CDC Advocating a Dangerous Reduction
On June 1, 2016, U.S. health officials announced a new set of recommendations regarding the salt content of processed foods. The stated goal is to help Americans reduce sodium intake to levels recommended by the Institute of Medicine (IOM) in 2004 and 2005, termed AI (for adequate intake), which were set at 1500 mg per day (3.7 grams salt) for adults up to age fifty, 1300 mg per day (3.3 grams salt) for adults between fifty and seventy, and 1200 mg per day (3 grams salt) for adults older than seventy. The maximum recommended sodium intake was set at 2300 mg per day (5.7 grams salt or slightly more than one teaspoon).1
An AI is specifically defined as the intake found in a healthy population, but no First World population has a sodium intake anywhere as low as the 2004/2005 IOM targets.2 In comparison to the sodium adequate intake of 1500 mg per day for adults, the average sodium intake in the U.S. and Canada is 3300 mg per day (8.3 grams salt or just over one and one-half teaspoons). Despite the Institute of Medicine’s commitment to base its nutrient intake recommendations on the evidence, the 2004/2005 Dietary Reference intakes for sodium are not supported by evidence.
High blood pressure is a known risk factor for cardiovascular disease (CVD) and cardiovascular mortality, and reducing elevated blood pressure lowers that risk. These findings derived from studies on subjects with hypertension led to the theory that lowering sodium intake in nonhypertensive individuals would lower blood pressure in them as well and would thereby reduce the risk of heart disease. There are two components to this presumption: 1) lowering salt intake in normotensive individuals will lower blood pressure meaningfully, and 2) lowering salt intake in normotensive individuals will reduce adverse health outcomes. Both presumptions are false.
A key role of sodium is the maintenance of blood pressure. Adequate body sodium content is necessary for maintenance of blood volume and renal perfusion, and these variables are strongly defended by the body. When our salt consumption is too low, defense mechanisms include salt hunger to increase sodium intake and reduction of urine and sweat to reduce sodium losses. When salt intake is too high, salt receptors in the tongue “flip” from positive to negative, which tends to decrease intake of salty foods.
RECENT STUDY ON ADVERSE EFFECTS OF LOW SODIUM INTAKE
About the same time that U.S. health officials announced their new initiative to reduce salt intake, The Lancet published a large population-based study which showed persuasively that the risk of mortality and serious cardiovascular events increases significantly when salt intake drops below 3000 mg per day (two-thirds teaspoon) in an adult of average weight.3 The study also found that sodium intake in excess of seven grams per day (over three teaspoons salt) was associated with an increased risk in those with hypertension, but not in those without hypertension. The study included 133,118 individuals (63,559 with hypertension and 69,559 without hypertension), with a median age of fifty-five years, from forty-nine countries. The association between salt intake as estimated by twenty-four-hour urinary sodium excretion and the composite outcome of death and serious cardiovascular events was assessed over a median of 4.2 years for both groups of subjects. The lead authors, Mente, O’Donnell and Rangarajan, are associated with Hamilton Health Services of Ontario, Canada. (For details on the 2016 Hamilton study, see box below.)
It is instructive to compare the results of the 2016 Hamilton study with those of an earlier (2014) study by the same authors.4 The study included 101,945 participants (compared to 133,118 in the recent study). In this study, the researchers did not separately determine the effect of sodium on hypertensive and normotensives subjects. Compared to the sodium reference range of 4 to 6 grams per day, an increased risk of death and CVD events were associated with sodium excretion of over 7 grams per day (hazard ratio 1.15) and with sodium excretion of less than 3 grams per day (hazard ratio 1.27).
Most importantly, the study found that sodium excretion equal to the “adequate intake” promoted by health officials of 1.5 grams per day was associated with a large increased risk of death and serious CVD events compared to the average reference level of 4.5 grams per day (hazard ratio 1.80). It is noted that the average of the reference range of 4.5 grams per day, which approximates the optimum sodium intake of hypertensives, is three times the “adequate intake” of 1.5 grams per day promoted by U.S. health officials.
This study also looked at potassium excretion. Compared with potassium excretion of less than 1.5 grams per day, higher potassium excretion was associated with reduced risk of the composite outcome. Mean potassium intake was 2.1 grams per day.
The association of sodium intake with risk of death and CVD events was evaluated with respect to significant variables, including HDL/LDL ratio, dietary factors including caloric and potassium intake, and the presence of heart disease, cancer, diabetes and high blood pressure. Adjusting for potassium intake reduced the risk of the composite outcome somewhat for both high and low sodium intakes. Adjusting for high blood pressure reduced the risk of high sodium intake but not low sodium intake. As with the 2016 study, the study authors concluded that the increased risk associated with sodium excretion above 7 grams per day was due to hypertension while the increased risk of intakes less than 3 grams per day was due to other causes. Elimination of subjects under treatment for heart disease, cancer and diabetes from the assessment did not significantly alter the composite outcomes.
