The Meaning of the Word Salt
Original Himalayan crystal salt contains all the elements of which the human body is comprised. From the periodic table of elements we are familiar with 94 natural elements (stable as well as unstable).
Apart from inert gases, all of the elements (84) can be found in crystal salt. Hence crystal salt contains all natural minerals and trace elements that are found in the human body. We perceive crystal salt as being the totality of all natural elements. This may not be entirely correct according to chemistry; however we will continue to use the term crystal salt in this context. The number of the respective elements contained in the crystal salt is biophysically irrelevant to this study.
The word salt comes from the Latin term sal, which again comes from the word sol. Sol is synonymous with the “Sole, the water and salt solution and is the Latin word from sun. Mythologically, and from its definition, sole means “liquid sunlight,” the liquid materialization of the sun’s energy, liquid light energy, bound into a geometrical structure, capable of creating and sustaining life. This literally explains where life on Earth came from: from the sole of the primal oceans.
THE SALT FIX (Dr. James DiNicolantonio)
”Consider Scandinavian novelist Isak Dinesen’s famous line, “The cure for anything is salt water: sweat, tears or the sea.”
There’s poetic truth in this, but it also speaks to our biological reality as humans. Our physical inner world was born of the sea, and we carry the saltiness of the ocean inside us. Salt is an essential nutrient that our body depends on to live. Its proper balance is an equilibrium that our bodies strive to return us to, again and again.
But over the past century, our culture has defied this biological drive, has smeared the urge for salt as a self-destructive “addiction.” We’ve all heard the guidelines. We know that we’re supposed to eat low-saturated-fat diets, say no to cigarettes, go for a jog, learn to relax—and dramatically cut down on salt. This list of admonishments certainly gets a lot of things right. But there’s one big problem with it: most of us don’t need to eat low-salt diets. In fact, for most of us, more salt would be better for our health rather than less.
Meanwhile, the white crystal we’ve demonized all these years has been taking the fall for another, one so sweet that we refused to believe it wasn’t benign. A white crystal that, consumed in excess, can lead to high blood pressure, cardiovascular disease, and chronic kidney disease: not salt, but sugar.
Thankfully, the mainstream press is starting to catch on that sugar is a wolf in sheep’s clothing, with low-sugar diets rising in popularity every day. And even fat has been getting a fresh look, as we’re now encouraged to seek out the beneficial kinds in fatty fish, avocados, and olives.
So why do we still see labels on salty foods that make the saltshaker look downright toxic? Why do we keep reading fearmongering headlines about salt in mainstream, reputable media, like these?
Eating Too Much Salt Is Killing Us by the Millions
—Forbes, March 24, 2013
1.6 Million Heart Disease Deaths Every Year Caused by Eating Too Much Salt
—Healthline News, August 14, 2014
”The truth is, our most hallowed health institutions cling to outdated, disproven theories about salt—and their resistance to the truth is putting our public health at risk. Until the low-salt dogma is successfully challenged, we’ll be stuck in this same perpetual loop that keeps our bodies salt-deprived, sugar-addicted, and ultimately deficient in many critical nutrients. Many of us will continue struggling with insatiable hunger and hold on to weight around the middle despite following recommended lifestyle changes.
If you’re diligent about your health, you may have been struggling to achieve the low-salt guidelines that limit you to 2,300 milligrams of sodium (basically 1 teaspoon of salt) per day—or even 1,500 milligrams (⅔ teaspoon of salt) if you are older, are African American, or have high blood pressure. Indeed, according to the Centers for Disease Control and Prevention (CDC), more than 50 percent of people in the United States are currently monitoring or reducing their sodium intake, and almost 25 percent are being told by a health professional to curb their consumption of sodium.
If you are among them, you may have been buying less-tasty “low sodium” versions of your favorite foods. You may feel a twinge of guilt when you sneak a handful of your partner’s popcorn at the movies. You may have picked olives out of your salad and ignored every recipe’s call to “salt to taste.” Perhaps it’s been years since you’ve had a warm, salty pretzel or a bowl of satisfying puttanesca, full of savory capers, out of fear of those evil grams of sodium.
You may have been mightily struggling to restrict yourself, not knowing that your salt cravings are totally, biologically normal, akin to our thirst for water. Scientists have found that across all populations, when people are left to unrestricted sodium consumption, they tend to settle in at 3,000 to 4,000 milligrams of sodium per day. This amount holds true for people in all hemispheres, all climates, all range of cultures and social backgrounds—when permitted free access to salt, all humans gravitate to the same threshold of salt consumption, a threshold we now know is the sodium-intake range for optimal health.
Your body has been talking to you, and it’s time to listen. The good news is, you probably don’t need to cut down. In fact, you may need even more salt. Instead of ignoring your salt cravings, you should give in to them—they are guiding you to better health.
In these pages, I’m going to set the record straight and upend everyday myths about the supposed negative effects of salt. I’ll tell the story of how humans evolved from the briny sea, how our biology shapes our taste for salt—and how this taste is actually an unfailing guide. I’ll tell the story of the Salt Wars of the Salt Wars of the past century—the varying dietary guidelines that have led us so far astray. I’ll explain how our essential physiological need for salt is increased by the demands of modern life and how we’re actually at a greater risk for salt depletion than ever before. (Two-thirds of the world’s population now struggles with three or more chronic health conditions, many of which increase the risk of low salt levels in the body.) I’ll talk about how many commonly prescribed medications, beloved caffeinated beverages, and widely touted dietary strategies actually promote salt depletion. I’ll examine how many of the negative health effects that have been blamed on salt are really due to excess sugar consumption—and how eating more salt can be instrumental in breaking the sugar addiction cycle.
Along the way, I’ll also include recommendations for how to use salt to improve your exercise performance and increase muscle gain, and how not to fall short in crucial iodine. I’ll give specific recommendations on how to strategically increase your intake of the right kinds of salt, in the amounts your body needs (because some people need more salt than others). You’ll learn how eating the salt your body desires can improve everything from your sleep, energy levels, and mental focus to your fertility and even sexual performance. Finally, I will cover numerous medications, disease states, and lifestyle choices that lead to salt wasting, so you can have a better idea if you are at risk of salt deficit.
As I share these findings, you’ll also hear stories from many people, including those struggling with chronic diseases, such as high blood pressure, heart failure, obesity, or kidney disease, and hard-charging elite athletes looking for a competitive advantage. You’ll hear about how eating certain kinds of salt—or simply giving in to salt cravings—helped these people feel healthier, have more energy, improve athletic performance, resolve long-standing chronic conditions, and even lose weight. People such as AJ, a man in his early thirties with hypertension who’d been advised to reduce his salt intake—but found his blood pressure unchanged, his energy levels plummeting, and vicious headaches recurring. It was only after AJ reintroduced salt—as much as he wanted—while he reduced his carbohydrate intake that the headaches stopped, he lost 65 pounds, and he reduced his blood pressure by eighty points. (See AJ’s full story on this page.) And then, finally, in the last chapter of the book, I’ll pull all of these lessons together and spell out five simple steps to tap into your instinct for salt, get more of the healthiest types of salt, and reverse years of salt imbalances in your body.
In hearing the story about the power of salt, you may find yourself as baffled as I am by the continued resistance to the clear research findings. I’ll examine the forces behind this stubborn refusal to accept the truth—and prove that the time for adherence to this long-outdated dogma has come to an end. We need to recognize that science has moved on, and our dietary guidelines need to move on as well. In the names of our hearts, our health, and our happiness, we need to help salt reclaim its rightful and vital place on our table. Simply put, our lives and happiness depend on it.
ADD SALT, REMOVE POUNDS
When my friend Jose Carlos Souto, MD, first treated AJ, he was obese and hypertensive (220/170 mmHg), and had frequent headaches. According to the standard recommendation, AJ had tried to reduce his salt consumption, thinking it would improve his health. Soon thereafter, he began to feel tired all the time and had started to develop unexplained chills every now and then—and his blood pressure remained high. Dr. Souto decided to try another approach—he advised him to go on a low-carb diet and to start eating the amount of salt his body craved. Almost immediately, his energy returned and his chills disappeared. His headaches reduced dramatically. And while his blood pressure remained high for a while, as he began to lose weight, his blood pressure declined at the same time. A year later, he had lost 65 pounds—and, lo and behold, his blood pressure stabilized at 140/90 mmHg, without any medications.
Mutta eikö suola nosta verenpainetta?
For more than forty years, our doctors, the government, and the nation’s leading health associations have told us that consuming salt increases blood pressure and thus causes chronic high blood pressure.
Here’s the truth: there was never any sound scientific evidence to support this idea. Even back in 1977, when the government’s Dietary Goals for the United States recommended that Americans restrict their salt intake, a report from the U.S. Surgeon General admitted there was no evidence that a low-salt diet would prevent the increases in blood pressure that often occur with advancing age.1 The first systematic review and meta-analysis of the effects of sodium restriction on blood pressure did not occur until 1991, and it was almost entirely based on weak, nonrandomized scientific data—but by then, we had already been telling Americans to cut their salt intake for nearly fifteen years. By that point, those white crystals had already been ingrained into the public’s mind as a primary cause of high blood pressure—a message that remains today.
