Credible and Incredible Salt Research
Credible and Incredible Salt Research
Most people in the USA consume far more salt than the preponderance of credible scientific research indicates is healthy. Unfortunately, despite the fact that the best quality research has consistently shown that excessive salt intake is a major cause of hypertension (HTN), CVD, and numerous other ills, there continues to be numerous studies with poor quality data being published and making headlines. Those headlines and articles are often filled with quotes from these poor quality studies that question the efficacy of reducing salt are premature and may even be harmful. These studies are often funded by the Salt Institute and the commercial food industry who profits from the addition of unsafe amounts of salt to most convenience foods and restaurant meals. These same commercial interests use these poor quality studies to undermine public health efforts to reduce excessive salt intake. Let's take a closer look at two recent publications on the health effects of dietary salt. One study represents cutting edge research that adds yet more credible evidence to our knowledge about how current salt intakes harm the body. The second study, while widely touted in the media as yet another study that seriously questions public health efforts to reduce salt intake adds nothing new to our understanding about the pathological effects of excessive salt consumption.
Dr. Moore's Study Is More of the Same
The first new study followed more than 2,600 men and women for 16 years and reported that consuming less sodium is not really associated with lower blood pressure. Media reports largely proclaimed these new findings as call into question the limits on sodium intake recommended by the 2015 US Dietary Guidelines for Americans (less than 2300mg) and since 2011 by the American Heart Association (no more than 1500mg). The author of this study was Lynn L. Moore, DSc, Associate Professor of Medicine at Boston University School of Medicine. She presented her findings at the American Society for Nutrition Scientific Sessions and annual meeting during the Experimental Biology 2017 meeting held in Chicago in April 2017. “We saw no evidence that a diet lower in sodium had any long-term beneficial effects on blood pressure,” said Moore. “Our findings add to growing evidence that current recommendations for sodium intake may be misguided.” For the study, the Dr. Moore and colleagues followed 2,632 men and women ages 30 to 64 years old who were part of the Framingham Offspring Study. Sodium intake was based on data from several days of food diaries. The participants all had normal blood pressure at the study’s start but over the next 16 years, the study participants who food diaries indicated they consumed less than 2500mg of sodium daily had higher blood pressure than the participants who consuming more than 2500mg of sodium. The results of Dr. Moore's study were consistent with earlier and even larger observational studies. For example, the data from the PURE study, which was published a few years ago came to the same dubious conclusions. Like Dr. Moore's study, Dr. O'Donnell et. al. analysis of the PURE data also reported a J-shaped relationship between sodium intake and CVD risk.[1] (also see my article in the October 2014 CFFH newsletter titled "Do New Studies Refute Benefits of Reducing Salt?"). Both Dr. O'Donnell's and Dr. Moore's studies reported a higher risks of CVD was seen in those consuming the lowest levels of salt/sodium. They noted the correlation between apparently "dangerously low" levels of sodium intake at levels consistent with the new US Dietary Guidelines (<2300mg/day) and especially the even more ambitious AHA guidelines (<1500mg/day). Both of these studies did find those with the highest levels of salt intake also had increased CVD risk but those with sodium intakes in the middle (about 3000 to as much as 6000mg sodium/day - which is the range consumed by most Americans) actually had the lowest risk of CVD events. “Our new results support these other studies that have questioned the wisdom of low dietary sodium intakes in the general population,” said Moore. The problem is all long term observational studies that mistakenly blame lower salt for increased risk of dying such as Dr. Moore's and Dr. O'Donnell's do a very poor job of measuring salt intake and/or suffer from confounding factors.
Dr. O'Donnell study used a single spot urine sample to estimate long-term sodium intake. However, this method for assessing sodium intake and provides little reliable evidence of a subject's salt intake over the long term. The use of a spot urine sample grossly underestimates the associations between salt intake and adverse health outcomes. It is well known that false associations (i.e. J- or U-shaped associations) may be generated when using spot urine samples are used to assess a subject's usual salt intake. Equations used to estimate 24-hour urine salt consumption from spot urines contain other confounding variables that are known strong health risks (e.g. age, gender, urine creatinine, body weight) generating further concern about the use of these equations for estimating usual salt consumption in observational outcomes studies. Even less accurate than single spot urine samples for estimating an individual's salt intake are food diaries (used for Dr. Moore's study), diet recalls, and food frequency questionnaires. For more detailed information about the numerous methodological issues that have long been known to confound observational studies examining the association between salt intake and disease see a review article on this topic by Laura Cobb and others in the Journal of the American Medical Association. This AHA Scientific Advisory report concluded: "Methodological issues may account for the inconsistent findings in currently available observational studies relating sodium to CVD. Until well-designed cohort studies in the general population are available, it remains appropriate to base sodium guidelines on the robust body of evidence linking sodium with elevated blood pressure."[2]
Russian Cosmonaut Study
In marked contrast to the very imprecise measurement of salt intake and excretion seen in the O'Donnell et. al. study and more recently Moore et.al. study are the very precise measurements of salt intake and excretion utilized in a study of young healthy volunteers in a very controlled environment that was meant to simulate many of the challenges of future flights to Mars. This study was headed by Dr. Jens Titze at Vanderbilt University. The results of Dr. Titze's study have over turned conventional scientific wisdom on how the human body regulates electrolyte and water balance in the face of large increases in dietary salt intake. The results also provide new insights into the Western epidemics of obesity, diabetes and heart disease and how excessive salt intake actually is promoting those serious health problems.
