The Salt Fix: Why the Experts Got It All Wrong–and How Eating More Might Save Your Life

Overall score

Scientific accuracy

Reference accuracy

Healthfulness

How hard would it be to apply the book's advice? Fairly easy

Book published in 2017

Published by Harmony Books

First Edition, Hardcover

Review posted June 29, 2022

Primary reviewer: Hilary Bethancourt

Peer reviewer: Travis Masterson

Table of contents

1. Introduction
2. Scientific accuracy
3. Reference accuracy
4. Healthfulness
5. Most unusual claim
6. Other
7. Conclusion
8. Updates

Claim 1

High-salt diets do not cause high blood pressure or heart disease.

Supporting quote(s) and page number(s)

Page 34: “If salt caused heart disease – chest pain leading to sudden death – and Europeans were consuming 40 grams of salt per day in the 1500s, there should have been hundreds of thousands of reports of heart disease during this time.”

Page 67: “Looking at population data, it’s clear that high-salt diets don’t seem to cause strokes and heart attacks. If anything, we see that high salt intakes lower the risk of cardiovascular disease and premature death.”

Page 69: “[R]educing your salt intake to around 2,300 milligrams per day (1 teaspoon of salt) may only lower your blood pressure by a meager 0.8/0.2 mmHg.”

Page 69: “[A]pproximately 80 percent of people with normal blood pressure are not even sensitive to these meager blood-pressure effects of salt; among those with prehypertension (a precursor to high blood pressure), roughly 75 percent are not sensitive to salt, and among those with full-blown hypertension, about 55 percent are immune to salt’s effects on blood pressure.”

Page 71: “[H]igh salt loads may actually cause the blood vessels to relax.”

Page 102: “[E]ven if you happen to binge on salt, we know that our kidneys simply reabsorb less. No harm, no foul.”

Criterion 1.1. How well is the claim supported by current evidence?

1 out of 4

This claim received a score of 1, indicating that it is not supported by current evidence.

A large body of scientific literature on this topic suggests that this claim is incorrect. Summaries of animal experiments, observational studies, migration studies, population-based interventions, and randomized-controlled trials paint a compelling picture of high salt consumption contributing to higher blood pressure. Because high blood pressure is considered one of the major risk factors for cardiovascular disease, high salt intake has also been associated with increases in cardiovascular disease events, cardiovascular-related mortality, and total mortality (these associations are linear dose-response, which means the more salt a person eats, the higher their risk of cardiovascular disease is likely to be, even when accounting for age, smoking, physical activity, and other risk factors).

It is true, as The Salt Fix notes, that a number of observational cohort studies and meta–analyses of observational studies have reported J- or U-shaped associations, whereby both lower and higher sodium intakes are related to cardiovascular events or mortality. However, these non-linear findings have been largely attributed to methodological issues with the way these studies are conducted.

It is possible that high sodium intake is just an indicator of consuming highly processed diets, and diets higher in processed foods are associated with greater risk of cardiovascular disease and mortality. Yet research has demonstrated that higher exposure to sodium in drinking water is associated with higher blood pressure among young, coastal-dwelling Bangladeshis even after controlling for other dietary factors or sodium intake. Even in a lean, highly active pastoralist population with little to no access to processed foods, higher water salinity appears to be related to higher blood pressure.

However, these examples are taken from observational studies, which we consider fairly weak evidence. When we look at stronger evidence such as randomized controlled trials, there is evidence that reducing sodium intake can reduce blood pressure. For example, several meta–analyses of randomized controlled trials have provided evidence of a dose-response relationship between sodium intake and blood pressure (i.e., showing that greater reductions in sodium lead to greater reductions in blood pressure). This appears to be particularly true in individuals with elevated blood pressure.

Those meta-analyses excluded interventions that combined sodium reductions with other treatments, like increasing potassium intake (which may also reduce blood pressure). Still, it is also worth noting that several double-blind controlled trials that randomized participants with hypertension to either continue using normal table salt (100% sodium chloride) or use an alternative salt with reduced sodium and added potassium (and sometimes magnesium) report significant reductions in blood pressure and rates of cardiovascular events. These studies were conducted in places where table salt used in cooking (as opposed to processed foods) is a prominent source of salt in the diet.

Salt defenders have argued that the increase in potassium as a result of low-sodium salt substitutes may be more influential than a decrease in sodium for reducing blood pressure. Yet just because increasing potassium intake may help reduce blood pressure does not mean there aren’t still added benefits from reducing sodium. For example, one highly cited randomized-controlled trial demonstrated that sodium reductions were associated with reduced blood pressure among participants randomized to either a standard American diet or a healthier diet with more fruits and vegetables (i.e., more potassium). In other words, the reduction in sodium was beneficial regardless of whether it was combined with a diet higher in potassium. However, the combination of a healthy diet and reduced sodium intake had a greater effect on reducing blood pressure than either intervention in isolation. This suggests that the best strategy to reduce or maintain a healthy blood pressure would include both reduction in salt intake and increasing intake of potassium-rich foods.

It is true that, as The Salt Fix argues, participants of experimental studies who have normal blood pressure at the start of the study tend to experience smaller reductions in blood pressure when they restrict salt compared with participants who start out with prehypertension or hypertension. There is nothing surprising about that finding; someone who is already in a healthy range of any health measure has less room for change. Individuals with normal blood pressure experience less pronounced reductions in blood pressure with exercise/physical activity interventions than individuals with prehypertension or hypertension. Yet we would not use that evidence to suggest that normotensive individuals have no need to follow physical activity recommendations. We would likewise not expect someone with normal weight to experience as much weight loss as someone with overweight/obesity in response to transitioning from a highly processed, high-sugar diet to a more whole foods diet. Yet we would still recommend that individuals of any weight status follow a healthy, whole foods diet so that those with a healthy weight can prevent weight gain and those with overweight or obesity might lose weight or at least prevent further weight gain.

The dietary recommendations on salt, therefore, are set not just to help those with high blood pressure to reduce their blood pressure but also to help people without high blood pressure prevent it. Data has shown that even infants and children can experience sodium-related rises in blood pressure, and the effects of high sodium intake early in life may persist into later life. Furthermore, even if excess salt intake does not cause an immediate effect on blood pressure for many individuals, it can over time have adverse effects on endothelial, artery, and kidney function, eventually contributing to the development of hypertension, heart disease, and chronic kidney disease.

The Salt Fix suggests that only 20% of the population is considered salt-sensitive and that only those salt-sensitive individuals need to worry about limiting their salt intake. However, research suggests that salt sensitivity is not solely a genetic trait that someone has or doesn’t have. Instead it appears to be more of a spectrum, and we can become increasingly salt-sensitive over time, as excess salt intake can contribute to damage to the kidneys and other organs and tissues. Salt sensitivity may increase further as individuals develop hypertension or other conditions, such as type 2 diabetes, that accelerate kidney damage.

In summary, the bulk of the evidence suggests that regular consumption of excess salt intake tends to cause blood pressure to rise and can tax other organs (e.g., kidneys), all of which may contribute to the development of cardiovascular disease. Some individuals may be more sensitive or resistant to the effects of salt depending on genetic, physiological, dietary, and lifestyle factors. A healthy diet, consumption of adequate potassium, and exercise may help lower blood pressure independently of salt intake. Nevertheless, the evidence suggests that moderating salt intake, in addition to a healthy diet and lifestyle, is a prudent step toward preventing onset and progression of hypertension and disease.

