread assumptions about how to protect against heart disease -- the nation's leading killer. Another recent major study found that driving blood cholesterol levels as low as possible did not necessarily slow the progression of heart disease.
Many earlier studies had shown that tightly controlling blood sugar significantly reduced the risk of many complications. The new study -- known as the Action to Control Cardiovascular Risk in Diabetes, or Accord, trial -- was designed to convincingly test whether various aggressive treatment strategies reduced the risk of heart disease -- the main cause of death among diabetics.
The study involves 10,251 patients ages 40 to 82 at 77 sites in the United States and Canada at high risk for heart disease for any reason, such as high blood pressure, high cholesterol or obesity. About half were placed on a regimen combining diet and exercise with commonly used drugs designed to lower their blood sugar levels to those of the average person with diabetes, while the other half were put on a more intensive regimen designed to drive levels closer to those of someone without diabetes. The patients were further divided into those who also received blood-pressure-lowering medication or drugs to improve their cholesterol levels.
Over about four years, about half of the patients getting intensive treatment achieved blood sugar levels close to normal, and about half the patients in the standard treatment group achieved levels close to the average diabetic.
But a special 10 member panel that was monitoring the study alerted the organizers that 257 patients r eceiving intensive treatment had died, compared with 203 receiving standard treatment, a difference of 54 deaths -- or 3 per 1,000 participants per year, officials said. About half the excess deaths were from heart disease.
Stein interviewed Cleveland Clinic cardiologist Steven Nissen, who seemed chastened, admitting: "This suggests that there are things drugs do that we don't understand."
The potential for unanticipated (and adverse) consequences is why we give lip service to supporting evidence-based medicine. Then along comes a plausible answer to an important problem and we must show discpline and humility to say: sounds great, let's find some money and test it out to see if it's true.
In August 2006, international experts joined the Salt Institute in urging the U.S. Department of Health and Human Services to find funding for a controlled trial of the question: will lowering dietary sodium improve health, specifically cardiovascular risk and mortality? We were told, in effect, that this was our problem and we should fund the study despite the fact that HHS's own U.S. Preventive Services Task Force has determined there is no evidence supporting population advice to reduce dietary salt.
It's time for some discipline and humility, HHS. And some funding.
Medical experts dispute the importance of curtailing dietary salt. Experts focused on blood pressure favor cutting salt. Experts focused on reducing heart attacks and protecting cardiovascular health disagree and favor an approach of improving overall dietary quality. A new study suggests the 30-year debate may have been irrelevant; human physiology has multiple systems that ensure proper intakes of salt and water to protect health. As Mort summarized recently on SaltSensibility , the body has redundant systems and is self-regulating. No matter what the experts may advise, our unique consumption level for salt is "hard-wired" into our systems to protect our health against do-gooder meddling:
This latest publication shows that this multi-factorial system is so robust and includes so many failsafe mechanisms that it continues to fully function even after large sections of its system are shut down. Employing a complex cascade of physiological functions from powerful hormones, such as aldosterone, to pressure sensitive receptors in the brain, this water thirst and salt appetite mechanism moderates our behavior so that we are driven to quickly replenish the volume and ionic balance of our blood, so that it is pressurized sufficiently for our heart to circulate it through our bodies. When fluids and electrolytes are lost, such as with sweating, physical exertion, diarrhea or other circumstances, we immediately get a water thirst signal. So we drink water to make up the loss. After a delay, our salt appetite kicks in to ensure that the ion levels are replaced. If we don't respond on time to the salt appetite, we die.
The article, "Central regulation of sodium appetite " appears in the February issue of Experimental Physiology.
In a strikingly clear and comprehensive manner, the paper entitled "Central regulation of sodium appetite ," by Joel Geerling and Arthur Loewy of the Department of Anatomy and Neurobiology, Washington University School of Medicine in St Louis, MO, elaborates the mechanisms responsible for our appetite for salt. The physiological apparatus we have evolved over the eons to maintain a fully operational cardiovascular system is largely dependant upon maintaining both a balance and sufficient quantities of the two nutrients most essential to life, water and salt. This fundamental system is can be found in fish, reptiles and all mammals. Life depend on it.
In order for us to survive, our circulatory system must have an adequate volume of blood that is under sufficient pressure to supply all our tissues with the nutrients they need and to remove all the toxic byproducts of metabolism. It is a finely tuned balance of water and salt that allows this to happen. Any amount of water or salt that is consumed in excess of our needs is quickly eliminated through our kidneys. However, an equally important issue is ensuring that we have ingested enough water and salt to make up for any losses we experience. This is where the incredible mechanism controlling the thirst for water and the appetite for salt comes in.