According to physiology textbooks, the excretion of dietary salt inevitably leads to greater water loss into the urine and thereby tends to reduce total body water content and increase thirst and water consumption. But that’s not what Dr. Titze and his team observed under tightly controlled conditions. On the contrary, he said, “we showed the biological principle of salt excretion is water conservation and water production.” It takes a lot of energy to conserve water in the face of increased salt excretion. To accomplish water conservation on a higher salt intake the human body must either consume more calories and/or utilize its own energy stores and break down muscle mass. “This predisposes to overeating," and “The resulting metabolic response looks a lot like diabetes.” Dr. Titze noted.
Dr. Titze very carefully controlled what his subjects ate and precisely measured how much salt and water they consumed and excreted in their urine. Between 2009 and 2011, his team studied four men during a 105-day pre-flight phase and six others during the first 205 days of a 520-day phase that simulated a full-length manned mission to Mars and back. Dietary salt intake in this tightly controlled environment was either 6, 9, or 12 grams daily. All other variables were tightly controlled. Russian scientist Natalia Rakova, M.D., Ph.D., first author of the clinical study, made sure the men ate every crumb of their meals and collected every drop of urine every day.
In 2013 Dr. Titze had reported sodium excretion occurred not on a daily basis but excretion fluctuated with a weekly rhythm. That observation, which went against the prevailing dogma, suggested sodium was stored in the body. He observed that levels of aldosterone, which regulates sodium excretion, and cortisol (a glucocorticoid hormone) also fluctuated weekly. In the Russian cosmonaut study his team found that when dietary salt was increased from 6 to 12 grams a day, the men surprisingly drank less water, not more. That suggested they must be somehow conserving more and/or producing more water.[3]
In a subsequent study in mice, Dr. Titze and colleages confirmed what they observed in their human subjects. Again the higher salt intake induced a catabolic state driven by elevated glucocorticoid levels. Muscle protein was broken down at faster rate and their amino acids were converted into urea by the liver. Urea is usually thought of as a waste product that is eliminated into the urine. However, Dr. Titze’s group showed that urea helps create the driving osmotic force that allows the kidney to reabsorb more water from the collecting tubules and return it back to the blood instead of letting it follow the excreted salt into the urine and out of the body. The kidneys thus act as a biological barrier for water conservation to prevent dehydration when salt intake is high. Until now salt and water balance had focused only on the kidney. This new study also found the liver and skeletal muscle play a role in regulating salt and water metabolism. Of course, elevated glucocorticoids and the metabolic abnormalities they cause including muscle wasting is a high price to pay for avoiding dehydration. This data suggests high-salt modern diets may be promoting sarcopenia as well as CVD, osteoporosis, insulin resistance, elevated BP, kidney stones, and perhaps increased hunger and body fat gain.[4] The alternative to breaking down muscle would be increasing protein and calorie intake, which may be why the cosmonauts in this study complained they were hungrier when their dietary salt intake was increased from 6 to 12g daily. Water conservation in response to a higher salt diet may have several pathological consequences. “We have always focused on the role of salt in arterial hypertension. Our findings suggest that there is much more to know — a high salt intake may predispose to metabolic syndrome,” Titze said. This suggest elevated blood pressure is a symptom of salt toxicity so treating hypertension with drugs is in effect treating yet one symptom of salt toxicity while ignoring its cause - excessive or toxic salt intake.
Bottom Line:
While the news media focuses on seriously methodologically flawed studies such as those of Dr.Moore's or O'Donnell's that continue to question whether or not added dietary salt contributes to elevated blood pressure and/or CVD, the far more credible scientific data from researchers such as Dr. Jens Titze continue to provide us with a better understanding of how excess dietary salt promotes not only hypertension and CVD but also may well promote many other serious ills. The lack of training of physicians in medical school about how the modern Western diet promotes disease continues to focus on elevated blood pressure as a primary disease (of supposedly unknown cause) that will require anti-hypertensive drugs to control. While most MDs largely ignore the cause of hypertension it is becoming increasingly clear that elevated blood pressure is but one of many likely pathological consequences of excessive dietary salt intake. The cure rate of hypertension with drugs is zero. By contrast, hypertension can in most cases be cured in but a few weeks by adopting a healthy DASH-style diet with no more than 1000 to 1500mg of sodium daily.
By James J. Kenney, PhD, FACN
References
[1] O'Donnell MJ, Mente A, Ranjarajan S, et al. Urinary sodium and potassium excretion, mortality, and cardiovascular events. N Engl J Med 2014;371:612-33 or http://www.nejm.org/doi/pdf/10.1056/NEJMoa1311889
[2] http://circ.ahajournals.org/content/early/2014/02/10/CIR.0000000000000015
[3] Rakova N, Kitada K, Lerchi K, et. al. Increased salt intake induces body water conservation and decreases fluid intake. J Clin Invest. 2017 available at: https://doi.org/10.1172/JCI88530
[4] https://doi.org/10.1172/JCI88532
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