Criterion 1.2. Are the references cited in the book to support the claim convincing?

1 out of 4

The book’s references received a score of 1, indicating that they do not provide convincing support for the claim.

The studies cited to support the book’s claim that humans evolved on high-salt diets were not convincing. For example, one study describing orangutans in the tropics catching and eating fish is cited in the book to suggest that our pre-human ancestors were forced by climate changes to seek out wetlands, resulting in diets consisting of salty fish and aquatic vegetation (page 20). This is taken as evidence that “the diet of pre-human primates (and thus early humans) would not have been low in salt; in fact, it could have been extremely [sic] high in salt” (page 21). Yet, the study cited merely serves as an example of how our pre-human ancestors may (in theory) have caught fish prior to the development of tools; it tells us nothing about how often they were eating fish and aquatic plants or how much sodium was being consumed on a daily basis. Given how hard it is to catch fish with bare hands, this is hardly a strong argument for a high intake of fish, let alone salt.

The book suggests that sodium intake was also high among non-coastal pre-human ancestors. It supports this notion by citing a Daily Mail article, as opposed to the original study, which uses data from baboons to suggest that Paranthropus boisei, thought to be a distant cousin of humans, may have been incorporating tiger nuts (containing 3,383 mg of sodium per 100 grams) into their diets. However, this study provides no indication of whether our human ancestors were eating these foods, how much they may have been eating at a time, and how regularly they may have consumed them. Even if we were to assume that our early ancestors were eating high amounts of sodium, tiger nuts (and other foods sources) also contain considerable amounts of potassium, which help maintain the balance of sodium and other electrolytes in the body.

The book points to a paper that describes aborigine populations eating 2-3 kg of meat in one sitting to suggest that our hunter-gatherer human ancestors would potentially be consuming ~3,450 mg of sodium in one sitting. However, the study notes that such occasions were only episodic, as hunting success rates were generally low. That same study also describes research demonstrating that even chimpanzees experience elevations in blood pressure when fed high-sodium diets, undermining the claim that sodium intake is unrelated to blood pressure.

Some other evolutionary claims made in the book are completely unsubstantiated. For example, that “Our ancestors also likely had salt licks and drank rainwater, providing clear evidence that previous estimates of sodium intake during our evolution are most likely drastic underestimations” (page 25). But with no citation for the claims that humans consumed salt licks or that rain water is high in sodium, these appear to be merely speculations.

The historical accounts of various European populations purportedly consuming a range of 13-100 g/day of salt between the 16th-19th centuries are also not convincing evidence that salt is harmless to health. While historical accounts (if we can trust them to be accurate) provide examples of the amount of salt humans may be capable of eating, they provide no evidence of what impact those high-salt diets may have had on health. Just because humans might be capable of eating and excreting large amounts of salt does not mean consuming large amounts of salt everyday is a healthy consumption pattern. After all, humans are capable of drinking large amounts of alcohol and filtering it through the liver, but long-term daily consumption of high quantities of alcohol will eventually take a huge toll on the liver.

The book doesn’t differentiate between the implications of short-term versus chronically high salt intake. For example, one experimental study was cited to argue that our kidneys can handle excretion of massive amounts of sodium, but the experiment lasted for only three days. Such a study says nothing about our kidneys’ ability to excrete such large amounts of sodium long-term. As we age, kidney function is known to decline, so we can’t assume that our kidneys can handle “massive” amounts of sodium at all stages of life.

In Chapter 4, there is a text box titled “Populations that consume ample amounts of salt in which hypertension is virtually absent” (page 82). None of the studies cited in that box provide convincing support for the claim either. These studies merely report average sodium excretion or intake levels and average blood pressure among the populations studied; none of them test relationships between sodium intake and blood pressure within individuals. The cited papers in the box do discuss how factors other than increased salt intake, including higher psychosocial stress, higher body weight, lower physical activity, or other dietary factors (e.g., lower potassium intake, higher alcohol consumption), may account for  increases in blood pressure that are observed with populations as they transition to more modern, industrialized lifestyles. However, some of the studies, including one that was cited repeatedly for nine of the 15 different populations listed, undermine the claim, as they demonstrate that populations with higher average salt intakes tend to have higher average blood pressures. Though, again, these cross-population comparisons are considered a weak form of evidence because they don’t account for other dietary and lifestyle factors that could influence blood pressure at the individual-level.

Some of the meta-analyses of randomized controlled trials and the systematic review cited in The Salt Fix to refute the idea that salt reduction has a meaningful benefit on blood pressure (at least among people without high blood pressure) were conducted in the 1990s. More recent meta-analyses and reviews, including ones that do and do not demonstrate a significant reduction in blood pressure among people without high blood pressure, were not cited in the book. However, contrary to the main point of the book, the meta-analyses cited actually suggest that sodium reduction is beneficial for reducing blood pressure among people with hypertension.

In summary, the book relies too much on low-quality evidence (e.g., speculation, historical accounts, ecological and cross-sectional studies, and short-term experiments) to support its claim that high-salt diets do not cause hypertension or heart disease. There is no disputing the claims in the book that sodium is an essential nutrient and that higher potassium intake, a generally healthy diet, a physical activity regimen, maintaining a healthy weight, and managing stress will help prevent and manage blood pressure and cardiovascular disease risk. However, none of that evidence provides convincing support for the claim that a high sodium intake is not at least one of the contributors to the development of hypertension and cardiovascular disease or that lowering/moderating sodium intake won’t provide additional health benefits for those aiming to prevent or manage hypertension and cardiovascular disease through diet and lifestyle. There may be people who, at least temporarily, can handle high levels of salt/sodium intake without experiencing negative effects on their blood pressure. That doesn’t mean that regular high salt intake over the years won’t lead to health consequences.

Criterion 1.3. How well does the strength of the claim line up with the strength of the evidence?

1 out of 4

The claim received a score of 1, indicating that the claim is substantially overstated.

The data provided by The Salt Fix and more up-to-date sources do not support the suggestion that humans evolved to consume high-salt diets. Nor do inferences on salt intake among human ancestor, early human, or 16th-19th century human populations provide evidence on what levels of salt intake are optimal for preventing the development of hypertension and cardiovascular disease. This is especially true for modern human populations that are sedentary, living in climate-controlled environments (i.e., not losing large amounts of sodium through sweating), consuming inadequate amounts of potassium and minerals that help regulate sodium excretion, or have overweight or obesity or other health conditions that put them at risk of hypertension and cardiovascular disease (e.g., insulin resistance or chronic kidney disease).

It is true that salt is not the only factor that contributes to elevated blood pressure and cardiovascular disease. Indeed, as suggested in the book, excess dietary sugar and sugar-sweetened beverages appear to contribute to hypertension and cardiovascular disease. Likewise, a variety of factors other than salt reduction, including weight reduction, physical activity, increased potassium intake, overall healthy dietary patterns, caloric reductions, and moderating alcohol intake, may also help reduce blood pressure and cardiovascular disease risk independently of salt intake. But none of these facts mean that salt should get a free ride and be used indiscriminately. Salt is an essential nutrient and should be consumed in adequate quantities. However, the bulk of the evidence indicates that chronically high salt intake is a notable contributor to hypertension and cardiovascular disease among the general population and should, therefore, be used in moderation for both the prevention and management of disease.