The advice stemmed largely from the most basic of scientific explanations: the “salt–blood pressure hypothesis.” This hypothesis held that eating higher levels of salt leads to higher levels of blood pressure—end of story. But that wasn’t the full story, of course. As with so many old medical theories, the real story was a bit more complex.
The hypothesis went like this: In the body, we measure blood pressure in two different ways. The top number of a typical blood pressure reading is your systolic blood pressure, the pressure in your arteries during contraction of your heart. The bottom number is your diastolic blood pressure, the pressure in your arteries when your heart is relaxed. When we eat salt, so the theory goes, we also get thirsty—so we drink more water. In the salt–high blood pressure hypothesis, that excess salt then causes the body to hold on to that increased water, in order to dilute the saltiness of the blood. Then, the resulting increased blood volume would automatically lead to higher blood pressure.
”That’s the theory, anyway. Makes sense, right?
All of this did make sense, in theory, and for a while there was some circumstantial evidence supporting this claim. Data was gathered on salt intake and blood pressures in various populations, and correlations were seen in some cases. But even if those correlations were consistent, as we all know, correlation does not equal causation—just because one thing (salt) may sometimes lead to another thing (higher blood pressure), which happens to correlate with another thing (cardiovascular events), that does not necessarily prove that the first thing caused the third thing.
Sure enough, data that conflicted with the salt–blood pressure theory continued to be published right along with data that supported it. A heated debate raged in the scientific community about whether salt induced chronically elevated blood pressure (hypertension) versus a fleeting, inconsequential rise in blood pressure, with advocates and skeptics on both sides. In fact, compared to any other nutrient, even cholesterol or saturated fat, salt has caused the most controversy. And once we got on that salt–high blood pressure train, it was hard to get off. Governments and health agencies had taken a stance on salt, and to admit that they were wrong would cause them to lose face. They continued the same low-salt mantra, refusing to overturn their premature verdict on salt until they were presented with overwhelming evidence to the contrary. No one was willing to get off the train until there was definitive evidence that their presumptions were wrong—instead of asking, “Did we ever have any evidence to recommend sodium restriction in the first place?”
We believed so strongly in sodium restriction because we believed so strongly in blood pressure as a metric of health. Low-salt advocates posit that even a one-point reduction in blood pressure (if translated to millions of people) would actually equal a reduction in strokes and heart attacks. But evidence 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. Among those with prehypertension (a precursor to high blood pressure), roughly 75 percent are not sensitive to salt. And even among those with full-blown hypertension, about 55 percent are totally immune to salt’s effects on blood pressure.
That’s right: even among those with the highest blood pressure, about half are not at all affected by salt.
The stringent low-salt guidelines were based on a guess: we essentially gambled that the small benefits to blood pressure that we see in some patients would extend to large benefits for the whole population. And while taking that gamble, we glossed over the most important point: why salt may increase blood pressure in some people but not in others. Had we focused on that, we would’ve realized that fixing the underlying issue—which has nothing to do with eating too much salt—completely fixes one’s “salt sensitivity.” We also presumed that blood pressure, a fleeting measurement known to fluctuate depending on many health factors, was always impacted by salt. And because of that baseless certainty, we presumed that overconsumption of salt would logically result in dire health outcomes, such as strokes and heart attacks.
Our mistake came from taking such a small sample of people—unethically small!—and wildly extrapolating their benefits from low-salt eating without ever mentioning the risks. Instead, we 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 our risk of heart disease—such as increased heart rate; compromised kidney function and adrenal insufficiency; hypothyroidism; higher triglyceride, cholesterol, and insulin levels; and, ultimately, insulin resistance, obesity, and type 2 diabetes.
You start craving sugar and refined carbs like crazy, because your body believes carbohydrate is your only viable energy source. And, as the now-familiar story goes, the more refined carbs you eat, the more refined carbs you tend to crave. This overeating of processed carbs and high-sugar foods virtually ensures fat cell accumulation, weight gain, insulin resistance, and eventually type 2 diabetes.
What’s clear is that we have been focusing on the wrong white crystal all along. We demonized sodium before we had the evidence. And our health has been paying the price ever since. Had we left salt on the table, our health problems in general—and especially those pertaining to sugar—might be a little less dramatic.
It’s time to set the record straight. It’s time to drop the guilt, grab the shaker, and enjoy salt again!
”That experience prompted me to take a deeper look into the low-salt guidelines. The deeper I looked, the more I could see that maybe the advice we had been giving people, to cut their salt intake, wasn’t correct after all. Around the same time, in 2013, I took a position as a cardiovascular research scientist at Saint Luke’s Mid America Heart Institute. After joining Saint Luke’s, I published nearly two hundred medical papers in the scientific literature, many relating to the impact of salt and sugar on health. Based on these academic publications, that same year I was offered a position as the associate editor of BMJ Open Heart, an official journal of the British Cardiovascular Society.
In total, I’ve spent nearly a decade examining the research on salt and working with clinicians to untangle the complexity of our salt intake and get to the heart of the issue. Should we do away with these outdated restrictions? Who really needs less salt—and who needs more? How much—and what kinds—are optimal? And perhaps most exciting, how might increasing our salt intake actually help us turn back the tide of obesity and stem the rising epidemic of type 2 diabetes that threatens to overwhelm our nation, and the entire world?
”Low salt is miserable.
Low salt is dangerous.
Our bodies evolved to need salt.
Low-salt guidelines are based on inherited “wisdom,” not scientific fact.
All the while, the real culprit has been sugar.
And finally: salt may be one solution to—rather than a cause of—our nation’s chronic disease crises.
Your body drives you to eat several grams of salt (around 8–10 grams, equal to 3,000–4,000 milligrams of sodium) every day to remain in homeostasis, an optimal state in which you put the least amount of stress on the body. But you could literally live the rest of your life—and probably a much longer one—if you never ingested another gram of added sugar.
Now, I understand that it will take a bit of time to unlearn years of indoctrination about the evils of salt—which is why I wrote this book. In these chapters, you’ll learn the entire story. (By the end, in chapters 7 and 8, you will find specific recommendations for how you can find and implement your ideal salt intake.) But that understanding begins with reeducation about the myriad ways our lives can be healthier, stronger, and longer when we welcome salt back into our lives.
If salt has always played such a fundamental role in human health, how did we ever begin to doubt it? Perhaps salt’s ubiquity was one of the factors in its downfall; perhaps we simply took it for granted. In order to understand how we could have gone so far off course, we first have to understand the critical role salt has always played in human health, from the moment life slithered out of the sea right up until the birth of modern medicine. By looking closely at salt’s crucial role in our past, we can start to restore its tarnished reputation and honor salt’s place in our future.
We cry salt, we sweat salt, and the cells in our bodies are bathed in salty fluids. Without salt we would not be able to live.
Just a small dash of salt can take a bland dish and heighten all of its flavors, making it taste extraordinary. Salt knocks out bitterness and makes food taste sweeter, reducing the need for sugar. And just as much as we relish the satisfaction and savory heartiness that salt adds to our food, salt plays a fundamental role in dozens of critical functions in our bodies.
Salt is needed to maintain the optimal amount of blood in our bodies; it’s even needed by the heart to pump blood throughout our bodies. Salt is essential for digestion, cell-to-cell communication, bone formation and strength, and prevention of dehydration. Sodium is also critical to reproduction, the proper functioning of cells and muscles, and the optimal transmission of nerve impulses to and from organs such as the heart and brain. Indeed, our bodies rely on elements called electrolytes—such as sodium, potassium, magnesium, and calcium—in our bodily fluids to help carry out electrical impulses that control many of our bodies’ functions. Without an adequate sodium intake, our blood volume goes down, which could lead to the shutting down of certain organs, such as the brain and kidneys.
Simply put, if we eliminated all sodium from our diets, we would die.
Our brain and body automatically determine how much sodium we eat, reabsorb, and excrete. The ability of our body to conserve salt and water is thought to be controlled by our hypothalamus, a part of our so-called reptilian brain that both receives and transmits signals that drive us to crave salt or feel thirsty.
Those signals, if we honor them, lead us to naturally create optimal levels of water and salt in the body—because those powerful instinctual drives are a direct result of evolutionary facts of life. The first living creatures on the planet were bathed in seawater, and when they came onto land, they took salt from the ocean with them.1 And, today, millions of years later, the makeup of our human body fluids still mimics that of the ancient ocean.
Out of the Ocean
The ocean covers 71 percent of the earth’s surface, but because of its massive volume, the ocean also makes up 99 percent of the earth’s total living space.2 Sodium chloride, aka salt, constitutes 90 percent of the entire ocean’s mineral content,3 the same percentage of mineral content found in our blood. The only difference between the two is in concentration—the ocean is four to five times as salty as our own blood (around 3.5 percent NaCl versus 0.82 percent NaCl).4 Besides the ocean, salt can also be found in smaller seas, rock salt, brackish water, salt licks, and even rainwater. The vast amount of salt we find in numerous areas around the world only underscores the importance of salt to all forms of life.
The similarity between the mineral content and concentration of our own blood and seawater has been known for decades.5 Cells can’t survive outside a narrow range of electrolyte levels in the extracellular fluid that bathes them. In order for a species to leave the ocean and survive on land, several salt-regulating systems had to develop and evolve. Those systems operate all over our bodies, including in our skin, adrenal glands, and kidneys.