The average sodium excretion of study participants was 4.9 grams per day, about 50 percent more than the average sodium intake of 3.3. grams per day in the U.S and Canada. The higher average intake of study participants was due largely to the high intake of Chinese participants who comprised 49 percent of participants and whose average sodium intake was 5.2 grams per day. Canadians comprised 9.6 percent of study participants. None of the study participants were from the U.S. In the 2016 Hamilton sodium study, 11 percent of participants had sodium excretion of less than 3 grams per day and hence were at significantly increased risk of death and CVD. In contrast, it is estimated that about 40 percent of the population of the U.S. and Canada are at increased risk due to sodium intakes of less than 3 grams per day.
On the high end of sodium consumption, 11 percent of hypertensive study participants had sodium intake greater than 7 grams per day and were therefore also at significant increased risk. In contrast, a negligible percentage of the population of the U.S. and Canada are at increased risk due to sodium excretion of more than 7 grams/day.
Potassium intake of study participants averaged 2.1 grams per day compared to about 2.9 grams per day in the U.S. Compared to study participants, the higher potassium intake in the U.S. results in a modest reduction of risk among those with sodium intake of less than 3 grams per day but that reduction in risk is offset by somewhat lower average sodium intake. The increased risk associated with low sodium intake in the U.S. is estimated to be similar to the risk observed in the 2016 Hamilton sodium study participants (hypertensives hazard ratio 1.34, normotensives hazard ratio 1.26)
Thus, a high percentage (about 40 percent) of the populations of the U.S. and Canada is already at significant increased risk of death and major CVD events due to low sodium intake. Further sodium reduction will increase the numbers at risk and is therefore not advisable.
THE CDC WEIGHS IN
On June 1, 2016, the same day that CDC announced the new recommendations regarding the salt content of processed foods, the agency published an article, “Dietary Sodium and Cardiovascular Disease Risk: Measurement Matters,” which was an attempt to discredit recent studies (including the Hamilton sodium studies) showing that sodium intake of less than 3 grams per day significantly increases risk of death and serious CVD events, and to support their contention that sodium intake of 1.5 grams per day is adequate for adults.5
Under the heading “Lower Sodium Intake and Increased Cardiovascular Risk: Association or Causation?” the CDC article erroneously claims that the 2016 Hamilton sodium study found that “both low and high intakes of sodium as compared to ‘usual’ intake (defined as 3-5 grams per day) were associated with increased risk of cardiovascular disease.” This statement is not consistent with the conclusion of the 2016 Hamilton study, which found that sodium intake greater than 7 grams per day was associated with increased risk of death and major cardiovascular events only in those with hypertension (hazard ratio 1.23) and not in those without hypertension (hazard ratio 0.9). The error suggests a lack of understanding of the 2016 Hamilton sodium study’s conclusions.
To address the question of whether low sodium intake causes cardiovascular disease, the CDC “applied Hill’s classic criteria of determining whether an observed association is causal: strength, consistency, specificity, temporality, biologic gradient, plausibility, coherence, experiment and analogy.”
Under the “strength” criteria, the CDC discusses several factors that could explain the association between low sodium intake (below 3 grams per day) and cardiovascular incidence that appears in studies such as the 2014 and 2016 Hamilton sodium studies. CDC speculates that the observed association between low sodium intake and increased CVD risk may have been due to a higher proportion of participants in the low sodium group, compared to groups with higher intake levels, who had diabetes, hypertension, and pre-existing cardiovascular disease at baseline and therefore may have consumed less sodium, leading to a noncausal association between sodium intake and increased cardiovascular events. However, in the Hamilton sodium studies, assessments of the association between sodium excretion and CVD risk were made in which subjects with such preexisting conditions were excluded, with no significant effects on outcomes.
CDC claimed that investigators did not take into account the presence of chronic kidney disease (CKD), which increases CVD risk and may result in lower sodium intake. However, patients with CKD typically have above-average sodium intake, not lower.6 It is further noted that the studies cited by CDC in support of their theories did not exclude those with CKD.
The CDC article noted that spot urine tests are not accurate and inferred that studies such as the 2014 and 2016 Hamilton sodium studies used “convenient but potentially biased methods to estimate individual intake”. But the Hamilton sodium studies used twenty-four-hour sodium excretion tests, not spot urine tests, and included over one hundred thousand subjects; they were therefore more accurate than the small studies cited by CDC, studies that used various sodium excretion measurements.
In summary, none of the CDC’s suggested criticisms of the Hamilton sodium studies are valid.
Under the “consistency” criteria the CDC cites twenty different studies to support their cause. While it is not practical to address all of the studies, I have reviewed two—the Trials of Hypertension Prevention7 (TOHP) and a 2016 study by Mills and others,6 which looked at sodium intake and CKD—in the sidebars on pages 34 and 35. CDC’s interpretations of these studies are inaccurate and in certain details, just plain wrong.