Overall (average) score for claim 1

1 out of 4

Claim 2

Low-salt diets (i.e., keeping salt intake within recommended ranges) are detrimental to cardiovascular and metabolic health.

Supporting quote(s) and page number(s)

Page 10: “[W]e focused on those extremely minuscule reductions in blood pressure, completely disregarding the numerous other health risks caused by low salt intake – including several side effects that actually magnify [original emphasis] our risk of heart disease – such as increased heart rate; compromised kidney function and adrenal insufficiency; hypothyroidism; higher triglycerides, cholesterol, and insulin levels; and, ultimately, insulin resistance, obesity, and type 2 diabetes.”

Page 28: “Our sodium pump uses approximately 70 percent of the basal energy expended by the kidneys, making a low-salt diet an energy hog and a tremendous stress to the kidneys. This is one way that low-salt diets can lead to weight gain, by slowly depleting our energy stores and leading us to become more sedentary.”

Page 28: “Similar to the way a low-salt diet depletes energy of the kidneys, it does the same to the heart. When we restrict our salt intake, our heart rate goes up, reducing our blood and oxygen circulation throughout our body and increasing the heart’s need for oxygen.”

Page 40: “The known consequences of salt restriction, such as low sodium and chloride in the blood, have long been independently known to increase risk of death.”

Page 69: “[M]any people with normal blood pressure, prehypertension, and hypertension may even get a rise [original emphasis] in their blood pressure if they restrict their salt intake.”

Page 70: “[L]ow-salt diets may actually cause [original emphasis] the very disease they are supposed to prevent and treat, hypertension.”

Page 72: “[T]hose who experience a higher heart rate and blood pressure on salt restriction may have decidedly worse [original emphasis] health outcomes, a fact that would affect a much larger portion of the population.”

Page 74: “[L]ow-salt diets would increase the overall stress on the heart and arteries and hence increase the risk of hypertension and heart failure.”

Page 76: “[L]ow-salt diets were found to cause insulin-resistant blood vessels, leading to increased vasoconstriction, the same problem found in patients with hypertension. Thus it’s not a huge leap to say that, even without the help of sugar, low-salt diets were probably contributing to hypertension by causing insulin resistance.”

Page 87: “[L]ow-salt diets have been found to compromise kidney function, decrease high-density lipoprotein (HDL; “good” cholesterol), and reduce adiponectin, a substance released by fat cells thought to improve insulin sensitivity.”

Page 88: “Salt restriction also increases fasting norepinephrine, a substance that increases heart rate.”

Page 88: “[L]ow-salt diets could actually cause overgrowth of the heart and kidneys, which could lead to heart failure and kidney disease-the very diseases we have been told high-salt diets cause.”

Page 89: “Less than 2,300 milligrams per day or more than 6,000 milligrams per day is associated with an increased risk of death and cardiovascular events – but the risk is higher with low salt intakes than high salt intakes.”

Page 91: “Consuming too little salt can set into motion an unfortunate cascade of changes that result in insulin resistance, an increase in sugar cravings and out-of-control appetite, and what’s been dubbed “internal starvation (aka “hidden cellular semistarvation”), thereby promoting weight gain.”

Page 91: “[C]ompared to someone who hasn’t slashed his or her salt intake, a low-salt diet may cause you to absorb twice as much fat for every gram you consume.”

Page 94: “[E]ven moderate salt restriction (2 grams of salt per day) could increase insulin response to an oral glucose tolerance test in patients with high blood pressure.”

Page 95: “When salt restriction reduces blood circulation, less blood flows to the liver, interfering with the liver’s ability to break down insulin-a possible mechanism explaining how low-salt diets raise insulin levels.”

Criterion 1.1. How well is the claim supported by current evidence?

1 out of 4

This claim received a score of 1, indicating that it is not well-supported by current evidence.

Salt plays a very important role in the functioning of the human body, which is why it is considered an essential nutrient. One metabolic health condition brought up by The Salt Fix is hyponatremia, the condition of too little sodium in the blood that may be associated withincreased morbidity, mortality, and cognitive problems. However, this condition is primarily seen among ill and hospitalized patients and the elderly; it is much less common in the general population.

Also, hyponatremia is often considered more of an issue of water imbalance than of low salt intake. It is often caused by 1) conditions that affect the body’s ability to properly excrete water which leads to higher water content in the blood, 2) drinking high amounts of fluids relative to salt intake, as might be the case in heavy alcohol drinkers or elderly on “tea and toast” diets, or 3) heavy use of thiazide diuretics and other medications that disrupt water homeostasis in the body and cause increased excretion of salts and other solutes. So, for the general population hyponatremia is not a common concern.

However, there is a contentious debate about whether recommended sodium intakes (<2.3 g/day) might be associated with increased risk of cardiovascular disease. The current concern is borne from two major lines of evidence:

1) Reviews of clinical trials demonstrating increased concentrations of cholesterol and triglycerides in the blood, as well as increased renin, aldosterone, adrenaline and noradrenalin, in response to salt restriction. Elevations in these markers are considered potential risk-factors for cardiovascular disease.

2) Data from observational studies and a handful of follow-up randomized controlled trials reporting so called “J-shaped relationship” between usual salt intake and cardiovascular disease. The J-shape refers to there potentially being a  higher risk of cardiovascular events, cardiovascular mortality, and all-cause mortality among those with both the highest (>7 g) and the lowest lower intakes (<3 g) of sodium relative to those in the middle ranges of sodium intake.

Both of these lines of evidence have been fiercely contested in the scientific literature, however. It is true that rapid and drastic decreases in salt appear to cause reduced blood volume, which results in acute increases in blood lipid concentration and activates the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous systems. The role of the RAAS is to maintain blood pressure, so it is precisely because of the short-term activation of this system that blood pressure falls only slightly in the first couple weeks of salt restriction (or rises only slightly following short-term increases in salt). Large increases in RAAS activity can also explain why some people experience an increase in blood pressure initially when lowering sodium intake.

However, these increases in the RAAS and sympathetic nervous system appear to be short-lived responses to rapid changes in sodium intake as the body works to reach a new balance, which appears to occur within four weeks. When salt reduction trials of less than four weeks are excluded from meta-analyses, the data suggests that increases in blood lipids, renin activity, aldosterone, and catecholamines are minimal and not necessarily clinically relevant. Moreover, researchers have argued that it remains unclear if renin or aldosterone are risk factors for cardiovascular disease in the general population. Unlike blood pressure, these markers are not established biomarkers of cardiovascular disease.

Studies reporting J-shaped relationships between usual salt intake and cardiovascular related events of death have also been criticized for methodological issues that bias their results. One major methodological issue is the use of a single 24-hour or single morning or spot urine collection for estimating “usual” salt intake. When only a single 24-hour or spot urine sample is available (as opposed to the gold standard of multiple 24-hour urine samples), mathematical formulas are used to estimate “usual” sodium intake.