This latest publication shows that this multi-factorial system is so robust and includes so many failsafe mechanisms that it continues to fully function even after large sections of its system are shut down. Employing a complex cascade of physiological functions from powerful hormones, such as aldosterone, to pressure sensitive receptors in the brain, this water thirst and salt appetite mechanism moderates our behavior so that we are driven to quickly replenish the volume and ionic balance of our blood, so that it is pressurized sufficiently for our heart to circulate it through our bodies. When fluids and electrolytes are lost, such as with sweating, physical exertion, diarrhea or other circumstances, we immediately get a water thirst signal. So we drink water to make up the loss. After a delay, our salt appetite kicks in to ensure that the ion levels are replaced. If we don't respond on time to the salt appetite, we die - a situation which was described in an earlier article where a young woman died in a water-holding contest.
It has been repeatedly suggested that policies must be developed to reduce the amount of salt in processed foods. In fact, some countries already have or are in the process of considering policies to effect this. Will these policies be effective? What indication is there that people who are provided with a lower-salt food supply will actually reduce their intake of salt? Based upon this latest publication on salt appetite, individuals faced with foods that are mandated to be low in salt may make up for this in other ways. They may eat considerably more food in order to get more salt or they may simply pick up the salt shaker and add more voluntarily.
The recent publication by as described in a recent article legitimately brings up the question of minimum levels of salt intake. Based upon their data, we can justifiably ask whether the current recommended daily values are prudent. Should the 2,300mg daily upper limit for sodium be reconsidered? Should the Institute of Medicine recommended daily adequate intake of 1,500mg sodium be reconsidered?
Our thirst for water is a basic mechanism we have evolved in our fight for survival. So is our appetite for salt. It is time we realize that the two mechanisms are interdependent and basic to our survival. Any policies promulgated to regulate our consumption of salt must bear this in mind and be based on the most rigorous science. If not, harm will be done.
The long-standing debate on the impact of salt on health has been characterized by claims that salt reduction would improve cardiovascular health. In contrast, there is a considerable body of documented knowledge that asserts this claim as being without scientific merit. Despite this, the FDA has been asked to revise the regulatory status of salt and establish restrictive food labeling regarding salt. The outcome of restrictive sodium labeling may induce the food industry and consumers to significantly cut back on salt consumption. The reverse side of this issue, that is, the negative health impacts of a population-wide reduction in sodium intake is a subject of great significance and one that is seldom discussed.
In an analysis of 219 patients with essential hypertension in the early 1970s, heart attacks and strokes were observed when plasma rennin was elevated. It was concluded that renin may be a risk factor for heart attacks (1). In 1991, Alderman et al reported on the relationship of reduced-salt related high rennin levels with increased myocardial infarction rates (2). This relationship was again confirmed in 1997 (3).
In 58 trials of hypertensive persons, reducing sodium intake to 118 mmol/24 h (urinary sodium excretion) lowered systolic blood pressure (SBP) by 3.9 mm Hg and diastolic blood pressure (DBP) by 1.9 mm Hg. In 56 trials of normotensive persons, reducing sodium intake to 160 mmol/24 h resulted in a reduction of 1.2 mm Hg on SBP and 0.26 mm Hg on DBP. However, another consequence of this drop in sodium consumption was a significant 3.6-fold increase in the levels of plasma renin and a 3.2-fold increase in the level of aldosterone. These increases were proportional to the degree of sodium reduction and were accompanied by a significant decrease in body weight, and an increase in noradrenaline, cholesterol, and low-density lipoprotein cholesterol levels (4).
In his introduction of Dr. Michael H. Alderman as Editor-in-Chief of the American Journal of Hypertension, renowned hypertension researcher, Dr. John Laragh stated that Dr Alderman rightly "questioned the popular wisdom of unselectively advising salt avoidance for all hypertensives, and for all normotensive people, - a popular public health strategy which will surely chronically raise all of their plasma renin values and may have other unintended adverse consequences. (5)"
The primitive Yanomamo Indians of Brazil do not use added salt in their diet. As a consequence, this group provides an opportunity to study the hormonal regulation of sodium metabolism in a culture with a life-long restriction of dietary sodium. Results indicate that urinary excretion of sodium is very low, however, plasma renin activities were elevated when compared to other societies. The findings suggest that the hormonal adjustments to life-long low sodium intakes are similar to those achieved in acute sodium restriction of civilized man. In other words, there is a constant struggle to retain salt through the employment of the renin-angiotensin-aldosterone system, together with all its other consequences. Yanomamo Indians have a life expectancy of 48.5 years.