The majority of subjects in both studies were overweight and obese.8 Obesity is associated with increased sodium excretion and with increased cardiovascular risk. As a consequence, both studies give an erroneous illusion of a strong association between sodium excretion and cardiovascular risk. BMI and sex risk variables entirely explain all of the observed increase in cardiovascular risk in the TOHP trials. In the CKD study, BMI and sex were the primary cardiovascular risk variables but sodium excretion also contributed to cardiovascular risk of hypertensives. but only in the highest quartile of sodium excretion.
The TOHP trials and the CKD study cited by CDC as evidence that cardiovascular risk is increased by sodium intake above 1.5 grams per day both show that, on the contrary, sodium intake below 3 grams per day increases cardiovascular risk.
Under the “experiment” criteria, the CDC cited a Cochrane Review of experimental salt reduction studies as evidence that reducing salt intake lowers cardiovascular risk.9 The review consisted of eight small studies published between 1978 and 2007, of which five studies involving 5,912 participants included cardiovascular data during follow-up. Individually the five studies showed no significant results, but “pooling the studies across normotensive and hypertensive trials gives modest evidence of benefit for cardiovascular events at the longest follow-up (random effects 0.77).” However, a closer look shows that the observed modest benefit of salt reduction was due entirely to the three studies that included hypertensives, whereas no significant benefit was observed in the two studies that included only those without hypertension. Further, the claim of “modest benefit” was confounded by a number of factors:
1. Two of the three studies that included hypertensive subjects were salt substitution studies where salt reduction was achieved by substituting potassium-enriched salt for regular salt, thereby providing “a major increase in potassium and a moderate reduction in sodium intakes.”10,11 The CDC failed to include the author’s conclusion that the results that showed modest evidence of benefit “were strongly driven by the China Salt Substitution Study,”10 in which the reduction in CVD risk was most likely due to increased potassium intake, which has been shown to reduce CVD risk among Chinese subjects.
2. The 2007 follow-up study of the combined “Trials of Hypertension Prevention (TOHP)” studies12 was one of two studies of subjects without hypertension. This paper compared the percentage of subjects with CVD events in the experimental group, which reduced sodium intake and took nutritional supplements, with the control group, which did not reduce sodium intake and took no supplements. The results were confounded by the use of supplements in the experimental group but not in the control group and further confounded by the fact that the majority of subjects were overweight or obese. (Note: The TOHP trials discussed under the “consistency” criteria involved only the control group.)
3. In some of the studies, sodium intake was not determined by measuring sodium excretion and may be inaccurate.
In contrast to the CDC analysis, the authors of the Cochrane Review stated, “There is insufficient power to confirm clinically important effects of dietary advice and salt substitution on cardiovascular mortality.”9 A comment published in the Sao Paulo Medical Journal stated that “recent evidence from the Cochrane systematic review has cast doubt on the efficacy of dietary sodium restriction.”13
OTHER ADVERSE EFFECTS OF REDUCED SALT INTAKE
While maintenance of adequate blood pressure is a vital function of salt, including both the sodium and the chloride content, salt has many other important physiological functions as discussed in detail in Wise Traditions (Summer 2011).14 Sodium is critical for developing glial cells in the brain and is involved in muscle contraction including heartbeat, nerve impulses and the digestion of body-building protein. Sodium is active in the absorption of other nutrients in the small intestine and is the major electrolyte responsible for regulating water balance, pH and osmotic pressure. Chloride, the other component of salt, helps preserve the acid-base balance in the body, aids potassium absorption, supplies the essence of stomach acid, and enhances the ability of the blood to carry carbon dioxide from respiring tissues to the lungs.
OTHER RECENT ARTICLES ON ADVERSE EFFECTS OF LOW SALT INTAKE
A 2006 study showed that sodium restriction increases the risk of heart failure, death and hospitalization. The study sought to evaluate the impact of sodium restriction on heart failure outcomes. A total of two hundred sixty heart failure patients were divided into one hundred thirty sodium-restricted patients with sodium intake under 2500 milligrams per day, and one hundred thirty sodium-unrestricted matched controls with sodium intake over 2500 milligrams per day. The groups were followed for three years. Sodium restriction was associated with a significantly higher risk of death or heart failure hospitalization (42.3 percent versus 26.2 percent, hazard ratio 1.85).15
A study from Japan found that salt restriction during gestation causes retardation of fetal growth, thereby leading to low birth weight or a decrease in birth rate. Such retardation of growth along with the up-regulation of the renal angiotensin system due to salt restriction leads to underdevelopment of the cardiovascular organs or decreases the number of nephrons in the kidneys, leading to hypertension in adulthood. Moreover, salt restriction is associated with a decrease in insulin sensitivity. Part of metabolic disease in adulthood may be programmed through epigenetic changes due to salt restriction.16
A 2016 study found that low salt intake reduces the heart rate, which increases CHD risk. As heart rate is independently associated with the development of heart failure and increased risk of premature death, a potential decrease in heart rate could be a harmful side effect of sodium reduction.17
A 2013 study found that low salt intake increases chronic kidney disease risk. In the study of almost fourteen thousand participants from the National Health and Nutrition Examination Survey (2001-2006), subjects in the highest quartile of sodium intake (4267 milligrams per day or more) had lower odds of CKD compared to subjects in the lowest quartile (2116 milligrams per day or less) (hazard ratio 0.46 unadjusted, 0.79 adjusted).18
No first-world population has a sodium intake anywhere as low as the “adequate intake for adults” of 1.5 grams per day that health officials are promoting. Adequate body sodium content is necessary for maintenance of blood volume, renal perfusion and many other physiological functions, and these variables are strongly defended by the body.