A single urine sodium mesaurement is a poor estimate of typical intake of a nutrient that can vary substantially day-to-day, and the formulas used to estimate usual intake from a single measurement rely on data on age, sex, and weight, all of which may themselves be related to both disease and salt intake. Therefore, these formula estimates of sodium intake tend to misestimate and misclassify levels of sodium intake when compared with the gold standard. One group of researchers demonstrated that the J-shaped relationship between sodium intake and cardiovascular mortality that was observed with the use of only a single urine sample disappeared and was directly linear when using the gold standard of multiple 24-hour urine samples for estimating sodium intake.

Another major issue with these studies’ methods is that they include participants with pre-existing conditions that may put them at higher risk of cardiovascular disease and also cause them to restrict their salt intake. This leads to an issue called reverse causation. When people voluntarily lower their sodium intake because of  pre-existing conditions that put them at risk of death, it becomes hard to distinguish between the effects of low sodium on mortality risk versus other underlying health issues that caused people to both reduce sodium and die earlier.

However, the salt defenders have argued that the studies showing linear relationships are using small study samples, thus lacking adequate participants in the low-salt range to be able to detect an association. They further contend that pre-existing conditions that could lead to reverse causation are adequately controlled for in statistical analyses and that misclassifications by single urine sample are random and not systematic. Hence, they claim that, even if imprecise, the formula estimates of sodium intake from a single urine sample generally categorize people into the correct percentile of sodium intake. Salt defenders insist that, at the very least, there is no compelling evidence that sodium intakes below 2.3 g/day are beneficial relative to “moderate” intakes of 2.3-4.5 g/day. A more recent meta-analysis of six prospective cohort studies challenges this argument, however, as it found that within the range of 2 to 6 g/day of sodium there was a dose-response relationship between sodium and cardiovascular disease risk (i.e., each 1 g/day increase in sodium above 2 g/day was associated with increased cardiovascular disease).

Finally, with regard to the effect of low-sodium diets on metabolic health, the evidence is limited. In a meta-analysis of trials testing the effects of low-sodium diets found average increase in insulin levels but not glucose levels was observed when pooling data from randomized crossover trials. However, the authors of that study caution readers to be careful in the interpretation of those results for a number of reasons. First, there was substantial variation across studies in the effect of low sodium on insulin (i.e., some trials observed strong relationships between sodium restriction and insulin and others didn’t). Second, many of the studies lasted only a few days to a week (i.e., short-term studies can’t tell us how sodium restriction would influence insulin levels in the long-term). Third, in many of the trials the low-sodium diet contained less than 1500 mg/day (i.e., less than what current recommendations suggest is adequate intake of sodium). Given insulin’s effect on sodium retention, it is not particularly surprising that insulin might rise in the short-term (just as renin, aldosterone, and adrenaline rise acutely in response to sudden decreases in sodium intake) as the body attempts to regain homeostasis, especially in instances of less-than-adequate sodium intake. But just as the renin decreases as the duration of sodium restriction increases, we might expect insulin to do the same. Unfortunately, there aren’t enough long-term trials testing this to be sure.

In summary, the broader body of literature does not support the claim that keeping sodium within recommended ranges (1500-2300 mg/day) is detrimental to cardiovascular and metabolic health in the general population.

Criterion 1.2. Are the references cited in the book to support the claim convincing?

1 out of 4

The references in The Salt Fix received a score of 1 for claim 2, indicating that they do not provide convincing support for the claim that diets that restrict sodium to recommended ranges of 1500-2300 mg/day are detrimental to cardiovascular and metabolic health.

One problem with the fear-inducing suggestions in the book that salt restriction can increase risk of death is that they are based on studies of people who end up with dangerously low sodium levels in the blood, not because of salt restriction but because of use of thiazide diuretic drugs. As mentioned in section 1.1 of Claim 2, extremely low levels of sodium in the blood, a condition known as hyponatremia, is most commonly observed among elderly or hospitalized patients. There is no strong evidence that the general population keeping sodium between recommended ranges of 1500-2300 mg/day is at risk of hyponatremia unless they have other underlying health conditions, are taking medications that affect water balance, or regularly lose a lot of sodium through sweating.

The Salt Fix points to several observational studies suggesting that consuming less than 2300-2600 mg/day of sodium may increase risk of cardiovascular events and death. Yet each of these studies was followed by a flood of commentary (see string of articles listed under “Comment in” below the abstract of each of the three aforementioned links), many of which were pointing out methodological issues with these studies that raise concerns for their findings of J- or U-shaped relationships between sodium and cardiovascular disease. As mentioned in section 1.1 above, one major source of bias is misclassification of sodium intake due to incomplete collection of 24-hour urine samples, use of only a single 24-hour urine sample, use of only a single morning urine sample, and problems with the mathematical formulas used to estimate “usual” sodium intake from only a single urine sample. It is important to realize that salt intake can vary widely from day to day, so estimating “usual” salt intake from just a single day’s analysis is likely going to misclassify many individuals.

Another major issue is potential reverse causation; this refers to the fact that people in the “low-salt” group could have decided to reduce their salt intake because they were already told they had hypertension or cardiovascular disease; so it’s the disease causing the low salt intake and not low salt intake causing the disease. Other methodological issues that could bias the results of these observational studies include inappropriate adjustment for factors in the causal pathway (i.e., statistical adjustment for blood pressure when that is the pathway through which salt contributes to cardiovascular disease) or incomplete adjustment for potential confounding variables (i.e., not accounting for differences in family history of disease or other dietary and lifestyle factors that may be related to both salt intake and disease or mortality risk). None of these methodological issues or critiques are acknowledged in The Salt Fix.

The few studies cited to support the suggestion that “many” people may experience a rise in blood pressure on salt restricted diets (pg 69) generally used extreme (far below adequate) levels of sodium reduction; tended to be of short duration; were not randomized; and/or in some cases were not purely testing dietary sodium restriction (e.g., also administered furosemide, a drug used to reduce body fluid). Similarly, the meta-analysis cited in The Salt Fix to argue that salt restriction is detrimental for cholesterol levels and heart rate has been criticized for including studies of short duration and rapid, dramatic decreases in salt intake. Short-term studies, especially those with dramatic decreases in salt intake, are not helpful for understanding the long-term health effects of restricting salt intake to recommended levels. This is because sudden and large drops in sodium intake will lead to a decrease in blood volume and activation of the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system. These are compensatory responses of the body to prevent huge reductions in blood pressure, and they can lead to short-term increases in cholesterol and heart rate initially. In the long-term, however, as well as with more gradual changes in salt intake, the body gets used to the new pattern of lower salt intake and the activation of these compensatory mechanisms is less pronounced. Even the authors of the aforementioned meta-analysis cited in the book stated in a later manuscript that there is little evidence that the changes in blood cholesterol observed in short-term studies are permanent. Other researchers have also argued that the small increases in triglycerides and other blood lipids observed with salt restriction were “​​not significant or clinically relevant.”

The cited experimental studies suggesting that salt restricted diets may cause insulin resistance are also limited sources of support because of their short duration (<2 weeks). Moreover, as noted in the meta-analyses of trials cited in the book (and mentioned in section 1.1), there is substantial variability in findings across studies; some studies find elevated insulin and others find no difference in insulin when trial participants were put on sodium-restricted diets. In addition, the very-low-sodium diets used in many of the trials (<50 mmol/day – or 1150 mg/day of sodium) is below what is considered adequate intake. Thus, those studies are not even testing the effects of simply moderating sodium (keeping it below 2300 mg/day) as suggested by dietary guidelines. Certainly none of the cited research has “proven” (pg. 95) that moderately low-salt diets increase insulin levels over the long run.