The precise ionic calibrations that facilitate cell life have not changed substantially since the beginning of life itself.6 Even now, our bodies retain salt in times of scarcity and excrete excess salt when we don’t need it. This ability to regulate the amount of salt in our bodies and to seek it out in times of need has allowed us to survive and thrive in almost every type of geographical region in the world—but, in essence, our blood still reflects the ancient ocean where life began and from which it evolved.
Compared to the dramatic changes in the form, structure, and function of organs that occurred during vertebrate evolution, the fact that the electrolyte makeup of the extracellular fluid has generally remained constant7 suggests that salt balance is an evolutionary adaptation. This adaptation remains tightly regulated for sustaining life for all vertebrates, including marine and freshwater fish and turtles, reptiles, birds, amphibians, and, yes, mammals.8 That fact is foundational to the theory that all animals—including humans—are thought to have evolved from creatures that originated in the ocean.
Once sea invertebrates developed a closed circulatory system, they would have needed to evolve organs called kidneys to help them reabsorb and excrete salt and water (among other things). Until then, the salty ocean would have been integrated into the invertebrate itself. From an evolutionary perspective, then, the kidneys likely first evolved in the sea and would therefore consider salt a friend, not an enemy. This fact seems to be lost in our current debate about optimal salt intake.
An organism’s ability to retain and excrete salt is critical in order to provide the proper cell function and hydration that sustains life. There is no better example of this than fish that are able to live in both freshwater and salt water. Most of these fish can actively reabsorb or excrete sodium via their gills, allowing for drastic environmental change in saltiness.10 The gills of these fish serve much like the kidneys of a human, reabsorbing or excreting sodium depending on whether they have too much or too little salt in their body, thereby helping to maintain normal electrolyte and water balance. Another evolutionary adaptation to maintain salt and water homeostasis is the heavy armor-plating seen in freshwater reptiles. This adaptation allows maintenance of normal electrolyte and fluid balance, as the shell counters the drastic difference in osmotic stress of living in a freshwater environment—where the concentration of salt is much less than that of blood.11
Despite significant changes in the saltiness of the animals’ environments, their organs continued to evolve in order to maintain normal salt concentrations, and hence water balance, in the blood, no matter where their travels took them—even as they took those first critical slithers onto land.
Crawling Up on Shore
Tetrapods, the first four-limbed vertebrates, are thought to be the last common ancestor of amphibians, reptiles, and mammals. These animals were first able to leave the seas by swallowing air into their gut.12 Once these creatures were on land, their kidneys had to adapt from living in the salty environment of the sea to one that was relatively salt-scarce.
While there are many theories about the origin of land-based animals and the rise of vertebrates from invertebrates, our kidneys and our salt cravings are big clues that we more likely evolved from marine animals rather than freshwater animals.13 If we did come from the sea, the evolutionary ability to retain sodium would have been a requirement, one that allowed the maintenance of blood pressure and circulation of blood through the tissues once on land
These animals, once bathed in salt water, were now faced with the relative salt scarcity of the desert, rain forest, mountains, and other nonmarine environments. Thus, not only was it important to retain salt, but a “hunger” for salt would have evolved in these animals to ensure that their needs were met. This “hunger” would provide a physiological signal—an appetite—to seek out salt whenever a deficit was on the horizon. Their brand-new closed circulatory systems would give them an enhanced ability to maintain sodium and water homeostasis, mostly due to the evolution of the kidneys, bladder, skin, intestines, and other endocrine glands not present in ancient marine invertebrates.15
In the animal kingdom, there are no dietary guidelines, of course—no medical directives to create a conscious effort to restrict salt intake. Indeed, many animals (especially those hunting in the sea) ingest large amounts of salt simply as a matter of course during their daily lives. Take, for example, reptiles, birds, and marine mammals, such as the sea lion, sea otter, seal, walrus, and polar bear, that hunt prey living in the ocean. These animals take in large amounts of salt, both from the animal itself and from salt water, during a kill, particularly if they eat oceanic invertebrates, which have the same salt concentration as the ocean.16 For these marine mammals, the salt content of their blood is not very different from that of terrestrial mammals17—and since they are ingesting sea water, which is four to five times as salty as their blood, that salt must be excreted via their kidneys.
Or, to say it bluntly: their kidneys must be able to excrete massive amounts of salt.
This basic physiology of the kidneys is the same in humans. In fact, research has shown that patients with normal blood pressure and kidney function can easily excrete ten times as much salt as we normally consume in a day.
Millions of years ago, climate changes that featured intense dry seasons were thought to have forced nonhuman primates to seek out wetlands.19 Their diet would have consisted of aquatic vegetation, with a sodium content five hundred times that of terrestrial plants.20 This may also be when nonhuman primates started eating meat, which they would have first encountered when fish and aquatic invertebrates were trapped in aquatic vegetation—providing primates with the original seafood salad.21 Once these foods were “inadvertently” eaten, nonhuman primates probably got a taste for them and started seeking them out deliberately. Their first fish were thought to have been easier prey, such as catfish that were injured, washed ashore, or trapped in shallow ponds. (Catfish were plentiful where ancestral primates and early humans roamed, making this a plausible notion.
This dietary switch—toward consuming more fat and omega-3s—certainly makes sense for its potential to foster the development of a larger (more human-sized) brain. Dozens of nonhuman primates have been reported to eat fish and other aquatic fauna that would have supplied their diet with ample amounts of salt.22 They would have encountered such things as shark eggs, shrimp, crabs, mussels, razor clams, snails, octopus, oysters and other shelled invertebrates, tree frogs, invertebrates in the river mud, snapping turtle eggs, water beetles, limpets, tadpoles, sand-hoppers, seal-lice, and earthworms.23 These abounded at seashores and in swamps, freshwater and marine water, and other tropical and temperate locations. Based on this list, it’s obvious that the diet of prehuman primates (and thus early humans) would not have been low in salt; in fact, it could have been extremely high in salt.
The Case Is Clear
From an evolutionary standpoint, evidence does not suggest that we evolved on a low-salt diet. Instead, much of our evolutionary theory seems to support the fact that we evolved on a high-salt diet. So where does this persistent misconception about our original diet come from?
The idea that our human ancestors consumed very little salt, generally less than 1,500 milligrams of sodium per day, is both old and current.35 Some of the debate about evolutionary diet seems to stem from one influential paper on the topic, which was published in 1985 in the New England Journal of Medicine, one of the world’s most prestigious medical journals. The authors of this paper estimated that during the Paleolithic era (from about 2.6 million years ago until about 10,000 years ago), our intake of sodium was just 700 milligrams per day.
But this figure was based on the sodium content of select land animals (and only the sodium content of the meat) as well as land plants available to hunter-gatherers. This estimate does not include the sodium that would have been obtained from tiger nuts, insects, or aquatic vegetation or prey, nor does it include the other large stores of sodium found in animals besides the meat, such as that found in the skin, interstitial fluid, blood, and bone marrow (which we know hunter-gatherers did eat). We can’t forget that, aside from their meat, animals themselves (muscle, organs, viscera, skin, blood) are extremely good sources of salt. For example, muscle contains approximately 1,150 milligrams of sodium per kilogram. Australian Aborigines would eat 2 to 3 kilograms of meat per sitting during a kill.37 This is equal to 3,450 milligrams of sodium per day, the exact amount of sodium that current-day Americans consume (when they’re not straining to achieve the low-salt guidelines, that is!).
Organs of animals are even higher in salt than meat: just 10 ounces of bison ribs (about one-quarter of a kilogram) provides 1,500 milligrams of sodium, the same amount in just 13.5 ounces of bison kidney or 2 pounds of bison liver. And remember, this doesn’t even include the salt that is found in the skin, interstitial fluid, blood, and bone marrow.
Early humans probably got salt in other ways as well. Some would have also eaten soil, as is still done by Kikuyu women of Africa, who are known to make dishes from sodium-rich soil.38 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.
How did these glaring contradictions—that humans throughout history consumed only a fraction of today’s salt intake, that salt causes high blood pressure, and that high blood pressure causes heart disease—take hold of the medical field so completely? And how have they maintained their iron grip for almost a century?
The truth is, a small number of emphatically held assumptions derailed scientific progress for decades—if not generations. To trace the roots of these beliefs and find the truths behind them, let’s first look at how humans interacted with salt as civilization unfolded. By understanding the history and psychology of our relationship with salt, we can trace the progression from a few researchers’ mistaken assumptions and how—through a lethal combination of inertia, publication bias, and nefarious interests motivated by the food industry—those assumptions became established medical dogma and public health guidelines.
Mining for White Gold
Humans have been consciously producing salt, by scraping salt from dried desert lake beds or mining salt from the earth, for at least eight thousand years.3 Salt mining started in China but spread to various regions around the world—including Egypt, Jerusalem, Italy, Spain, Greece, and ancient Celtic territories. These territories also traded salt and salted foods, such as fish and fish eggs, olives, cured meats, eggs, and pickled vegetables, to various regions around the world, a trade that’s been occurring for thousands of years. Almost every important Roman city was located near a source of salt, and the average Roman consumed 25 grams of salt, equivalent to 10 grams (10,000 milligrams) of sodium per day, more than 2.5 times our current average intake.