The recent large 2016 Hamilton sodium study confirmed previous studies which found that sodium intake of less than 3 grams per day, compared to a 4 to 5 grams per day reference level, is associated with a significantly increased risk of death and serious CVD events due to factors other than hypertension. The risk associated with low sodium intake remains unchanged when adjusted for variables such as heart disease, cancer and diabetes. The study also found that those with hypertension, but not those without hypertension, are at increased risk when sodium excretion exceeds 7 grams per day.
The CDC criticisms of studies showing that sodium intake below 3 grams per day increased CVD risk contain no valid arguments. Ironically, data from two studies cited in the CDC article under the “consistency” criteria support the conclusion that sodium intake of less than 3 grams per day increases cardiovascular risk. The small studies that the CDC cited under the “experiment” criteria in support of their contention that reducing sodium intake below current levels can reduce CVD risk are flawed by confounding factors such as excess weight in study subjects, substitution of potassium for sodium, and providing nutritional supplements to experimental subjects but not to controls.
Approximately 40 percent of the total population of the U.S. and Canada has sodium intake of less than 3 grams per day (supplied by about one and one-half teaspoons of salt) and is therefore at significantly increased risk of death and major CVD events. In contrast, a negligible percentage of the hypertensive population of the U.S. and Canada is at increased risk of CVD events because of a sodium intake exceeding 7 grams per day. Consequently, the reductions in sodium intake recommended by health officials will significantly increase the population at risk due to low sodium intake but will benefit only a negligible number of hypertensives who are at increased CVD risk due to high sodium intake. The recently announced government efforts to reduce the salt content of processed foods will undoubtedly further increase the percentage of population at risk due to inadequate salt intake.
THE 2016 HAMILTON SALT STUDY
This important study found that in those without hypertension, the outcome of death or serious cardiovascular
events occurred in 4.3 percent of the population whereas in those with hypertension, the outcome of death or serious cardiovascular events occurred in 10.7 percent of the population. In those with hypertension, sodium excretion below 4 grams per day and above 5 grams per day was associated with increased risk of death and serious cardiovascular events. The reference range of 4 to 5 grams per day was used in assessing the risk of sodium excretion above and below the reference range. The risk was significant compared to the reference range when sodium excretion was less than 3 grams per day (hazard ratio 1.34) and when sodium excretion was greater than 7 grams per day (hazard ratio 1.23). The researchers determined that the increased risk of sodium excretion above the reference range was due to hypertension while the risk associated with sodium excretion less than 3 grams per day was due to other causes.
In those without hypertension, compared to 4 to 5 grams per day, the increased risk of death or serious CVD events was significant only when excretion was less than 3 grams per day (hazard ratio 1.26.) When sodium excretion exceeded 7 grams per day there was no significant change in risk (hazard ratio 0.90). The study concluded that compared with moderate sodium intake of 4 to 5 grams per day (two to two and one-half teaspoons salt), high sodium intake, greater than 7 grams per day is associated with a significantly increased risk of death and serious CVD events in hypertensive populations only, but not in the normotensive population. The association of low sodium intake, less than 3 grams per day, with increased risk of the composite outcome was observed in those with or without hypertension.
THE TRIALS OF HYPERTENSION PREVENTION (TOHP 1 and 2)
The Trials of Hypertension Prevention (TOHP 1 and 2) are cited by CDC as examples of studies that “support a
positive linear association from low to high levels of sodium intake and increased cardiovascular risk,” and as examples of the use of multiple, non-consecutive twenty-four-hour determination of sodium excretion as the “gold standard” of sodium measurement. The cited study, published in 2014,6 was a follow-up study to the original TOHP trials, which began in 1987 and 1990 and were completed in 1994. The purpose of the original trials, which were conducted with subjects without hypertension who were almost exclusively overweight and obese, was to assess the effects of stress, supplements and sodium on blood pressure. The original studies included an intervention arm of subjects who were counseled about sodium reduction and diet, and were provided with supplements of calcium, magnesium, potassium and fish oil, and a control arm that was left to their own devices.