In summary, the short-duration of many cited studies and the methodological issues of the longer observational studies referenced in The Salt Fix cast doubts on the claim that keeping sodium intake within recommended ranges of 1500-2300 mg/day is harmful to long-term cardiovascular and metabolic health for the general population.

Criterion 1.3. How well does the strength of the claim line up with the strength of the evidence?

1 out of 4

The claim received a score of 1, indicating that the claim is substantially overstated given the available evidence.

It is true that there may be short-term compensatory physiological responses to a sudden drop in sodium intake (especially if drastic) that can lead to temporary elevations in blood lipid concentrations, heart rate, and even an increase in blood pressure. However, these effects are typically not seen for more modest changes in sodium intake and tend not to be apparent after the body has had sufficient time to reach fluid and sodium homeostasis.

As for the studies suggesting that lower intake of salt increases risk of cardiovascular disease and related events or death, there are too many methodological issues and high potential for reverse causation in those studies. More recent studies than those cited in the book suggest that, when sodium intake is measured more reliably and individuals with pre-existing conditions are excluded, there is no evidence that lower sodium intakes (in the adequate range but within recommended thresholds) are related to higher risk of disease or mortality.

Finally, there are too many conflicting results on the effects of low-sodium diets on insulin resistance and a lack of long-term studies to have confidence in claims that metabolic health is adversely affected by salt restriction.

Overall (average) score for claim 2

1 out of 4

Claim 3

Increasing salt intake above recommended thresholds will help reduce sugar cravings and support efforts to lose weight.

Supporting quote(s) and page number(s)

Page 71: “[H]igh salt loads may actually cause the blood vessels to relax.”

Page 72: “Ingesting adequate amounts of salt allows your body to maintain normal blood pressure without having to activate an arsenal of hormones to compensate.”

Page 73: “If someone were to simply consume 3,000 to 5,000 milligrams of sodium per day, those same salt-retaining hormones would stay suppressed. This fact alone is solid evidence that this level of sodium intake places the least stress on the body and is logically the body’s preferred salt consumption zone to maintain homeostasis.”

Page 86: “[E]ven in those who have increases in blood pressures, there are benefits to higher salt intake, such as lower heart rate, reduced insulin levels, more balanced adrenal hormones, and better functioning kidneys, all of which likely outweigh any risk of higher blood pressure.”

Page 96: “[A] high-salt diet has been proven to enhance insulin signaling.”

Page 98: “[I]ncreasing your salt intake, even above what’s generally considered normal intake, may help improve your insulin sensitivity.”

Page 100: [E]ating enough salt to satisfy our salt cravings may just be the key to kicking our sugar cravings for good.”

Page 106: “Those who seem to be consuming extremely high amounts of salt (putting salt on every meal they eat) may unconsciously be protecting their optimum blood volume.”

Page 110-111: “Eating the level of salt that your body drives you to consume, rather than trying to consciously restrict your salt intake, will help ensure that you avoid harms during salt depletion, and by doing so may help prevent problems with sugar and other drugs of abuse.”

Page 125: “[S]odium surplus keeps your salt-retaining hormones down, protecting your body from the resulting wear and tear on vital organs.”

Criterion 1.1. How well is the claim supported by current evidence?

1 out of 4

This claim received a score of 1, indicating that it is not supported by current evidence.

There is no convincing evidence that increasing salt intake will reduce sugar cravings or sugar intake. Research looking at the relationship between salt and sugar intake is based on observational data, which we consider weak evidence because it tends to be heavily biased by other factors. For example, elevated salt consumption may just be an indicator of eating more processed foods or a less healthy diet, making it difficult to isolate the effects of salt.

Current research suggests that higher salt intake tends to coincide with higher consumption of sugar sweetened beverages, but it’s not clear from this research if or how salt intake directly affects sugar cravings and intake. One observational study using cross-sectional data did suggest that sugar intake was higher among those consuming the least amount of sodium. However, such a study can only demonstrate correlations and cannot be used to make inferences on whether it was the salt intake that influenced the sugar intake or vice versa. Futhermore, there is often so much error in self-reported dietary intake and inability to adjust for all of the other dietary and lifestyle factors that may account for patterns in salt and sugar intake that findings from cross-sectional and observational studies should be taken with a grain of salt (pun intended).

Further evidence against the claim is found in studies suggesting that salt can (up to a threshold) increase palatability of food. This could potentially drive increased caloric intake, which would result in weight gain rather than weight loss.

Animal experiments have also suggested that high-salt diets could be associated with increases in body fat, potentially due to high-salt diets stimulating endogenous fructose production and metabolism and inducing leptin resistance (i.e., resistance to the hormone that regulates body fatness).

One human experiment also found that a very high (18 g/day) intake of sodium was associated with elevated levels of ghrelin (the appetite stimulating hormone), which could be another pathway through which high salt intake could encourage overeating. However, it is not clear if more moderate levels of sodium intake would cause the same changes in humans.

These findings provide plausible mechanisms through which elevated salt intake could theoretically promote increased weight and fat storage, but this has no direct relation to sugar craving. Cross-sectional studies consistently report positive relationships between salt intake and risk of overweight and obesity, even when controlling for total energy intake. However, there are few longitudinal studies and randomized controlled trials exploring causal relationships. In other words, the research has yet to demonstrate that a reduced sodium intake will promote weight loss (beyond that caused by greater loss of body water). At the same time, the evidence provides no indication that increasing salt intake will be beneficial for efforts to reduce caloric intake, sugar cravings, or body weight.

Criterion 1.2. Are the references cited in the book to support the claim convincing?

0 out of 4

The book’s references received a score of 0, indicating that they undermine the book’s claim.

The Salt Fix makes the claim that a low-salt diet may cause more fat absorption, The experimental study referenced to support that claim was conducted with mice and found that a high sodium diet led to reduced fat absorption due to reduced digestive efficiency. However, the amount of salt (4% of the weight of their diet) given to mice to induce that effect would be extremely high if using the authors estimation of an average human diet weighing ~ 1.2 g/day: ~48 g/day of salt or ~19.2 g/day of sodium, which is over 8 times the recommended threshold for humans. Moreover, it’s questionable that reduced digestive efficiency is a healthy condition we would want to induce for the sake of weight loss.

The book also cited research suggesting that salt may activate the brain’s reward systems and thereby drive overeating, which could lead to weight gain rather than weight loss.

Overall, the research cited in The Salt Fix points toward sugar being a major contributor to obesity, but it does not demonstrate that low-salt diets worsen the problem.

Criterion 1.3. How well does the strength of the claim line up with the strength of the evidence?

0 out of 4

The claim received a score of 0, indicating that the claim is greatly overstated.

None of the studies cited in the book suggest that low salt intake causes increased sugar intake or weight gain. If increased salt intake were the solution to weight loss and reduced sugar cravings, we would not have the high and growing prevalence of obesity and metabolic disease that we have worldwide because most of us consume more than the recommended salt intake already. Salt increases palatability of food, making it easier to overeat; it is therefore more likely that salt would contribute to weight gain than to weight loss.

