Salt & Human Health: Salt & Health Newsletter

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.

Posted by Mort Satin at 08:53 AM | Permalink

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 Shapiro, Boaz, Matas, Fux, and Shargorodsky 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.

Posted by Mort Satin at 04:06 PM | Permalink

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).

Posted by Mort Satin at 11:22 AM | Permalink