Between 2000 and 2005, information on cardiovascular events was collected by phone and letter from the trial
subjects who could be located. Data on the available 2,275 subjects in the control arms of the combined TOHP trials were used to estimate the association between measured sodium excretion from the trials and subsequent cardiovascular events. The authors concluded that the study “showed a linear 17 percent increase in (cardiovascular disease) risk per 1000 mg (per day) increase in sodium,” a claim that is not supported by the data and is just plain wrong. In fact, as shown in the following analysis, the data from the study support the findings of the 2016 Hamilton sodium study, which found sodium intake of less than 3 grams per day significantly increases the risk of death and CVD events whereas sodium intake of above that amount does not significantly affect CVD risk in those who do not have hypertension. About 92 percent of subjects were overweight or obese. The study found that the percentage of CVD events in overweight subjects (BMI over 25) was 53 percent higher than the risk of normal weight subjects (BMI less than 25). Obesity is associated with increased sodium excretion and with increased cardiovascular risk. The sodium excretion of the study subjects of 3.8 grams per day was significantly higher than the average sodium excretion of around 3.4 grams per day in the U.S. and Canada. The percentage of CVD events of males was 215 percent higher than that of females. While age also affects cardiovascular risk, age was similar across sodium excretion categories and hence not a significant factor.
Table 1 below includes pertinent data on BMI and number and percentage of males by category of urinary sodium
excretion, together with the percentage of subjects in each category who experienced CVD events during follow-up.
From Table 1 it can be seen that both BMI and the percentage of male subjects increased with increasing sodium excretion, and that the percentage of subjects who had CVD events increased from the second highest category of sodium excretion to the highest. Based on the observed increased cardiovascular risks associated with BMI and sex variables, the increase in CVD events of 3.1 percent from the second to the highest sodium excretion category (9.9 percent to 6.8 percent) is explained entirely by the BMI and sex variables. The finding that increased sodium excretion did not contribute significantly to cardiovascular risk is consistent with the 2016 Hamilton sodium study, which showed that increased sodium intake above the reference level of 4 to 5 grams per day did not increase risk of CVD events in those without hypertension (hazard ratio 0.9).
In the lowest category of sodium excretion, with an average of 1.9 grams per day, the percentage of subjects that had CVD events was higher (7.2 percent) than that of the second category (6.8 percent), with average excretion of 3 grams per day, even though the average BMI and percentage of high-risk males was lower in the lowest category. After adjustment for the variables of BMI and sex, the CVD risk of the lowest category of sodium excretion, relative to the 6.8 percent of the second category, should be 5.3 percent. The observed risk of 7.2 percent is 36 percent higher than the 5.3 percent expected risk, which indicates that sodium intake below 3 grams per day significantly increases CVD risk. Thus the data in fact support the findings of the Hamilton sodium studies, showing that intake below 3 grams per day increases CVD risk!
SODIUM EXCRETION AND RISK OF CARDIOVASCULAR DISEASE IN PATIENTS WITH KIDNEY DISEASE
A second study cited by the CDC under the consistency criteria, “Sodium excretion and risk of cardiovascular disease in patients with chronic kidney disease”7 included 3757 subjects with chronic kidney disease (CKD), 55 percent males, who experienced 804 CVD events during 6.8 years follow-up. The authors concluded that “among patients with CKD, higher urinary sodium excretion was associated with increased CVD risk,” a conclusion that is greatly exaggerated.
Data from a study on the characteristics of CKD patients, 55 percent of whom are male, found that typically, 18 percent of CKD patients are of normal weight (BMI <25), 29 percent are overweight (BMI 25-30) and 53 percent are obese (BMI >30), 84 percent have hypertension and 42 percent have diabetes.8 Obesity is a risk factor for CKD and hypertension, and is associated with increased sodium excretion. The data suggest that the high percentage of overweight and obese subjects in the CKD study was similar to that in the aforementioned TOHP trials, a conclusion that is strengthened by the high average sodium excretion of 3.9 grams per day in the cited study compared to 3.8 grams per day in the TOHP trials and the average of 3.3 to 3.5 grams per day in the U.S. and Canada. Hypertensive subjects were excluded from the TOHP trials but not from the CKD study, so hypertension was a cardiovascular risk factor in the CKD study for those with high sodium intake (above 6 grams per day).
The percentage of CKD patients who had cardiovascular events during follow-up was higher (18.4 percent) in the lowest quartile of urinary sodium excretion (average excretion 2.5 grams per day) than the 16.5 percent in the second quartile (average excretion 3.3 grams per day). The finding is consistent with the results of the aforementioned TOHP trials and the Hamilton sodium excretion studies. Adjusting the results for sex and BMI further increases the cardiovascular risk associated with sodium intake below 3 grams per day in the lowest quartile of sodium excretion. As in the TOHP trials, the authors did not acknowledge the fact that the study data showed increased cardiovascular risk associated with a sodium intake less than 3 grams per day.
The available data appear to show that the increased cardiovascular risk among those with sodium excretion greater than 3.0 grams per day is explained entirely by the variables of BMI, sex and hypertension. It is concluded that increased sodium intake is a cardiovascular risk factor only for hypertensives with sodium intake above about 6 grams per day.
INFLAMMATION, AUTOIMMUNITY AND SALT: A RESPONSE TO LOREN CORDAIN
By Jack Cameron
On August 17, 2015, Loren Cordain posted an article entitled “Inflammation and Autoimmunity” on his website, thepaleodiet.com, in which he argues that added salt causes inflammation and autoimmunity. A careful look at his argument is warranted.