Overall (average) score for claim 3

0.3 out of 4

Overall (average) score for scientific accuracy

0.8 out of 4

Reference 1

Reference

Chapter 4, reference 76. Rocchini et al. The effect of weight loss on the sensitivity of blood pressure to sodium in obese adolescents. N Engl J Med. 1989;321(9):580-585.

Associated quote(s) and page number(s)

Page 78: “Another 1989 study found that obese teenagers who lost 8 percent of their starting weight were able to correct their salt-sensitive blood pressure.”

Criterion 2.1. Does the reference support the claim?

3 out of 4

This reference received a score of 3, indicating that it offers moderate support for the claim. This was an experimental study with two components. The researchers first examined changes in blood pressure and other health measures on 2 weeks of a high sodium (5750 mg/day) followed by 2 weeks on a low-sodium (<690 mg/day) in adolescents (10-16 years old) with obesity (n=60) and without obesity (n=18). They found that lowering sodium intake led to significant reductions in blood pressure. They then put the adolescents with obesity on a 20-week weight loss diet. Of the 51 adolescents who completed the weight-loss program, 36 lost at least 1 kg of weight. Those who lost at least 1 kg of weight saw no difference in blood pressure when then put on the same sequence of a high-sodium followed by a low-sodium diet, whereas the 15 adolescents who lost no weight did continue to see a difference in blood pressure when on a low-sodium diet.

So this reference in general provides strong support for the overall argument that weight loss might reduce the sensitivity to sodium’s potential effects on blood pressure. The reason this did not receive full points is only because the claim makes it sound like all adolescents lost 8% of their body weight or like that percent of body weight was the threshold beyond which an improvement in salt-sensitivity was observed. Yet the minimal blood pressure change in response to sodium restriction was reported for the group of 36 adolescents who lost at least 1 kg. Those 36 lost an average of 7.5 kg, which is 8% lower than the average starting weight of 92.7 kg among the group of 60. But some lost less body weight and some more, and it’s not clear from this study what percentage of body weight loss would be associated with improvements in salt sensitivity.

Reference 2

Reference

Chapter 4, reference 117.  Harsha et al. Effect of dietary sodium intake on blood lipids: results from the DASH-sodium trial. Hypertension. 2004;43(2):393-398. 

Associated quote(s) and page number(s)

Page 87: “Even the famous DASH-Sodium trial-the foundation of the most well-known low-salt diet-found that salt restriction increased triglycerides, LDL, and the total-cholesterol-to-high-density-lipoprotein ratio (TC:HDL).”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2, indicating that it offers weak support for the author’s claim.

The DASH-Sodium Trial was a multicenter, randomized controlled feeding trial that compared three levels of sodium intake (“high” of 3450 mg/2100 kcal, “intermediate” of 2300 mg/2100 kcal; or “low” of 1150 mg/2100 kcal) among study participants randomized to either the DASH diet (emphasizing fruits, vegetables, whole grains, low-fat dairy, nuts, poultry, and fish and restricting red meat, sweets, fats, and sugar-sweetened beverages) or “control” diet modeled off of a typical American diet. The study cited was conducted with adults who had either prehypertension or stage 1 hypertension. All participants started by consuming the same high-sodium control diet for 2 weeks. They were then randomized to consume either the the DASH diet (n=197) or control diet (n=193), eating high, intermediate, and low-sodium versions of each diet for 30 consecutive days in randomized order. Energy intake was adjusted for each participant to maintain body weight throughout the study.

The authors of the cited study reported no significant effect of dietary sodium on total cholesterol, LDL cholesterol, HDL cholesterol among participants consuming either the DASH diet or the control diet. Triglycerides were only slightly higher (by 0.06 mmol/L or 5.3 mg/dL) in the low- relative to high-sodium version of the conventional American diet but this difference was neither statistically significant nor deemed clinically relevant. There was no impact of sodium intake on triglycerides among those consuming the DASH diet. Likewise, among those consuming the conventional American diet, the total cholesterol-to-HDL cholesterol ratio was slightly higher (4.63) in the lower sodium group compared with the intermediate (4.53) and high sodium (4.53) groups. But because there was no clear dose-response relationship and because neither total or HDL cholesterol changed significantly, the authors expressed doubt that this difference in the cholesterol ratios in the control group was clinically relevant.

Reference 3

Reference

Chapter 4, reference 110. DiNicolantonio et al. The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease. Prog Cardiovasc Dis. 2016;58(5):464-472.

Associated quote(s) and page number(s)

Page 86: “Yudkin was able to show over and over again that numerous abnormalities found in patients with coronary heart disease (elevated lipids, insulin, and uric acid and abnormal platelet function) could be caused by just a few weeks on a high-sugar diet.”

Criterion 2.1. Does the reference support the claim?

3 out of 4

This reference received a score of 3, indicating that it offers support for the claim. However, it was not the primary literature by Yudkin, the author to which this claim refers, that was cited here. Instead, the article cited is a review article written by the author of The Salt Fix; the article reviews the literature on the role of sugar and saturated fat in coronary heart disease.

Reference 4

Reference

Chapter 8, reference 5. McCarty and DiNicolantonio. The cardiometabolic benefits of glycine: Is glycine an ‘antidote’ to dietary fructose?. Open Heart. 2014;1(1):e000103.

Associated quote(s) and page number(s)

Page 169: “Consuming 5 grams of glycine (preferably in powder form mixed with water) three times daily thirty to forty-five minutes prior to meals may help reduce high blood pressure, improve fatty liver disease, and drop a few extra pounds of fat.”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2, indicating that it offers weak support for the claim. The reference is an editorial, co-authored by the author of this book, that reviews some of the research on the potential benefits of glycine on cardiometabolic health. The paper cites a randomized controlled trial that observed a decrease in systolic blood pressure among male (and not female) study participants randomized to consume 15 grams of glycine per day for three months. Most of the research discussed in the paper on the topic of glycine in relation to fat loss or fatty liver disease was conducted with rodents, which we would consider a weak form of evidence for making claims on supplementation for human health.

Reference 5

Reference

Chapter 3, reference 24. Kempner. Treatment of hypertensive vascular disease with rice diet. Am J Med. 1948;4(4):545-577. 

Associated quote(s) and page number(s)

Page 36: “[Dr. Kempner’s] analysis of his case reports suggested that a low-salt diet, consisting mainly of rice and fruit, was effective in treating most of his patients who had malignant hypertension, chronic kidney disease, and even diabetes.”

Criterion 2.1. Does the reference support the claim?

4 out of 4

This reference received a score of 4, indicating that it offers strong support for the claim. This reference is cited multiple times in The Salt Fix as part of the historical backdrop to the low-salt recommendations that are purportedly flawed, according to the book. Indeed, Dr. Kempner in this referenced article discusses an extremely restricted “rice diet” consisting of primarily rice and fruit and allowing no more than 200 mg of chloride and 150 mg of sodium. This paper reports primarily on the blood pressure lowering observed on the rice diet in patients with hypertension, but it also discusses previous publications on the therapeutic effects of the rice diet for diabetes and chronic kidney disease.

Reference 6

Reference

Chapter 1, reference 2. Overlack et al. Divergent hemodynamic and hormonal responses to varying salt intake in normotensive subjects. Hypertension. 1993;22(3):331-338.