In ancient times, humans invented creative methods of salt production. They drilled brine wells in the earth and boiled the brine down to salt crystals. They extracted salt deposits from dried riverbeds. They actively evaporated seawater from human-made lakes and ponds, mined mountain salt, and extracted salt from the soil in the desert or the burned ashes of marsh plants. Or they simply boiled marsh water and peat.
Before refrigeration, salt was the main antimicrobial and preservative agent, helping to maintain the freshness of foods for weeks or even months when canned properly. Salt was considered so valuable that it was used to pay Roman soldiers and was a symbol of a binding agreement. In fact, the absence of salt on a Roman dinner table was interpreted as an unfriendly act, raising suspicion. It was the life force of the ancient world.
By the sixteenth century, Europeans were estimated to consume around 40 grams of salt per day; in the eighteenth century, their intake was up to 70 grams, mainly from salted cod and herring,6 an amount four to seven times the current intake of salt in the Western world. In France, in 1725, where detailed records were kept regarding salt revenue because of heavy taxation, the daily salt intake was between 13 and 15 grams per day.7 In Zurich, Switzerland, it was over 23 grams. Salt was consumed in even higher quantities in Scandinavian countries: consumption levels topped 50 grams of salt in Denmark, and Nils Alwall even estimated that in the sixteenth century, daily consumption of salt in Sweden approached 100 grams (again, mainly from salted fish and cured meat).8
All of this suggests that the consumption of salt throughout Europe during the last several hundred years was likely at least twice, and even up to ten times, what it is today. Now let’s look at the rise of chronic disease in Europe. And how did our hearts fare during this heyday of unbridled salt consumption?
We already know that salt intake was extremely high in Europe during the 1500s, somewhere between 40 and 100 grams of salt per day. If salt caused heart disease—chest pain leading to sudden death—and Europeans were consuming around 40 grams of salt per day in the 1500s,14 there should have been hundreds of thousands of reports of heart disease during this time. Yet the first report did not occur until the mid-1600s.15 And the rates of heart disease only jumped to critical levels in the early 1900s. The rise of chronic disease simply does not parallel the rise of salt consumption—if anything, it’s inversely proportional.
So how did the current nutrition guidelines come to be? Research missteps, arrogance, funding conflicts, a stubborn refusal to relent—all these forces combined together to form them and keep them in place, even today.
An Idea as Old as It Is Inaccurate
The theory that salt raises blood pressure is over one hundred years old. Two French scientists named Ambard and Beauchard are credited for inventing the salt–blood pressure hypothesis in 1904 based on findings from just six of their patients.16 When these scientists gave these patients more salt, their blood pressure tended to go up. However, just a few years later, in 1907, Lowenstein published conflicting findings in patients with nephritis (inflammation of the kidneys).17 For close to the next century, scientists would tussle over the relative benefits and risks of salt consumption—although the quality of the research on both sides was far from equivalent.
The Salt Wars saga first spilled over into the United States in the early 1920s. Frederick M. Allen, a medical doctor from New York, and coworkers were the first to bring salt restriction to the attention of the American medical profession as a potential therapeutic strategy for lowering blood pressure. They published four papers, two in 1920 and two in 1922, that apparently set off the controversy in the United States. The core of these papers alleged that salt restriction lowered blood pressure in around 60 percent of those with hypertension. Allen used these case reports to champion salt restriction as a potential treatment for hypertension. Going further, he hypothesized that dietary salt irritated the kidneys, overworking them and eventually leading to elevations in blood pressure even in those who still had normal kidney function. But Allen had no proof. However, his rationale seemed sound; salt restriction was said to “spare the kidney, mainly by limiting the intake of salt.
However, numerous publications during this time refuted the idea that salt restriction was a good option for treating hypertension, and the idea fell out of favor.19 Over twenty years later, the “overworked kidney” theory of hypertension was plucked from obscurity and seemingly stolen by Walter Kempner, a researcher destined to create his legacy on this fallacy. Indeed, Kempner was stern in prescribing severe dietary restriction in order to relieve the kidneys of an increased workload, and this included salt restriction. He wrote, “There must be total war. Attacking one factor is not enough. Reducing the sodium is not enough; reducing cholesterol is not enough; reducing fluid and amino acids is not enough. Simple reduction is not enough, for all factors of renal work must be reduced to an absolute minimum.”20 Kempner would go on to receive worldwide recognition for the results he claimed to get with his Rice Diet—which just happened to be low in salt (one factor of about a dozen other dietary restrictions). The extrapolation of Kempner’s work as proof that low-salt diets are effective for treating hypertension is one of the most egregious instances of research misinterpretation in the entire Salt Wars saga.
Lewis K. Dahl
Dr. Lewis Kitchener Dahl was said to be a man of “strong conviction.”48 Dahl originally took an interest in the notion that certain populations who (apparently) consumed a low-salt diet did not have much hypertension, such as the Inuit. In contrast, those who consumed high amounts of salt, such as the Japanese, had a much higher rate of hypertension.49 This led him to study the effects of salt in rodents. However, there was a problem: Dahl knew that salt didn’t have much effect on blood pressure in normal rats. So he decided to selectively modify them through inbreeding over several generations in order to create what is now known as “Dahl salt-sensitive rats.” That’s right: Dahl created salt-sensitive rats in a lab, and then used them to prove his salt–blood pressure hypothesis.
In 1954, Lewis K. Dahl and Robert A. Love from the Medical Research Center, Brookhaven National Laboratory, Upton, New York, published a paper in the American Medical Association’s Archives of Internal Medicine that was later credited with reviving the idea that a high-sodium diet was driving the high prevalence of hypertension in the Western world.51 Primarily basing their assertions on epidemiological studies, Dahl and Love cited evidence that primitive societies who ate a low-salt diet were leaner, were more active, and didn’t develop high blood pressure—without acknowledging that these same societies seldom ate a high-sugar diet, either. For some reason, the idea that obesity itself could lead to hypertension (and that both could be driven by sugar) was not a popular theory at the time. The fact that there wasn’t a single publication until 1983 showing that sugar raises blood pressure in humans didn’t help matters.52 (And lest we cast stones at those researchers of yore and consider them myopic, acknowledge the fact that even today we generally don’t tend to think that one disease could be related to another. We like to separate diseases from one another and treat each disease via different specialists—but that’s clearly not how the body actually works.)
By the mid-1950s, despite many experts lobbying to the contrary, salt had already been demonized as the blood pressure–raising white crystal. To make matters worse, the sugar industry was working hard to help shift the blame off sugar and over to other dietary substances (like saturated fat).53 And this blame-shifting would also leave salt out to dry as the white crystal that causes hypertension—no one was even considering sugar. Why would they? At the time, sugar was considered completely harmless by most scientists, and certainly by most of the lay public.
Dahl was then one of the first to propose that added salt is a condiment—not a dietary need. In 1960, he published a review of the literature from studies he had gathered since 1954,54 showing that in five populations, as the intake of salt increased, so did the prevalence of hypertension. He even went so far as to conclude that humans could easily survive on less than 1 gram of salt per day. He cited some of his own studies in which the intake of salt was apparently dropped to around 100 to 375 milligrams per day, sustained for three to twelve months. He also referenced three people who’d apparently had a “proven” intake of salt between 250 and 375 milligrams for two to five years, and how a seventeen-year-old girl was able to “maintain salt balance” on an intake of just 10 to 12 milligrams of salt for several months (but no reference was provided for the latter).55 Despite all of this “evidence,” none of the work Dahl presented truly proved that low-salt diets were beneficial or without harm.
Dahl cited evidence that giving salt to rats that were genetically engineered to be susceptible to salt produced hypertension—without mentioning the equivalent human dose of salt in these studies. According to Bjorn Folkow, esteemed author of over four hundred articles on vascular physiology and a member of the Royal Swedish Academy of Sciences, that human equivalent would have been 40 grams of salt per day (or over four times a normal salt intake). That’s how much salt it would take to raise blood pressure in similarly salt-sensitive humans.56 In the salt-resistant rats—those that didn’t have a blood pressure “problem” with salt—even the human equivalent of 100 grams of salt per day still did not raise the blood pressure.
It’s safe to say that the rat studies cited by Lewis Dahl were completely irrelevant to humans. But Dahl was undeterred. To buttress his case, Dahl cited a 1945 JAMA publication as proof that low-salt diets lowered blood pressure in humans. One problem: that publication did not in any way show that salt restriction lowered blood pressure significantly in everyone. In fact, a closer look at that paper suggests the low-salt study may have actually killed people.57 One patient who was placed on the low-salt diet died soon afterward; another sustained circulatory collapse, which usually suggests a failure to maintain a supply of oxygen and nutrients to the tissues. When salt was added back into the diet, the patient with circulatory collapse improved (thank goodness).
These important points were not mentioned by Dahl in his paper. And yet Dahl was so convinced that salt causes hypertension, he concluded, “This idea [that salt causes hypertension] is today so widely accepted and used that dilation would belabor the obvious.” But perhaps it would have been instructive to have a bit more “obvious dilation” before pinning public health policy to this flawed theory for several more decades.