In the introduction, Cordain cites four studies that provide unconvincing and contradictory claims regarding the association between prevailing sodium intake and increased risk of stroke, hypertension and heart disease. One cited study, which attributes stroke to excessive salt intake, is a meta-analysis of thirteen studies published between 1966 and 2008 in which most measurements of sodium intake were highly inaccurate estimates based on food frequency questionnaires.22 The second is a review of fifty-two studies, which concluded that strokes are not caused by excess sodium but rather by insufficient potassium, a finding that is consistent with the preponderance of evidence.23 Cordain ignores more recent large clinical and epidemiological studies, which have found that sodium intakes of less than 3 grams per day significantly increase cardiovascular risk.3,4
In discussing sodium consumption, Cordain states incorrectly that the USDA recommended daily sodium intake of sodium is 2.3 grams. In fact, the USDA recommended daily “adequate intake” for adults is 1.5 grams for adults up to age fifty, 1.3 grams per day for adults between fifty and seventy years, and 1.2 grams for adults older than seventy years.2 The figure cited by Cordain of 2.3 grams is the USDA recommended daily maximum intake.
Cordain cites data from an 1984 book by D. Denton, which found that “hunter gatherers and non-westernized people worldwide” had average sodium intake from 0.234 to 1.131 grams per day. In sharp contrast to the sodium intakes in “non-westernized people worldwide” cited by Denton, surveys have found that the average daily sodium intakes are considerably higher: 5.3 grams in Asia, 4.9 grams in Africa and 4.6 grams in the Middle East. These values are derived from twenty-four-hour urinary sodium excretion measurements in studies involving over one hundred thousand participants.4 Cordain implies that sodium intake in “non-westernized people” is far lower than in the US, but in fact the average daily sodium intake in Asia, Africa and the Middle East is about 50 percent higher than the 3.4 grams per day in the U.S. and Canada.24,25
Cordain notes that Denton’s estimates of daily sodium intake are considerably lower than the “USDA recommended value of 2.3 grams” and much lower than the “wildly speculative values (3 to 7 grams) of sodium suggested by a non-scientific non-peer review Paleo blogger” (Kresser C. “Shaking up the salt myth, Healthy salt recommendations,” May 12, 2012). The “wildly speculative values” of 3 to 7 grams per day referred to by Cordain came from a cohort study published in 2011 in The Journal of the American Medical Association in which sodium intake of almost twenty-nine thousand patients with established cardiovascular disease or diabetes mellitus was estimated by twenty-four-hour urinary sodium excretion.26 During the follow-up of fifty-four months, the study found that daily sodium intake below three grams and above seven grams significantly increased cardiovascular risk. The finding that daily sodium intake below 3 grams significantly increased cardiovascular disease risk was supported by two subsequent studies that involved over one hundred thousand participants.3,4 When those with and without hypertension were evaluated it was found that sodium intake of about 7 grams per day increased the cardiovascular risk of hypertensives but not in those without hypertension.3
Cordain then estimates that a typical paleolithic diet with no added salt provides between 1.6 and 2.2 grams of sodium per day and concludes that it would not be possible to obtain “a popular blogger’s advice of 3 to 7 grams sodium per day” on a paleolithic diet with no added salt. Perhaps that is why humans have gone to such lengths to obtain salt.
It is noted that a sodium intake of less than 2 grams per day, which approximates the sodium intake of the paleo diet with no added salt, was associated with a 68 percent increase in cardiovascular disease risk during follow-up of fifty-four months in the study reviewed in the Kresser blog.26 Another study, which excluded subjects with cardiovascular disease, hypertension and diabetes, found that after thirty-three months, the cardiovascular risk of those with daily sodium excretion of 1.9 grams was 36 percent higher after adjustment for body mass index and sex than the risk of those excreting 3 grams.6
Cordain then turns his attention to the premise that diets high in sodium can have adverse effects on inflammation, immuniological function and autoimmunity, citing a half dozen studies involving dysfunction of the immune system, chronic systemic inflammation and autoimmunity. Most of these studies involve Th17 cells, which play an important role in maintaining mucosal barriers and contributing to pathogen clearance at mucosal surfaces, but also have been implicated in autoimmune and inflammatory disorders. The loss of Th17 cell populations at mucosal surfaces has been linked to chronic inflammation.
Cordain then asks the hypothetical question: “Would it be surprising that the typical western diet which includes 10 to 12 grams of sodium per day might have adverse effects upon the immune system and diseases of chronic inflammation?” It appears that Cordain has confused “sodium” with “salt” and meant to say “10 to 12 grams of salt,” not sodium. The average sodium intake in the U.S. and Canada is about 3.4 grams (about 1.5 teaspoons salt per day).
Two studies on the association between salt and immune function that Cordain discusses are analyzed below, together with a study on the association of salt intake with risk of all-cause mortality and end stage renal disease in those with type 1 diabetes.