Associated quote(s) and page number(s)

Page 9: “[E]ven among those with full-blown hypertension, about 55 percent are totally immune to salt’s effects on blood pressure.”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2, indicating that it offers weak support for the claim. This may in part be due to poor placement of the reference. This article is in reference to a study examining low- and high-salt intakes in normotensive patients. The sentences that precedes the sentence to which this reference is attached states, “[E]vidence in the medical literature suggests that approximately 80 percent of people with normal blood pressure (less than 120/80 mmHg) are not sensitive to the blood-pressure-raising effects of salt at all [sic]. Among those with prehypertension (a precursor to high blood pressure), roughly 75 percent are not sensitive to salt.”

This reference does support the preceding sentence that approximately 80 percent of people with normal blood pressure may not be overly sensitive to salt – at least in the short-term. In this randomized crossover single-blind study with 163 adults without obesity or high blood pressure, only 18.4% experienced a rise of >5 mmHg in mean arterial pressure when receiving capsules with 300 mmol (6900 mg) of sodium each day for 7 days. It would be inappropriate, however, to assume that a lack of a substantial blood pressure rise in response to only a week of eating a high-salt diet would necessarily translate into a lack of response to a long-term high-salt diet. As mentioned in the section on scientific accuracy, there is evidence to suggest that people can become salt sensitive over time with chronically high salt intake.

However, the other sentences about salt sensitivity among those with pre-hypertension and hypertension are presumably based on the discussion section of the referenced paper. The discussion mentions a previous study that categorized 51% of their hypertensive patients as salt-sensitive (but 26% of their normotensive patients as salt sensitive). They say that in other smaller studies, approximately 50% of hypertensive patients tend to be classified as salt-sensitive. The suggestion that “roughly 75 percent” of people with prehypertension are not salt-sensitive is perhaps based on the statement in the discussion of the referenced paper that, “With a study protocol similar to ours…salt sensitivity was found in 29.2% of 65 borderline hypertensive subjects.” It is not clear exactly which of the studies cited in the discussion of the referenced paper support the claim that 55% of those with hypertension are “totally immune to salt’s effects on blood pressure.” Moverover, the claim of “totally immune” cannot be supported by trials of short duration, and lack of an increase in blood pressure greater than 5 mmHg (the threshold used to define salt-sensitivity in the cited studies) does not mean there was no increase in blood pressure. Furthermore, the referenced article suggests that there are other factors that may influence how someone responds to an acute increase in salt intake (e.g., excess body weight and elevated insulin).

Reference 7

Reference

Chapter 2, reference 48. Moinier BM, Drüeke TB. Aphrodite, sex and salt–from butterfly to man. Nephrol Dial Transplant. 2008;23(7):2154-2161. 

Associated quote(s) and page number(s)

Page 29: “One of salt’s most intriguing properties is its importance for many facets of reproduction – from sexual desire and procreation to gestation and lactation…”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2, indicating that it offers weak support for the claim. There is no doubt that sodium, an essential nutrient for all life, would also be important for reproduction. However, the review article cited is not overwhelmingly informative on the role of different levels of sodium intake on different facets of reproduction in humans. Most of the research it reviewed in the referenced article comes from animal studies, which may not be generalizable to humans. The article also makes statements that appear more speculative than based on science. For example, it states that, “[F]ertility [among Yanomamo Indians of Northern Brazil] is low, with an average of only one live birth every 4–6 years despite the continuous exposure to the risk of pregnancy. This is possibly in relation with lifelong low salt intake and corresponding hormonal adjustments including elevated serum renin and aldosterone levels.” The problem with this statement is that there are many possible reasons why Yanomamo might have lower fertility. For example, infectious diseases, intestinal parasites, and lactational amenorrhea because of long breast feeding periods. Studies among Yanomamo cannot isolate sodium as the single nutrient contributing to this phenomenon.

Reference 8

Reference

Chapter 5, reference 26. Xavier AR, Garófalo MA, Migliorini RH, Kettelhut IC. Dietary sodium restriction exacerbates age-related changes in rat adipose tissue and liver lipogenesis. Metabolism. 2003;52(8):1072-1077.

Associated quote(s) and page number(s)

Page 96: “Researchers found that the activity of brown adipose tissue─the ‘good fat’ that burns calories─was reduced on a low-salt diet, indicating that low-salt diets may lower our basal metabolic rate, and possibly contribute to accelerated aging.”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2, indicating that it offers weak support for the claim. It is important to note that the study cited was conducted in rats just recently weaned. The researchers did indeed find that “chronic administration of [a low-salt diet] to rats [during the first three months post weaning] causes an excessive accumulation of fat that is accompanied by increases in liver lipogenesis and in the activity of white adipose tissue LPL and by a reduction in [brown adipose tissue] thermogenic capacity. The data suggest that sodium restriction exacerbates normal, age-related, developmental changes in lipid metabolism, and that the accumulation of body fat probably results from increases in the uptake of preformed fatty acids from the circulation and in the organism metabolic efficiency.”

However, this age range in rats would be comparable to the age range of early childhood through adolescence and early adulthood. Thus, as the authors note, the changes observed cannot necessarily be seen as accelerated aging but rather as a change in the developmental growth process. Moreover, it’s not clear how the low-salt diet of 0.06% for rats compares to the levels of salt consumed by humans trying to reduce salt intake. Overall, this study does not provide strong evidence that a low-salt diet in humans would lead to reduced basal metabolic rate and accelerated aging, and we would need to qualify what level of reduced salt (and for what period of time and at what stage in life) would potentially lead to such issues.

Reference 9

Reference

Chapter 6, reference 23 (second of two citations for this reference). Wald N, Leshem M. Salt conditions a flavor preference or aversion after exercise depending on NaCl dose and sweat loss. Appetite. 2003;40(3):277-284.

Associated quote(s) and page number(s)

Page 108: “[O]nce [salt depletion] is corrected, inhibitory signals will turn off the ‘liking’ for salt and turn on an ‘aversion’ signal.”

Criterion 2.1. Does the reference support the claim?

2 out of 4

This reference received a score of 2, indicating that it offers weak support for the claim. What this study demonstrated was that reportedly liking a root beer flavored beverage (purportedly a novel flavor for the Israeli university students in this study) consumed following 90-minute aerobic or basketball sessions was lower across time among young adults who both sweated the least and received capsules with 600 mg of sodium along with the beverage. In contrast, the self-rated liking of the beverage was higher among those who either took lower doses of encapsulated sodium or who tended to sweat more during the exercise sessions. The comparisons were made across different individuals as opposed to comparing how the same individuals’ preference or aversion to salt changed in response to their sodium levels. Also, participants were not even tasting the salt that they were taking in capsule form along with the beverage, so this study isn’t exactly testing the liking of or aversion to the salt flavor in relation to salt depletion.

Reference 10

Reference

[Chapter 4, reference 69. Pazarloglou M, Spaia S, Pagkalos E, Ioannidis H, Askepidis N, Varyemezis V. Evaluation of insulin resistance and sodium sensitivity in normotensive offspring of hypertensive individuals. Am J Kidney Dis. 2007;49(4):540-546.

Associated quote(s) and page number(s)

Page 76: “Those same people [who are believed to be genetically susceptible to salt] were found to have increased insulin resistance, and their degree of insulin resistance was also associated with increased mean arterial pressure.”