While there is little doubt that increased plasma rennin and aldosterone have a potential to result in increased myocardial infarction, a recent publication may reveal the mechanism of this action.
Aldosterone might affect arterial stiffening, in both the short and long term. Shapiro, Boaz, Matas, Fux, and Shargorodsky investigated the association between excess aldosterone, reflected by an increased aldosterone-renin ratio (ARR) and pulse wave velocity (PWV) in young healthy adults. In a single-center study, 60 subjects were evaluated for lipid profile, glucose, hs-CRP, renin and aldosterone (6). PWV was performed as a simple noninvasive recording and computer analysis of the two artery sites pressure waveform . The ARR was significantly and positively associated with PWV and had the potential to exhibit the direct effects of aldosterone on the vascular wall. Most significantly, the participants received instructions to consume intermediate levels of sodium proportional to energy intake, corresponding to 2,300 mg/day sodium per 2,100 kcal and to avoid foods notably high in sodium due to processing or foods with salt topically added - in other word to comply with the upper limit DV recommendations of the Institute of Medicine (7). This level of intake resulted in increased aldosterone and increased arterial stiffness.
There are a number of reasonable conclusions that can be derived from the above data. In the first instance, there is a strong possibility that a reduction in salt intake will elicit increased plasma aldosterone-renin output, thereby placing normotensive people at a greater risk for myocardial infarction. It appears likely that the arbitrarily derived IOM upper limit of sodium may not be sufficient to protect the majority of the population from arterial stiffening.
Finally, we must tread very carefully during any consideration of a change in the regulatory status of salt to ensure that we do not do the population more harm than good.
At this point in time, there is no justification to change the GRAS status of salt and there is sufficient information to reconsider increasing the IOM's DV of salt.
(1) Brunner, H. R., Laragh, J.H., Baer, L., et al, "Essential hypertension: renin and aldosterone, heart attack and stroke," N Engl J Med, 286, 441-449, (1972). (2) Alderman, M. H., Madhavan, S., Ooi, W. L., et al, "Association of the renin-sodium profile with the risk of myocardial infarction in patients with hypertension," N Engl J Med, 324, 1098-1104, (1991). (3) Alderman, M. H., Ooi, W. L., Cohen, H., et al, "Plasma renin activity: a risk factor for myocardial infarction in hypertensive patients," Am J Hypertens, 10, 1-8, (1997). (4) Graudal, N. A.., Galløe, A. M., abd P. Garred, "Effects of Sodium Restriction on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterols, and Triglyceride - A Meta-analysis," JAMA, 279,1383-1391, (1998). (5) Laragh,J. H., "Dr. Michael H. Alderman Takes the Helm as Editor-in-Chief of the American Journal of Hypertension, Am J Hypertens 19, 1197-1198, (2006). (6) Shapiro, Y., Boaz, M., Matas, Z., Fux, A., & M. Shargorodsky, "The association between the renin-angiotensin-aldosterone system and arterial stiffness in young healthy subjects," Clinical Endocrinology (OnlineAccepted Articles). doi:10.1111/j.1365-2265.2008.03176.x. (7) Dietary Reference Intakes For Water, Potassium, Sodium, Chloride, and Sulfate, Institute of Medicine of The National Academies, The National Academies Press, Washington, D.C. (2005).
In a story Saturday on "Heart Choices ," the Washington Post discusses the recent ENHANCE study showing, as they put it, the newer, more expensive anti-cholesterol drug Vytorin "is not known to be dangerous; it's just no better than the cheaper alternative." But the story goes on to draw a broader -- and much more important -- lesson:
lower LDL cholesterol itself is not the final goal; the goal is to lower the risk of heart disease and stroke. Only with the new study has it become known that Vytorin and Zetia are probably not superior to statins in improving health. Although another study looking directly as their effects on heart disease and stroke is underway, it looks as if consumers may hav been throwing away their money.