1. The cited study, “Sodium chloride drives immune system, chronic systemic inflammation and autoimmunity”27 is typical of the studies on the association between Th17 cells and immunity. In animal studies researchers have found that increased salt intake adversely affects Th17 cells. The study authors state that there has been a marked increase in the incidence of autoimmune diseases in the past half century, particularly MS and type 1 diabetes. While indeed the incidence of type 1 diabetes has increased a great deal during this century (by 21 percent between 2001 and 2009), there appears to have been no significant increase in the incidence of MS. Latitude is a major factor in MS; the incidence of MS in Canada about five times the incidence in the southern U.S. The authors suggest that the increase in MS and type 1 diabetes could be due to changes in diet and hypothesize that increased salt intake might be the cause. The flaw in this hypothesis, however, is that sodium intake did not increase between 1957 and 200324 and has increased only slightly between 1988 and 2010.24,28 Obviously the puzzling rapid increase in type 1 diabetes during this century is not caused by increased salt intake.
2. Another cited study regarding the association between Th17 cells and immunity, “A salty taste to autoimmunity,” found no clinical or epidemiological evidence supporting the effect of salt on autoimmunity.29
3. If high salt intake were the cause of increased type 1 diabetes risk, it would be expected that reducing daily sodium intake from the present median of 3.4 grams in the U.S. to the USDA “adequate intake” of 1.5 grams would significantly reduce the risk of type 1 diabetes. However, a recent study found the opposite to be true.30 The study included twenty-eight hundred adults with type 1 diabetes without end-stage renal disease (ESRD) who were followed for ten years to determine the incidence of all-cause mortality and ESRD. Urinary sodium excretion was associated with all-cause mortality, such that those with the highest urinary sodium excretion, as well as the lowest excretion, had reduced survival. This association was independent of age, sex, duration of diabetes, chronic kidney disease, cardiovascular disease and systolic blood pressure. The lowest risk of all-cause mortality occurred when daily sodium excretion was 3.0 to 3.5 grams which approximates the current median sodium intake in the U.S. The risk of all-cause mortality among those consuming the USDA “adequate” daily sodium intake of 1.5 grams was approximately 50 percent higher than those consuming the median sodium intake of 3.3 grams. The observed increase in mortality and CVD events among those with daily sodium excretion less than 3 grams is consistent with the findings of many other studies.3,4,6,7,22 During follow-up, one hundred twenty-six patients (4.5 percent) developed end-stage renal disease (ESRD). Urinary sodium excretion was inversely associated with cumulative incidence of ESRD such that those with the lowest sodium excretion had the highest incidence of ESRD. The risk of end-stage renal disease in those consuming the USDA recommended daily sodium intake of 1.5 grams was five times higher than those consuming the median intake of 3.3 grams.
Thus, the studies cited by Cordain regarding the association between sodium intake and autoimmune diseases found no epidemiological or clinical evidence that prevailing levels of sodium intake in the U.S. increase risk of autoimmune diseases such as MS and type 1 diabetes. On the contrary, the studies showed that among those with type 1 diabetes, sodium intake of less than 3 grams is associated with significantly increased risk of all-cause mortality and end stage renal disease. The USDA recommendation to limit sodium intake to 1.5 grams per day and Cordain’s advice to follow a “paleo diet” with no added salt are both likely to result in increased risk of cardiovascular disease, heart failure and chronic kidney disease, as well as increased all-cause mortality and ESRD from type 1 diabetes.
OTHER ADVERSE EFFECTS OF GOVERNMENT DIETARY GUIDELINES ON HEALTH
Decades of effort by government officials to reduce salt intake by the U.S. population have met with limited success due to the natural salt cravings that kick in when salt intake is not adequate. It has been estimated that about 40 percent of the U.S. population is at increased risk for cardiovascular events due to sodium intake of less than 3 grams per day. The pending plans to reduce the sodium content of processed foods will no doubt increase the percentage of people with inadequate sodium intake.
Other U.S. dietary guidelines that adversely affect health have been more successful at convincing Americans to substitute vegetable oils for animal fats, based on the disproven notion that saturated fat intake increases CVD risk. About 75 percent of milk consumed today is reduced in fat due to the government recommendation to drink only non-fat and lowfat dairy products. A recent large study found that those who consume the most whole-fat dairy products have a 23 percent lower risk of type 2 diabetes compared to those who consume the least.19 Consumption of non-fat dairy products had no effect on diabetes risk. The study also found that increased intake of soybean oil, which is high in linoleic acid and which constitutes 80 percent of vegetable oils consumed today, increases the risk of type 2 diabetes. Thus, government advice to drink only non-fat dairy products and increase vegetable oil consumption has significantly increased the incidence of type 2 diabetes in the U.S.
During the past century consumption of linoleic acid (LA) has increased from about 2.8 percent to 8 percent of calorie intake partly as a consequence of government recommendations to substitute vegetable oils for animal fats. Other recent studies found that the increase in LA intake is associated with the increased incidence of obesity and type 2 diabetes that has occurred during the past fifty years.20,21
Those who manage to overcome their natural desire for salt are also likely to be victims of other government dietary recommendations, which have adverse effects beyond the adverse effects of inadequate salt intake.