Criterion 2.1. Does the reference support the claim?

1 out of 4

This reference received a score of 1, indicating that it does not support the claim. This was a very small study conducted with 20 participants with a family history of hypertension and 10 participants with no family history of hypertension. Participants were given a standard diet containing 250 mmol (5750 mg) of salt/day for 7 days followed by the same diet with only 50 mmol (1150 mg) of salt/day for 7 days. Mean arterial pressure was measured, and a drop of 3+ mmHg between the high- and low-salt conditions was used to define salt-sensitivity.

The study found a similar proportion of individuals with salt-sensitivity among those with and without a family history of hypertension, and there was no relationship between salt-sensitivity and insulin resistance in their sample of 30 participants. These findings undermine the first part of the claim.

However, the study did report a trend toward higher mean arterial pressure among those with insulin resistance and a family history of hypertension; this finding was based on only 9 out of the 20 having insulin resistance. No such relationship was noted in those without a family history of hypertension, but that may also be because only 2 out of the 10 people in that group had insulin resistance.

This study is small and inconclusive and provides only weak support, at best for the latter part of the claim; it undermines the first part of the claim.

Overall (average) score for reference accuracy

2.3 out of 4

Summary of the health-related intervention promoted in the book

The key recommendation of The Salt Fix is to “giv[e] in to your innate, natural [salt] cravings” (pg 159) and eat as much salt as desired but strictly limit all sugars and refined carbohydrates. The book suggests that most people’s innate craving for sodium will lead to an intake of 3,000-5,000 mg/day (pg 170); the upper limit of sodium recommended in the book is 6 g/day (pg 162), which is 15.2 g/day or 2.5 teaspoons of salt. In contrast, the book suggests that added sugars be limited to no more than 30 g/day (pg 162) and ideally less than 20 g/day (pg 163), which is about 5 teaspoons of sugar.

In addition to listing all the “higher-nutrient” salts that can be added liberally to enhance the flavor of vegetables, meat fish, beans, legumes, nuts, and seeds, readers are told they can dig into the salted nuts, cured meats, olives, anchovies, aged cheeses, pickles, seaweed, and other whole salted foods. Ultra-processed foods should be avoided, however. Also, because the book recommends a variety of non-iodized salts, it suggests getting iodine from other food sources (e.g., seaweed, sushi, daily, and eggs).

To limit sugars, readers are advised to avoid sugar-sweetened beverages and juices. The book advises readers to become familiar with all the names sugar can take, read ingredient labels, and avoid foods with high amounts of hidden added sugars. The intervention also includes avoiding refined carbohydrates (e.g., white rice, pasta) and starchy vegetables (e.g., white potatoes – unless eaten slightly undercooked and cooled to optimize their resistant starch levels, p. 166-167) and eating barely ripe fruit (i.e., lower sugar content than ripe fruit) to satisfy sugar cravings.

Condition targeted by the book, if applicable

The conditions targeted by The Salt Fix include cardiovascular and metabolic diseases, including obesity, hypertension, diabetes, and heart disease. The book also promises that the program recommended will help people to “enjoy more energy, fewer infections, improved sexual and athletic performance, and faster metabolism.” (pg 159-160)

Apparent target audience of the book

The target audience of The Salt Fix is anyone who is currently eating a low-salt diet, or thinking about it.

Criterion 3.1. Is the intervention likely to improve the target condition?

1 out of 4

The intervention received a score of 1, indicating that the program is likely to have neutral effects on the target conditions in the medium-to-long-term relative to a typical diet.

Typical modern diets in the United States and globally already exceed dietary guidelines to limit sodium to less than 2,300 mg/day. So it is possible that the suggestions in The Salt Fix to consume 3,000-5,000 mg/day may not lead to drastic increases in salt above typical intake for most people. But the data suggest that a reduction in blood pressure without reducing salt intake would only be expected if there were a major shift to an overall better dietary quality, an increase in potassium intake, or weight loss. So it may be possible to experience small improvements in hypertension, and thereby cardiovascular disease risk, following the dietary recommendations in The Salt Fix if salt really were at least kept at moderate levels and just used as a vehicle to eat more potassium- and fiber-rich foods (e.g., vegetables, nuts, beans, and whole grains) while following the advice to avoid sugar (especially added sugar), refined grains, and the ultra-processed salty foods. This is especially the case if cutting added sugars from one’s baseline diet leads to an overall reduction in calories and potential weight loss. There is evidence that the removal or reduction of sugar-sweetened beverages and added sugars, major sources of added calories in the diet, could be advantageous for losing weight and preventing the development of hypertension, metabolic syndrome, and type 2 diabetes.

That said, it’s always easier to follow advice to add something to the diet (especially something as taste-enhancing as salt) than to remove things from the diet (especially tasty sugars and processed foods). So it’s easy to imagine scenarios in which people may follow the first pieces of advice to eat salt liberally without being as strict about the advice on cutting added sugars, refined carbohydrates, and processed foods. In a scenario in which more salt is consumed with an otherwise potassium-poor diet, especially if someone is not salt depleted and/or has any pre-existing health conditions, the science suggests that this program runs the risk of worsening cardiovascular health. There is certainly no convincing evidence that adding salt to the diet without reducing intake of added sugars and refined grains will benefit metabolic health. Furthermore, if someone is already or considering following a salt restricted diet in order to control their blood pressure but becomes inspired to add salt to their diet after reading The Salt Fix, they would be increasing their risk of hypertension and heart disease.

In summary, the book’s advice to reduce or eliminate added sugars and refined carbohydrates and eat more whole, minimally processed, and potassium-rich foods is healthful and likely to benefit metabolic and cardiovascular health. But the advice to eat salt liberally is likely not beneficial for blood pressure or heart health and could actually be quite harmful; the effects of increased salt intake on metabolic health remain unclear.

Criterion 3.2. Is the intervention likely to improve general health in the target audience?

1 out of 4

This intervention received a score of 1, indicating that it is likely neutral for general health in the medium-to-long-term.

The evidence does not point to a benefit in general health by simply adding more salt to the diet. The only cases in which added salt may be beneficial is if someone falls into the uncommon category of having frequent bouts of hyponatremia as a result of taking medications or having underlying genetic or health conditions that cause an increase in water retention and/or sodium excretion or are on an extremely limited/bland (e.g., “tea and toast”) diet.

At the same time, benefits to general health might be expected from following the book’s advice to restrict added sugars and refined grains. The research generally suggests that lower intake of added sugars (particularly sugar-sweetened beverages), refined grains, and ultra–processed foods is associated with lower risk of developing the target conditions listed above (obesity, hypertension, metabolic and cardiovascular diseases).

Therefore, it is possible that the healthful changes of eating less sugar and fewer refined foods could offset the unhealthful changes of increasing salt intake, but it is unclear that such a dietary change would necessarily have a net benefit to general health.

Criterion 3.3. Does the diet portion of the intervention promote an adequate nutrient intake for general health in the target audience?

3 out of 4

The diet received a score of 3, indicating that it is likely more than nutritionally adequate.

The book’s promotion of whole foods over processed foods and encouragement to increase intake of fruits, vegetables, nuts, dairy, and seafood should help ensure nutritional adequacy and higher diet quality, especially compared with a typical modern diet.

Overall (average) score for healthfulness

1.7 out of 4