Dahl even suggested that the high salt level in infant foods was to blame for the high infant mortality rate in the United States.58 When he gave certain baby formulas to salt-sensitive rats, they would end up dead. But of course human babies are much larger than rats, and salt-sensitive rats aren’t normal rats—but Dahl didn’t let that stop him. He issued a blanket proclamation that salt in baby formulas could be harmful to infants. Never mind that in his experiments, these salt-sensitive rats were developing malignant hypertension, which was leading to their death59—something that was not occurring in human babies. Based partly on Dahl’s work and ideas, the Committee on Nutrition of the American Academy of Pediatrics concluded that salt intake of infants was too high, and manufacturers began to lower the salt content of their foods.60
Quality in research counts—but somehow, throughout the Salt Wars, the power of sheer personal stubbornness and a hesitancy to question the status quo overwhelmed the power of academic rigor and integrity. And we’ve been paying the price ever since.
George Meneely and Harold Battarbee
Two authors likely had the greatest influence for getting salt restriction integrated into the 1977 Dietary Goals: George R. Meneely and Harold D. Battarbee from Louisiana State University Medical Center were among the most renowned scientists supporting the notion that salt restriction helps prevent and treat high blood pressure.61 Indeed, Meneely was actually the head of the physiology and biophysics department at Louisiana State, a position that afforded him a lot of clout and admiration. Both Meneely and Battarbee believed that a high-sodium/low-potassium diet was the principal driver of hypertension.63 They wrote that “excess salt” leads to expansion of the extracellular fluid volume and increased blood pressure—but they never specifically stated what amount of salt causes these consequences.
Even Meneely and Battarbee acknowledged that the idea that salt causes hypertension was just a theory in their 1976 paper titled “High Sodium-Low Potassium Environment and Hypertension.” Their paper was one of the most comprehensive reviews looking at salt and blood pressure at the time, and it was published just prior to the 1977 Dietary Goals. All this gave these authors a lot of notoriety. And the fact that the salt–blood pressure connection was just a theory got lost in the fanfare—and one can imagine, given the attention the authors were receiving, that they preferred not to soften the impact of their work. In fact, in the U.S. Senate report, Meneely and Battarbee were quoted in the Senate Report’s Supplementary Views, having testified before the Senate Committee in support of salt restriction.
What wasn’t given much attention by the U.S. Senate or the 1977 Dietary Goals, however, was that their theory was a combination of a high-salt and low-potassium intake that leads to hypertension, and still only in those who were genetically susceptible. These details were overshadowed by the big headline: salt leads to hypertension. But this little blip of coincidental timing turned out to have monumental impact on our nation’s health for the next forty years. The public was told that everyone would benefit from salt restriction and that it was a safe intervention to prevent and treat hypertension—something the evidence in the literature had never supported, before or since.
In 1977, George McGovern’s Senate Select Committee on Nutrition and Human Needs published the Dietary Goals, which recommended that all Americans restrict their salt intake to just 3 grams (1.2 grams of sodium) per day.65 This guideline was based on expert opinion at the time rather than sound evidence. Indeed, during this time, sound evidence was not a requirement to give dietary guidance to the nation; there was no demand for systematic reviews of the literature, or even evidence from clinical trials in humans. If you were considered an expert and had enough clout, your word would be considered “evidence.” A massive public health dictum that radically impacted food policy, industry regulations, school lunch programs, and physicians’ standard of care for subsequent decades was, in essence, based on the opinions of just a few scientists (and nonscientists, for that matter).
After the Dietary Goals were published in February 1977, two other hearings occurred to address around fifty additional opinions. These hearings were held on March 24 and July 26, and notes of these hearings were published in the Supplemental Views. These Supplemental Views offer a glimpse into the origin of the severe limits on salt intake: The Senate Select Committee relied mostly on the National Academy of Sciences (a nonprofit organization composed of the nation’s leading researchers) and George Meneely and Harold Battarbee for recommending a limit of just 3 grams of salt per day.66 We can thank Meneely and Battarbee for at least contributing to the 3-grams-per-day salt limit given to all Americans.67
By the time the second edition of the 1977 Dietary Goals was published, less than one year later, the limit of 3 grams of salt per day had been increased to 5 grams (around 2 grams of sodium). This might have been due to additional testimony provided to the Senate Select Committee indicating that even if someone obtained an entire 3 grams of salt as the iodized form, they still would not achieve the recommended amount of iodine per day (150 micrograms).68 (Even today, the populations of fifty-four countries are still considered iodine deficient, and our best way of obtaining iodine is—you guessed it—by eating iodized salt.)69 Again, the emphasis was on the minimum necessary to preserve life—hardly a metric for vital health.
The Supplemental Views reflected a robust dialogue about salt guidelines. They also referred to consumer warnings about salt restriction for people on medications that eliminate salt or lead to salt depletion. And even the American Heart Association was quoted as stating that “with the advent of effective sodium-eliminating diuretics, the need for strongly-restricted sodium diets has been sharply modified [emphasis added].” The American Medical Association (AMA) stated, “While epidemiological observations suggest a relation between salt ingestion and hypertension, they fail to support the hypothesis that salt consumption is a major factor in causing hypertension in persons in the United States [emphasis added].” And the Committee on Nutrition of the American Academy of Pediatrics stated, “The role of salt intake as an environmental factor in the induction of hypertension has still to be defined. For 80 percent of the population in this country, present salt intake has not been demonstrated to be harmful, i.e., hypertension has not developed [emphasis added].” In other words, three major medical establishments were wary of the low-salt advice given to all Americans at the very outset of the 1977 Dietary Goals.
Had these distinguished organizations pressed their case, rather than allow the flawed work of several individuals to represent the entire medical community, we might have never been asked to give up the saltshaker. Our health, and in particular our quality of life, might not have needed to suffer. But the Salt Wars were destined to rage on for another forty years, all the way up to today.
Formally Enshrining the Low-Salt Guidelines
Throughout the Salt Wars, studies consistently contradicted each other, the findings bouncing back and forth like a never-ending tennis match. Some studies showed that salt increased blood pressure, but others did not. The supporters of the salt–blood pressure hypothesis continually argued that the skeptics had little merit—and there were many advocates of the salt–blood pressure hypothesis.
Arthur Guyton, an American physiologist, was one of the most influential voices in the early 1980s. He believed that an increase in extracellular fluid from increased salt intake could lead to hypertension.72 However, he also believed that the kidneys would have to be compromised in order for this to occur, as it was well known that any extra salt in the body can easily be excreted by the kidneys.73 What was harming the kidneys and creating “salt-sensitive hypertension,” however, was not known at the time. (Spoiler alert: it’s the other white crystal.)
While some studies looking across populations found an association between salt consumption and blood pressure, this same effect could not be found when looking within populations. Meneely and Battarbee argued for a “saturation effect,” saying that when an entire population eats an excessive amount of salt, any evidence that could correlate salt intake with blood pressure would be hidden—when these effects were actually more likely attributable to lower potassium intake and higher consumption of sugar and refined carbohydrate.75 And this rationale seemed to work—but even the low-salt advocates found it hard to make a case for salt restriction. Only one out of four people is able to comply with rigid salt restriction, making it a rather futile public health policy.
”Despite the average person’s struggles to comply, Lewis Dahl was having none of it. He and other low-salt advocates simply demanded that the public needed to work harder to curb their salt appetite.77
In 1983, six years after the publication of the 1977 Dietary Goals, founder of the Hypertension Center at New York-Presbyterian/Weill Cornell Medical Center John Laragh78 and colleagues published a paper that exposed some of the misguided leaps, perpetuated by the low-salt advocates, that had led the country to adopting such stringent guidelines. Laragh and company alleged that, all told, fewer than two hundred patients had ever been tested with moderate salt restriction to treat hypertension.79 Laragh also stressed that most of the studies were of short duration and they didn’t look at hard endpoints (such as cardiovascular events or death). Despite these poor-quality results, every American had been told to restrict their salt intake by sweeping public health mandates. Additionally, no clear benefits had been found in those with normal blood pressure who restricted salt. The “benefits” of low-salt diets in patients with hypertension (again, based only on a few hundred patients) had been extrapolated to everyone in the United States, even those with normal blood pressure.
One of the best studies of the time was conducted in 1982, when British cardiovascular researcher Graham MacGregor and colleagues at Charing Cross Medical School in London tested just nineteen patients with mild to moderate essential hypertension in a placebo-controlled trial. The crossover trial tested a low-salt diet (1,840 milligrams of sodium per day) and a normal-salt diet (3,680 milligrams of sodium per day).80 While the average blood pressure was around 9/5 mmHg lower on the low-salt diet, some of the nineteen patients apparently had no significant benefit, and two patients actually experienced slight increases in blood pressure with salt restriction. Importantly, based on twenty-four-hour urinary potassium levels, the intake of potassium in the trial was low (around 2.2 to 2.5 grams per day, or about half the recommended intake of 4.7 grams of potassium per day.
What this trial actually showed was that compared to a normal-salt diet combined with a low potassium intake, a low-salt diet lowers blood pressure in some hypertensive patients but may raise blood pressure in others. In other words, mixed results. This study exemplifies the problems of extrapolating results from controlled clinical settings to the outside world. No one considered that adding salt to vegetables would increase our liking for them and hence how much of them we consume. In other words, using salt allows us to consume more vegetables (i.e., potassium), which leads to an overall improvement in our health and blood pressure. Instead, we were being given the wrong message based on evidence that had little to do with how people actually live.