This distinction between "risk factors" such as LDL cholesterol and "risk" of heart attack and strokes (not an extrapolation from the risk factor findings, but an examination of the actual health outcomes), is one too often ignored and central to understanding the current controversy over whether or not to encourage general reduction of dietary salt. Salt reduction may affect the "risk factor" of blood pressure in many individuals; it also affects other disease "risk factors" such as insulin resistance, plasma renin activity and sympathetic nervous system activity. What it seems NOT to affect is the "risk" or rate of cardiovascular disease, CV events like heart attacks and strokes or, ultimately, mortality.
The Post says "FDA could take some steps to prevent similar waste." We agree. Stop advocating salt reduction in the absence of any evidence that it reduces heart attacks or strokes.
This week's New Scientist features an excellent article by renowned science writer, Gary Taubes entitled, "The great diet delusion ." In it, he urges nutrition researchers and health authorities to wake up to the fact that people do not get fat simply because they overeat. For more than a century, medical dogma has stated that the only way to lose weight was to expend more energy than is consumed. While that may work in some cases, he goes beyond that into the physiological mechanisms of fat deposition and over-consumption. Citing examples from adolescent growth spurts, Taubes credibly describes the impact of hormones on growth and fat deposition. Carbohydrates, such as starches and sugars, stimulate the secretion of the hormone insulin which, in turn, accelerates deposition of fat.
Taubes, describes the conventional medical practitioners as being in denial of this phenomenon because acceptance of it would imply that Robert Atkins was correct in his diet recommendations all along. So they largely ignore it while witnessing the greatest epidemic of obesity and type II diabetes in history.
The Taubes article fits closely with the recent article entitled, "A Call for Higher Standards of Evidence for Dietary Guidelines," in the American Journal of Preventative Medicine by Marantz, Bird and Alderman and recently reviewed in SaltSensibility .
A study just published by the Journal of Agriculture and Food Chemistry reports on the role of broccoli as a cardioprotector. Broccoli contains high concentrations of selenium and glucosinolates, especially isothicyanate sulforaphane. Both selenium and sulforaphane are shown to protect the heart and the cardiovascular system. Sulforaphane induces the redox regulator protein, thioredoxin, which has a cardioprotective role by reducing oxidative stress.
A clinical study reported that eating fresh broccoli sprouts for a week lowered serum low density lipoprotein levels and a prospective study in Iowa showed a strong association between broccoli consumption and a lowering of the risk of coronary heart disease.
As reported earlier Ohio State University has recently completed organoleptic research indicating that the majority of individuals in three age groups (children, teens and adults) are most likely to eat broccoli when allowed to add sufficient salt to overcome broccoli's natural bitterness.
Here is a clear case of salt indirectly contributing to better heart health.
It is with some dismay that we saw the headline on the UK Food and Drink Federation website, "Salt: Brits Bought 2,000 Tonnes Less in the Past Year ." The article was timed to coincide with "Salt Awareness Week " sponsored by CASH (Consensus Action on Salt and Health) and described the "staggering reduction" in salt consumption which they attributed to the food industry's ongoing efforts to reformulate products to lower salt levels. The staggering reduction amounted to 0.3% which brought forth criticism from CASH chairman, Graham MacGregor, who said
- a fitting rebuttal to an industry that buckled under instead of insisting on food and nutrition policies based on science rather than politics.
It is interesting to note that neither CASH, the UK Food and Drink Federation nor the Food Standards Agency have ever asked that a legitimate health outcomes metric be put in place to show the health benefits to consumers of reducing salt consumption. Are they even interested in measuring the health benefits? Or will they simply follow the example of Finland and reduce salt consumption, then wait a decade or two to find out that their health benefits were reduced? Finland waged a 30-year battle to reduce salt consumption only to discover that there was no health benefit associated with it - on the contrary, their health outcomes performance was not even on a par with their neighbors that did not reduce salt.
The theme of CASH's National Salt Awareness Week , 2008 is Salt and Children. Despite the fact that the most recent National Academy of Sciences Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate (2004) stated:
CASH insists on making reduction recommendations for children. This sort of myth-information based upon statistical manipulation has been commented on earlier.
As was highlighted in a previous article , it is hoped that one day this seemingly inexorable march to misguided policies will halt, so that this issue may be managed by rational thinking and scientific evidence.
I recall an old colleague of mine in the United Nations who kept a sign on the wall behind his desk,
"Don't Just Do Something, Stand There!"
It was his way of trying to get people to think things through thoroughly, before rushing headlong into an intervention.
Legislation on food labeling , recommendations on Daily Values and the Dietary Guidelines are all examples of interventions that would have benefitted from my friend's advice. About the only thing that everyone can agree upon is that they are all largely ineffective and hold scant benefit for the consumer.