1. FDA News release: June 1, 2016: FDA issues draft guidance to food industry for voluntarily reducing sodium in processed and commercially prepared food.
2. Heaney, R. “Making sense of the science of sodium”: Nutr. Today. 2015 Mar: 50(2): 63-66 Published online 2015 Mar 26.
3. Mente, A, O’Donnell M, Rangaranjan S and others: “Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of four studies:” Lancet 2016 May 20. [Epub ahead of print].
4. O’Donnell, M, Mente A, Rangaranjan S. and others: “Urinary sodium and potassium excretion, mortality and cardiovascular events” N Engl J Med 2014 Aug 14: 371(7): 612-23.
5. Cogswell, M and others: “Dietary sodium and cardiovascular disease risk: Measurement matters”: N Engl J Med 2016 June 1 (Epub ahead of print).
6. Mills KT and others: “Sodium excretion and risk of cardiovascular disease in patients with chronic kidney disease” JAMA 2016 May 24-31;31(20):2200-10.
7. Cook, NR and others: “Lower levels of sodium intake and reduced cardiovascular risk” Circulation 2014;129:981-989.
8. Rahman M and others: Association between chronic kidney disease progression and cardiovascular disease: results from the CRIC Study: Am J Nephrol. 2014;40(5):399-407.
9. Adler AJ and others: Reduced dietary salt for the prevention of cardiovascular disease. Cochrane Database Syst Rev2014:12:CD0009217-CD009217.
10. China Salt Substitute Study Collaborative Group: “Salt substitution: a low cost strategy of blood pressure control among rural Chinese. A randomized controlled trial.” J. Hypertens 2007 Oct:25(10):2011-8
11. Chang HY, Effect of potassium-enriched salt on cardiovascular mortality and medical expenses of elderly men. Am J Clin Nutr2006;83:1289-1296.
12. Cook NR, “Long term effect of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention. BMJ 2007 Apr 28:334(7599);885-8
13. Santos, R. “Dietary sodium restriction and cardiovascular disease prevention: should we quit?” Sao Paulo Med J. vol.133 no.3 Sao Paulo June 2015
14. Fallon Morell, S “The salt of the earth: why salt is essential to health and happiness”: Wise Traditions, Volume 12 Number 2, Summer 2011.
15.. Doukky R and others: “Impact of dietary sodium restriction on heart failure outcomes:” JACC Heart Fail 2016 Jan:4(1):24-35.
16. Sakuyama H and others, “Influence of gestational salt restriction in fetal growth and in development of diseases in adulthood”. J Biomed Sci 2016 Jan 20: 23:12.
17. Graudal NA and others: “Reduced dietary sodium increases heart rate” Front Physiol 2016 Mar 24;7:111.
18. Sharma S and others: “Association between dietary sodium and potassium intake with chronic kidney disease in US adults: a cross sectional study” Am J Nephrol 2013;37(6):526-33.
19. Ericson U and others: “Food sources of fat may clarify the inconsistent role of dietary fat intake on incidence of type 2 diabetes”: Am J Clin Nutr. 2105 May;101(5):1065- 80.
20. Naughton SS and others: Linoleic acid and the pathogenesis of obesity: Prostaglandins Othr Lipid Mediat 2016 June 24.
21. Alvheim AR and others: Dietary linoleic acid elevates endogenous 2-AG and anandamide and induces obesity: Obesity (Silver Springs) 2012 Oct;;20(10) 1984-94.
22. Strazzullo P and others “Salt intake, stroke, and cardiovascular disease: meta analysis of prospective studies” BMJ 2009 Nov 24;339:b4567.
23. Aaron K and others. “Role of dietary salt and potassium intake in cardiovascular health and disease: a review of the evidence”. Mayo Clin Proc Sep;88(9).
24. Bernstien, AM and others: Trends in 24-hour urinary sodium excretion in the United States: 1957 to 2003: Am J Clin Nut 2010 Nov; 92(5):1172-80.
25. Mente A, and others “Assessment of urinary sodium and potassium excretion in Canadians using 24-hour urinary excretion” Can J Cardiol 2016 Mar;32(3):319-26.
26. O’Donnel, MJ and others “Urinary sodium and potassium excretion and risk of cardiovascular events” JAMA 2011 Nov 23;306(20):2229-38.
27. Kleinewietfield M and others: “Sodium chloride drives autoimmune disease by induction of pathogenic T17 cells” Nature 2013 Apr 25;496(7446)518-22.
28. Pfieffer CM and others “Urine sodium excretion increased slightly among U.S. adults between 1988 and 2010”; J Nut. 2014 May;144(5):698-705
29. van der Meer J and others: “A salty taste to autoimmunity” N. Eng J Med 2013 June 27;368(26): 2520-1.
30. Thomas M and others: “The association between dietary sodium intake ESRD and all-cause mortality in patients with type 1 kidney disease” Diabetes Care: 2011 Apr;34(4):861-6.
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation,Fall 2016