Sadly, MacGregor chose to stick with the flawed interpretation of these results and took up the mission of salt reduction on a global scale. After this study, MacGregor began his unrelenting one-man crusade against salt that has continued for decades and has positioned him on governmental and health agency advisory boards, wielding his influence widely. He’s been extremely effective in shaming industries and public health agencies into bending to his will.
MacGregor started Consensus Action on Salt and Health (CASH) in 199582 and followed up by creating World Action on Salt and Health (WASH) in 2005.83 With these two anti-salt research and advocacy groups, MacGregor had an elevated platform from which to spread his fervent belief that salt raises blood pressure and thus must raise the risk of stroke and heart attacks. Secure in that belief, he has been lobbying governments around the world relentlessly for decades to lower salt intake and the salt content of foods. In fact, CASH has been very successful and influential in getting UK food manufacturers to lower their salt content, despite the lack of research backing, and as many as eighty other countries are considering adopting the same guidelines MacGregor forced through in the UK. One reason his efforts may have been more persuasive is that he has lumped salt with other food additives—such as unhealthy fats and added sugar—which both boast much more plausible data showing negative health outcomes.
MacGregor has been emphatic about the evils of salt, his focus trained solely on the supposed benefits to lowered blood pressure as protection against heart disease. Meanwhile, these groups (CASH and WASH) simply dismissed the harms of low-salt diets. When small reductions in blood pressure were placed into “risk calculators,” these groups would shout from the rooftops about the benefits of low-salt diets.
The harms of low-salt, however, were never inserted in these calculators. Not surprisingly, they always concluded that “lowering salt will save lives” based only on reductions in blood pressure, but never by computing the harms of the higher heart rate, triglycerides, cholesterol, and insulin levels—all factors with much more thoroughly and rigorously documented links to heart disease. CASH and WASH have continued to promote that unproven direct link—that low-salt saves lives—for decades.84
Once an idea is entrenched in people’s minds, it is hard to supplant it. And the research to the contrary hadn’t been adequately translated and presented to the American public. Even the Dietary Guidelines for Americans, first published in 1980, have continued to tell Americans to cut back on their salt intake. Limited expert opinion turned into established public health policy, and health policy became unassailable low-salt dogma.
The first systematic review of trials testing the low-salt advice wasn’t published until 1991, almost fifteen years after the 1977 Dietary Goals told us to restrict our salt intake. This systematic review, performed by Law and colleagues, included seventy-eight trials, only ten of which were randomized.85 This systematic review became the basis for why the U.S. hypertension guidelines promoted low-salt diets in the general public, as it contended that a reduction of 2,300 milligrams per day of sodium would drop blood pressure by 10/5 mmHg in people with normal blood pressure and 14/7 mmHg in people with hypertension. Law and colleagues went on to state that low-salt diets could prevent seventy thousand deaths per year in Britain (based solely on the potential reduction in blood pressure). These strong statements were clearly aimed to unite a group worn down by the Salt Wars controversy.
However, these benefits on blood pressure were significantly greater than results found a few years later from higher-quality meta-analyses that included only randomized data. For example, in people with normal blood pressure, the newer, stronger meta-analyses of salt-restriction trials reported one-tenth the impact on systolic pressure and one-fiftieth the impact on diastolic pressure compared to the analysis by Law and colleagues (–1/0.1 mmHg compared to –10/5 mmHg)
Despite all of this higher-quality evidence showing that this reduction made only an inconsequential impact, in 1993 the Hypertension Guidelines in the United States (the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure [JNC 5])87 decided to cite the earlier Law meta-analysis to conclude that a modest reduction in the intake of sodium (1,150 milligrams of sodium) would reduce systolic blood pressure by 7 mmHg in people with hypertension and 5 mmHg in those with normal blood pressure.
Between 1991 and 1998, the Law 1991 meta-analysis was cited more than any other, despite being the weakest. Any findings in support of salt restriction were cited more than negative ones.88
Finally, a heavyweight stepped up to the plate. John D. Swales, a doctor, hypertension expert, and founding editor of the Journal of Hypertension, published a paper in 2000 showing that people with normal blood pressure only get a small reduction in systolic (1 to 2 mmHg) and diastolic (0.1 to 1 mmHg) blood pressure when they severely restrict their sodium intake.
Moreover, Swales wrote that the low-salt recommendations were based on data that had been “amplified by publication bias” (the tendency to publish positive rather than negative results); that the amount of salt restriction to obtain the small reductions in blood pressure was unachievable by the public; and that the results could be due to other changes in the diet besides just a reduction in salt. Swales also stated that there was a cost to lowering salt intake, both a social/quality-of-life cost and an economic cost. These considerations had long been looked down upon as almost irrelevant.
Swales went on to cite six meta-analyses of salt restriction in his paper, five of which contained only randomized trials and one meta-analysis that contained both randomized and nonrandomized studies. The five meta-analyses with randomized trials found that in people with normal blood pressure, salt restriction did not even reduce systolic blood pressure by 2 mmHg—not even 2 points! Only one meta-analysis of the five found a reduction in diastolic blood pressure greater than 1 mmHg—the rest were between 0.1 mmHg and 0.97 mmHg.
At best, the research suggested, salt restriction in people with normal blood pressure caused a reduction in blood pressure of only around 2/1 mmHg. Three of the meta-analyses concluded that dietary salt restriction was not supported by the evidence,90 with only one concluding that there was “great potential” with salt restriction.91 However, this “great potential” for salt restriction and blood pressure lowering was based on trials with a reduction in sodium intake between 1,748 milligrams and 3,680 milligrams, which is highly unlikely to occur in the general population. In fact, longer-performed sodium-restriction trials indicate that the public might be able to achieve a reduction in sodium intake of around 1,000 milligrams at the very most.92 In other words, the “great potential” of lowering blood pressure via salt restriction was based on a reduction of salt two to three times the amount the public would likely be able to achieve.
Many low-salt advocates argued that salt-restriction trials hadn’t been performed long enough to show a benefit, yet a systematic review of eight randomized controlled trials looking at salt restriction of greater than six months found similarly small reductions in systolic blood pressure (–2.9 mmHg in people with hypertension and –1.3 mmHg in people with normal blood pressure).93 More importantly, a systematic review by Law and colleagues suggested that it took just four weeks to get the maximal reductions in blood pressure with low-salt diets, and another review of randomized trials did not find progressive blood pressure lowering over time with salt restriction.
Perhaps most importantly, a meta-analysis performed by Midgley and colleagues underscored the influence of publication bias with the sodium-restriction trials. It found that trials that tested low sodium with positive results were more likely to be published compared to negative trials.95 Midgley emphasized that publication bias had led the scientific community to overestimate the blood-pressure-lowering benefits of salt reduction. This publication bias continues to distort the Salt Wars, even to this day.
The Huge Shadow of Intersalt
In 1989, the Food and Nutrition Board’s “Diet and Health: Implications for Reducing Chronic Disease Risk” set a maximum intake of 2,400 milligrams of sodium. This was based on the 1988 Intersalt study, a massive epidemiological study conducted at fifty-two population centers around the world, led by Dr. Paul Elliot from the Department of Epidemiology, London School of Hygiene and Tropical Medicine, London. The Food and Nutrition Board claimed that the Intersalt study proved that blood pressure increased with age if sodium intake was above 2,400 milligrams per day.96 One problem: the Intersalt study showed the opposite. Only five populations of the fifty-two studied consumed less than 2,400 milligrams daily, and four of them were primitive societies. The fifth population that consumed under 2,400 milligrams of sodium actually had a higher systolic blood pressure compared to several populations with a higher salt intake. In fact, one population consumed more than twice the amount of salt but had a lower systolic blood pressure. And when the four primitive societies were excluded from the other fifty-two populations, the data shifted—suddenly there was a clear downward slope for blood pressure as salt intake increased.
That’s right: as salt intake increased, blood pressure actually declined. The 2,400-milligram Daily Value for sodium (printed on every Nutrition Facts label) is the perfect example of the anti-salt warriors’ Napoleon complex: quick to exaggerate in order to make up for lack of evidence. There really never was good evidence for setting a limit of 2,400 milligrams of sodium per day, but this target was sealed onto every Nutrition Facts label and subsequently carried over to the 1995 Dietary Guidelines for Americans.
What is most chilling is the apparent decision by the Intersalt group not to publish data on heart rate. Heart rate was supposedly measured in the study, at least according to Bjorn Folkow, who reported that Paul Elliot (the corresponding author of Intersalt) had communicated to him that heart rate was measured in Intersalt.98 We likely will never know why this heart rate data was never published by the Intersalt group, but it’s well known that low-salt diets increase heart rate.99 Could Intersalt be just another example of “publish findings that support your theory and bury the ones that don’t”?
The official line is that the Intersalt group “declined to make their underlying data public…because of the need to preserve the independence of scientific investigation, the integrity of the data, and the confidentiality of information.”100 This explanation by these authors seems to be without any logic.