In a recent article entitled, "A Call for Higher Standards of Evidence for Dietary Guidelines," Am J Prev Med 2008: DOI: 1016/j.amepre.2007.11.017., authors Marantz, Bird and Alderman make the case that with their weak standards of evidence and tendency to focus on individual nutrients, the national dietary guidelines might actually do consumers a lot more harm than good.
As an example, they used the guidelines developed against the consumption of dietary fat, promulgated in the late 1970s. The authors noted that people were inadvertently led into believing that if they limited their fat intake, they could then go ahead and pig out on carbs - a phenomenon which may have contributed to the current epidemic of obesity and overweight in the U.S.
The flaw in reasoning was that no one believed that the guidelines could cause any harm, therefore only the weakest evidentiary support was needed to promulgate them. Indirect evidence, expert opinions and scientific "reasoning" were the main drivers of the guidelines. After all, they were only guidelines - what could be so bad?
In fact, once published, they took on an aura of credibility that far exceeded any scientific justification. Once promulgated and given the blessing of the medical establishment and the government, they were looked upon by the public, by the media and by teachers no differently than if they had been irrefutably proven by the most rigorous scientific experimentation. And government guidelines don't simply affect one or two of us - we are all influenced by government guidelines.
The authors write that in 2000, the Dietary Guideline Advisory Committee reversed an earlier 1995 recommendation to lower fat intake, indicating that it may have been premature and ill-advised. The Committee stated that "an increasing prevalence of obesity in the United States has corresponded roughly with an absolute increase in carbohydrate consumption."
Marantz et al also point to the advice given on salt intake as another example of the unintended consequences of a seemingly innocuous recommendation, noting that any blood pressure benefits may be trumped by the stream of harmful effects on plasma renin, insulin resistance, sympathetic nerve activity, and aldosterone levels. They further point to a recent finding of no difference in total mortality between randomized sodium-intake groups.
The authors final conclusion for a dietary guideline recommendation reminded me of my dear old friend;
"When adequate evidence is not available, the best option may be to issue no guideline."
Is desire clouding our objectivity or is there an emerging recognition that politically-correct medical science is imposing huge costs on our healthcare system? Junkfood Science led off this week with further coverage of the ethically-compromised ENHANCE trial, asking: "How much more are we spending for medications due to excessive mark-ups, but also for medications that may not provide the clinical benefits they purport?"
Blogger Sandy Szwarc revisits earlier posts (covered by our blog ), pointing out that reliance on a flawed process. We agree. Ignoring evidence-based results as has the U.S. Dietary Guidelines, produces scientifically-flawed recommendations. Just a glimpse of her perspective (which we heartily share):
Amidst all of the congressional hearings and media notice, and amidst the recent infestation of shark lawyers filing class-action lawsuits across the country over alleged cover-ups of the ENHANCE trial results, we mustn't lose sight of the far greater issue in all of this:
"The integrity of the scientific process ... in how drugs are researched and approved, and clinical guidelines are developed." JFS began covering the ENHANCE clinical trial issue last November . This trial provided an opportunity to examine the importance of randomized controlled clinical trials, the gold standards of evidence-based medicine. Sound trial designs that are fair tests include randomization; double-blinding; a placebo control group; control of study data and analysis of study data by bodies independent from drug company sponsors; and primary endpoints that are actual clinical outcomes, such as reduced premature deaths, versus false surrogate endpoints.
On January 17th, "How'd we get here ?" described the foundations of clinical trial evidence for drugs approved by the FDA that have been abandoned, and called into question the use of surrogate measures, like cholesterol, as proxies for actual clinical benefits to lives. When surrogate endpoints are used in order to expedite R & D for new drugs, post-market clinical trials are supposed to follow to provide the FDA evidence that these markers are valid and that the drugs actually save lives. But those studies never seem to come.
… Perhaps this hubbub will lead everyone to question their own assumptions and fears about health risk factors and to look closely at the evidence on cholesterol lowering for prevention of heart disease and whether it extends lives. Perhaps this hubbub will lead everyone to question their own assumptions and fears about health risk factors and to look closely at the evidence on cholesterol lowering for prevention of heart disease and whether it extends lives.
Our issue, of course, isn't cholesterol, but the same dynamic is playing out in the great salt debate. Let's keep the focus on the real issue: will reducing dietary salt improve health? Perhaps we can then realize the health improvements we deserve for the enormous investment society makes in our healthcare system.
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