An alternate explanation: if the heart rate data were indeed measured and published, Intersalt would have likely shown harm with low-salt diets. Indeed, as Folkow suggested, the total stress on the heart and arteries comes from a combination of blood pressure and heart rate—a fact well accepted by the medical community, except when it comes to sodium intake! Folkow concluded that low-salt diets would increase the overall stress on the heart and arteries and hence increase the risk of hypertension and heart failure.
The IOM’s 2,300-milligram UL of sodium was then incorporated into the 2005 Dietary Guidelines, which recommended that all Americans restrict their sodium intake to less than 2,300 milligrams.105 Additionally, “individuals with hypertension, blacks, and middle-aged and older adults [emphasis added]” were recommended to consume no more than 1,500 milligrams of sodium per day. Interestingly, 2005 was the first year that the Dietary Guidelines for Americans specifically recommended lowering salt intake to lower the risk of high blood pressure. Back in 1980, the Dietary Guidelines had stated that lowering salt mainly applied to people with high blood pressure (“the major hazard of excessive sodium is for persons who have high blood pressure”). How did that happen?
It may have been the influence of Lawrence Appel, MD.106 Appel was not only chair of the 2005 Institute of Medicine Panel on Dietary Reference intakes for electrolytes and water107 and a spokesperson for the American Heart Association—he was also on the board of WASH,108 a group whose stated purpose was to reduce sodium intake around the world. Appel had long focused only on blood pressure as a surrogate marker, translating that “benefit” on blood pressure with low salt intakes to definitive reductions in strokes and heart attacks. Like all low-salt advocates, Appel continued to ignore the harmful effects caused by sodium restriction on numerous other measures of health (called surrogate markers) such as increases in renin, aldosterone, triglycerides, cholesterol, LDL, insulin, and heart rate.
Despite his potential bias and conflict of interest as part of a group whose sole focus is to reduce sodium intake around the globe, Appel was also appointed as a member of the 2005 and 2010 Dietary Guidelines Advisory Committee. Sure enough, the Dietary Guidelines for Americans followed the IOM (of which Appel was chair regarding the recommendations for sodium intakes in the first place) and began specifically recommending low sodium intake for Americans. Indeed, those 2010 Dietary Guidelines for Americans were the first to recommend that 1,500 milligrams of sodium should be the goal for about half the U.S. population (including children and most adults). This applied to “persons who are 51 and older and those of any age who are African American or have hypertension, diabetes, or chronic kidney disease.”109 While the 1,500-milligram sodium-restriction level was removed from the 2015 Dietary Guidelines for Americans recommendations, the 2,300-milligram level remains.
Finally, we begin to see a bit of nuance in the guidelines. What had previously felt like a sledgehammer in search of a fly to smash, now began to hint at what we in the field have known for decades: low salt only works for a very small subgroup of people.
And at this point, we finally—finally—started seeing public health leaders begin to place more emphasis on the quiet killer that had been stalking us all along, damaging our kidneys (and, indeed, creating our issues with salt), generally laying waste to our overall health. The white crystal that was truly deserving of the “toxic” mantle: sugar.
Sugar’s Free Pass
Beginning in the 1950s, an American scientist named Ancel Keys was promoting the idea that dietary fat (and eventually saturated fat) was the cause of heart disease. At the same time, England’s John Yudkin thought the blame rested with sugar. But in 1961, the American Heart Association (AHA) officially demonized saturated fat, suggesting that Americans reduce their intake of animal fat and increase their intake of vegetable oils to reduce the risk of heart disease.111 Once the AHA had officially backed the fat-heart hypothesis—that saturated fat increased cholesterol levels and, thereby, the risk for heart disease—sugar was exonerated by omission. This black-or-white, one-or-the-other choice, made on behalf of the nation, was a major reason other researchers continued to struggle to be taken seriously when they suggested sugar was a driver of heart disease. In contrast, salt wasn’t exonerated, it was attacked, convicted of being an “unnecessary evil” by the National High Blood Pressure Education Program as early as 1972.
So, for years, sugar was a bit like Switzerland—neutral—and it was given a free pass on the dietary front. While salt (and fat) were viewed as harmful, sugar was considered harmless, no better or worse for you than any other food ingredient, as long as you burned more sugar calories than you took in.
This viewpoint was vigorously perpetuated by the Sugar Association, which has engaged in strong lobbying of Congress, the Department of Health and Human Services, and various health organizations to allow sugar to maintain its benign status for many years.113 The sugar industry has also worked hard to achieve a positive public image by sponsoring high-profile events such as the Olympics and investing in tooth decay prevention campaigns, and generally, relentlessly, shifting the focus of public health policy away from sugar.114 It even funded scientists who seemed to downplay the harms of sugar and who were placing the blame of our increasing waistlines on a lack of exercise rather than an overconsumption of sugar.115
In 1977, the sugar industry was citing Jean Mayer, a professor at the Harvard School of Public Health, who suggested that the obesity problem in modern societies was caused by inactivity. By shifting the focus of obesity away from “harmful calories” and toward “total calories,” sugar was able to fly under the radar of close scientific scrutiny. And because saturated fat contained more calories per gram than sugar, it took center stage as a driver of obesity, too.
In 1975, just a few years prior to the publication of the 1977 Dietary Goals, Alexander R. Walker published a paper suggesting that sugar was not a cause of hypertension or heart disease. He cited three of his own studies supporting this idea; all three were apparently funded in part by the sugar industry.117 This cozy relationship has been a common theme throughout history, in which authors who have conflicts of interest with the sugar industry consistently suggest that sugar is not inherently harmful,118 whereas authors without conflicts of interest with the industry generally report the opposite.
Strangely enough, the first edition of the 1977 Dietary Goals did recommend that we limit our consumption of added sugars to just 15 percent of our total calories,120 and the second edition trimmed this down further, to just 10 percent of our total caloric intake, for refined and processed sugars.121 Oh, how many lives might we have saved if that recommendation had resonated more loudly! However, over the subsequent years, the media mainly focused on salt (which hit the cover of TIME in 1982122), cholesterol (TIME, 1984123), and saturated fat (which had already hit TIME magazine in 1961124), and no one was taking the limits on the intake of sugar seriously. Indeed, over the next twenty years, from 1980 until 2000,125 the Dietary Guidelines for Americans told us that sugar did not cause diabetes or heart disease, despite clear evidence to the contrary.
In 1979, a study found that swapping the same number of calories of wheat starch with those of sugar was found to increase fasting insulin and insulin responses to a sugar load.127 Then, in 1981, Reiser and colleagues published another study showing that when wheat starch was replaced with sugar, even when calories were kept the same, more people eventually developed diabetes/prediabetes.128 Yet four years after this data was published, the 1985 Dietary Guidelines for Americans stated that “contrary to widespread belief, too much sugar in your diet does not cause diabetes.” This was a direct contradiction to the scientific literature.
I’ll be blunt: we were lied to.
The sugar industry had other strategies to keep the public naive to the harms of sugar. In the Supplemental Views to the 1977 Dietary Goals, the sugar industry stated, “It should be noted that sucrose (sugar)…does not displace other foods, but rather promotes their consumption. Though often referred to as empty calories, it is really Pure Calories with No Fat and No Cholesterol; it is an ideal energy source as an additive to other protein and nutrient providing foods [emphasis added].
That’s one Jedi-level mind trick right there.
By getting people to think of sugar as pure energy, the sugar industry helped create the general notion among the public that sugar was not inherently harmful. All we had to do was burn off the sugar calories, and we could consume as much as we wanted—and it was an appealing story to believe.
But, of course, the delusion that sugar calories are not harmful is simply not true: a sugar calorie is harmful, even more harmful than other carbohydrate calories, because of the way the sweet stuff affects insulin levels, brain chemistry, the immune system, inflammation, and many other physiological variables.129 Fortunately, more and more scientists are beginning to see through the obfuscation and are becoming convinced that sugar is a factor in the development of heart disease and other types of chronic disease.130 But back then, besides influencing the media and public perception regarding the harms of sugar, the sugar industry was undoubtedly also significantly swaying the scientific literature.
Throughout the years, the effects of conflicts of interest with the sugar industry were never quantified, until a recent systematic review of systematic reviews was published in 2013 in the journal PLOS Medicine. The review found that in studies with a conflict of interest with the food industry, 83.3 percent found no evidence linking sugar-sweetened beverages with weight gain/obesity. In contrast, when only studies without conflicts of interest with the food industry were analyzed, the same percentage (83.3 percent) found a positive association—that sugar-sweetened beverages have a definitive connection with weight gain and obesity. This one study provides just a small glimpse of how much science has likely been affected by these types of influences.131 This was a core message I stressed during my testimony in front of the Canadian Senate regarding the harms of added sugars in our diet.
Between their breakfasts of seaweed soup and rice and their evening meals of kalbi, barbecued beef short ribs, and a wide array of salty side dishes (banchan), the average Korean eats over 4,000 milligrams of sodium per day. They feast on tteokguk, a broth-based soup drowning in salt, or bulgogi, grilled meat marinated in a sea of sodium-packed soy sauce. They eat portions of kimchi—cabbage preserved in salt—with literally every meal.
Yet Koreans manage to somehow have one of the world’s lowest rates of hypertension, coronary heart disease, and death due to cardiovascular disease.1 This is known as the “Korean Paradox,” although you could swap out Korea for any one of thirteen other countries and get a lot more “paradoxes” regarding high salt intakes.
Three countries with the lowest rate of death due to coronary heart disease in the world (Japan, France, and South Korea) all eat a very high-salt diet.2 The Mediterranean diet, the eating pattern now widely recommended as a heart-healthy diet, is quite high in salt (think sardines and anchovies, olives and capers, aged cheeses, soups, shellfish, and goat’s milk). The French, who eat just as much salt as people in the United States, enjoy cheese, soup, traditional breads, and salted meats and have a low rate of death due to coronary heart disease.3 Norway eats more salt than the United States yet has a lower rate of death due to coronary heart disease. Even Switzerland and Canada have very low rates of death due to stroke despite a high-salt diet.4
Importantly, many of these high-salt-eating countries have very long life expectancies, including Japan, which has the longest life expectancy in the world.5 In contrast, Latvia, with a salt intake about half that of Japan (7 grams versus 13 grams) has a death rate more than ten times Japan’s.
While there are undoubtedly many factors that play into these numbers—such as the fact that most of the sodium in Korea comes from kimchi (salted fermented vegetables that likely have other beneficial properties) rather than processed foods7—the bottom line is that even in countries known for eating a lot of salt, coronary heart disease also seems to be the lowest in those that consume the highest amounts of sodium. Among women in Korea, for example, the group consuming the highest amounts of sodium has a 13.5 percent lower prevalence of hypertension compared to the group consuming the lowest amounts of sodium.8 And at least fourteen countries consume a diet high in salt but have a low rate of death due to coronary heart disease.9 (See the list on this page.) All of these countries consume the same amount of salt as people in the United States, if not more, and yet have a lower rate of death due to coronary heart disease.
We’ve all been told over and over again that salt raises blood pressure, which in turn increases risk of strokes and heart attacks. Looking at the 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. What’s going on? How do the Koreans (and French and Japanese) get away with eating so much salt while enjoying good heart health? Why isn’t all that salt raising their blood pressure? Let’s take a closer look at what really happens in the body when we eat a low-salt, normal-salt, and high-salt diet.
Perhaps the most disturbing thing about the low-salt guidelines is not how little effect they have on blood pressure when salt is restricted—but how great a negative effect they have on normal functioning, such as blood volume. When the intake of sodium is severely restricted, blood volume can go down by 10 to 15 percent.36 This change indicates the body is under stress of dehydration. At that point, the body is facing an emergency, and the salt-retaining hormones are released as a last-ditch means of maintaining the body’s homeostasis—to prevent a large drop in blood pressure.
In other words, a low-salt diet indicates a crisis for the body, not a recipe for optimal health. 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.37
So how did such bad science hang on for so long? The sad and simple truth is this: people were looking for easy answers.
How Low-Salt Eating Makes Sugar More Addictive
When left to their own devices, we’ve seen how animals (including humans) consume just the right amount of salt, and then stop. Either the salt craving goes away or our bodies excrete any excess. Nothing remotely similar occurs with sugar. While some people normally eat just a little bit of sugar, a large and growing group of people, particularly kids, consume refined sugar and/or high-fructose corn syrup in massive amounts, without an “off” switch. In fact, John Yudkin, MD, the founder of the Department of Nutrition in Queen’s College of London and an early anti-sugar activist, noted that up to 52 percent of total calories come from sugar in adolescents age fourteen to eighteen.33
And unlike cravings for salt, which are controlled by our bodies’ innate need for it, sugar cravings are produced by either a psychological desire or a physiological dependence on it. Regardless of how powerful these cravings are, they’re not signs that your body actually needs sugar! As we saw in the last chapter, consuming lots of sugar can contribute to the state of internal starvation, stimulating your appetite and nudging you to eat more—and more sweets, in particular. One of the worst offenders in triggering internal starvation is fructose, which is mainly derived from sugar beet, sugarcane, or corn. When fructose is stripped out of these naturally high-carbohydrate foods, then boiled down to concentrated form and added to other foods, it becomes more addictive and harmful than in its original state. If it seems crazy to think of a plant product becoming an addictive drug, think of cocaine from coca leaves or heroin from poppy seeds/pods—in essence, these are all concentrated addictive substances from plants.
With salt, we don’t see a continuous escalation in its intake. Contrast that with sugar. After the introduction of sugar in the diet of both animals and humans, scientists have charted a definitive thirtyfold escalation in its intake, with evidence of bingeing, tolerance, and structural changes in the brain in response to that consumption—all key criteria of addiction.35 Consider alcohol: some people will become alcoholics and will consume massive amounts, while others will not. English poet John Gower invented the term “sweet tooth” in his criticism of the indulgences of courtly life, and he understood back in the late 1300s that it was not normal to indulge in sugar or sweetness.36 Indeed, once a “sweet tooth” develops, people favor foods that once tasted too sweet, and what used to taste rather pleasant may now seem bland, and perhaps even slightly bitter. When the taste receptors change because of consuming a diet high in added sugars, a person may find it more difficult to enjoy nonsweet foods, precipitating a further sweetening of the diet.
Step 4: Add in Naturally Higher-Nutrient Salt
Most kitchens have a shaker of unassuming white table salt close to the stove or table. We’ve grown so accustomed to this as our default salt that we can sometimes forget that salt doesn’t just magically appear bleached white and perfectly granulated in nature! Not surprisingly, the healthier types of salts found in nature tend to be untouched by contaminants and less refined or processed. Salt naturally comes in many different flavors—smoky, earthy, nutty, peppery, sweet, or even sulfuric (smells like rotten eggs!). Experiment with different flavors to find your favorite. Some salts may have additional mineral content. Here’s a look at the breakdown of some popular “natural” salts and how they compare with standard table salt.
Water and Salt – the Essence of Life
How Salt Became Sodium Chloride
With the advent of industrial development, natural salt was “chemically cleaned” and reduced to the combination of sodium and chloride. Essential minerals and trace elements were removed as impurities. However, sodium chloride is an unnatural, isolated, unwholesome substance having nothing in common with salt. Similar to white, refined sugar, salt, once regarded as white gold, was converted into white poison. However, there is a higher reason for salt having been endowed with all the natural elements found in our bodies. Sodium chloride is an aggressive substance, which biochemically, is perpetually seeking an equalizing counterpart so that the body’s pH can always remain neutral. Sodium chloride needs its natural counterpart in order for it to produce its effect. The natural counterparts, such as potassium, calcium, magnesium and other minerals and trace elements, demonstrate, from a biophysical standpoint, specific frequency patterns. These patterns ensure the geometric structures in our body. When these structures are missing, we are without energy and are lifeless. Salt should not be used just to add flavour to our food, but for its vibration pattern, which is similar to our body!
How Table Salt Burdens the Body
While our body only requires the minute amount of 0.007 ounces of salt per day, most of us suffer from a lack of salt, even through we’re over-saturated with sodium chloride. When our consumption of salt is less than 0.007 ounces per day, salt craving kicks in. The average, per capita, daily consumption of table salt in the U.S. is between 0.4 ounces and 0.7 ounces. However, our body is only able to excrete 0.17 ounces to 0.25 ounces a day through our kidneys, depending on our age, constitution and sex. The body recognizes table salt as an aggressive cellular poison, an unnatural substance, and wants to eliminate it as quickly as possible in order to protect itself. This causes a constant overburden on our organs of excretion. In almost every preserved product, salt is used as part of the preservation process. So, by adding salt to the already-salted food, the body receives more salt than it can get rid of. The body now tries to isolate the over-dose of salt. In this process, water molecules surround the sodium chloride in order to ionize it into sodium and chloride to neutralize it. For this process, the water is taken from our cells as the body sacrifices its most perfectly structured cell water in order to neutralize sodium chloride. With this, the dehydrated body cells die.
The Consequences of Consuming Table Salt
The result of consuming common table salt is the formation of overly acidic edema, or excess fluid in the body tissue, which is also the cause of cellulite. That’s why doctors tell us to avoid salt. For every .035 ounces of sodium chloride that cannot be eliminated, the body used 23 times (23x) the amount of its own cell water to neutralize the salt. If the sodium chloride is still too high,, re-crystallization of the table salt occurs as the body uses available non-degradable animal proteins (as those found in milk), which also have no value and cannot be broken down and eliminated. The body uses these proteins to produce uric acid in order to get rid of the excess salt. As the body cannot dispose of uric acid, it binds itself with the sodium chloride to form new crystals that are deposited directly in the bones and joints. This is the cause of different kinds of rheumatism such as arthritis, gout, and kidney and gall bladder stones. This re-crystallization is the body’s band-aid solution for the cells and organs in order to protect the body from irreparable damage of irresponsible food intake. But in the long run, it poisons the system because those substances cannot be disposed of.
Place several Himalayan Crystal Salt stones in a glass container and add high quality spring water until full. After approximately 24 hours, look to see if the salt crystals have completely dissolved. If so, add a few more crystals. When the water can no longer dissolve any more salt, the salt crystals will sit at the bottom of the jar without dissolving. At this point the solution becomes saturated at 26%, which is stable and ready for consumption. Take 1 teaspoon of the 26% solution in a glass of water every morning before breakfast. The glass container can be refilled again and again with water and salt, to continue the process.