The Salt Fix İngizlice Kopya
Table of
Contents
How Low-Salt May Have Created the High Blood
Pressure Epidemic..................... 65
From Cradle to Grave: How Our Salt Thermostat Gets Derailed.............................. 80
You May Need More Salt to Help Manage Shock (Burns,
Trauma, and Hemorrhage) 92
You May Need More Salt to Counter Low Sodium Levels.......................................... 92
You May Need More Salt When Pregnant or Lactating............................................... 97
You May Need More Salt for Energy and Muscle Health.......................................... 101
You Need More Salt When High-Sugar Diets Lead to Salt
Wasting........................ 101
You May Need More Salt if You Have Inflammatory Bowel
Disease...................... 105
You May Need More Salt on Low-Carbohydrate Diets.............................................. 106
You May Need More Salt to Prevent Iodine Deficiency............................................. 107
and
my wonderful children, Alexander and Emmalyn
Title Page
Copyright
Dedication
Disclaimer
INTRODUCTION: DON’T FEAR THE SHAKER
1: But Doesn’t Salt Cause High Blood Pressure?
2: We Are Salty Folk
3: The War against Salt—and How We Demonized the Wrong White Crystal
4: What Really Causes Heart Disease?
5: We Are Starving Inside
6: Crystal Rehab: Using Salt Cravings to Kick Sugar Addiction
7: How Much Salt Do You Really Need?
8: The Salt Fix: Give Your Body What It Really Needs
EPILOGUE: REACH FOR THE RIGHT WHITE CRYSTAL
APPENDIX 1
APPENDIX 2
APPENDIX 3
NOTES
ACKNOWLEDGMENTS
1 -Introduction
………
Don’t Fear the Shaker
Consider Scandinavian novelist Isak Dinesen’s famous line, “The cure for
anything is salt water: sweat, tears or the sea.”
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.
Eating Too Much Salt Is Killing Us by the Millions
1.6
Million Heart Disease Deaths Every Year Caused by Eating Too Much Salt
—Healthline News, August 14, 2014
U.S.
Teens Eat Too Much Salt, Hiking Obesity Risk
For
the Good of Your Heart, Keep Holding the Salt
—Harvard Health
Blog, July 11, 2016
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.1
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 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.
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.
2 - But Doesn’t Salt Cause High Blood Pressure?
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 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?
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.2
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.
This question becomes increasingly urgent as the stresses of the modern
world inflict a compounded toll on our bodies. In addition to the salt we lose
by following our low-carb, ketogenic, or paleo diets, we’re also taking more
medications that cause salt loss; we’re enduring more damage to the intestine
that causes decreased salt absorption (including Crohn’s disease, ulcerative
colitis, irritable bowel syndrome [IBS], and leaky gut);
and we’re doing more damage to the kidneys by eating more refined carbohydrates
and sugar (decreasing the kidneys’ ability to retain salt).
Recent research even suggests that chronic salt depletion may be a
factor in what endocrinologists term “internal starvation.” When you start
restricting your salt intake, the body starts to panic. One of the body’s
defense mechanisms is to increase insulin levels, because insulin helps the
kidneys retain more sodium. Unfortunately, high insulin levels also “lock”
energy into your fat cells, so that you have trouble breaking down stored fat
into fatty acids or stored protein into amino acids for energy. When your
insulin levels are elevated, the only macronutrient that you can efficiently
utilize for energy is carbohydrate.3
Time for the Truth
After high school, I graduated from the University at Buffalo with my
Doctor of Pharmacy degree and began to work in the community as a pharmacist. I
became even more interested in salt when I found out that one of my patients
was complaining of fatigue, dizziness, and lethargy. While puzzling this out
with her, I remembered that she was on a medication (an antidepressant called
sertraline) that can increase the risk of low sodium levels in the blood. When
I put together her doctor’s instructions to cut her salt intake with the
additional prescription of a diuretic, I immediately suspected that she was
dehydrated because of salt depletion and that her blood sodium levels were low.
I suggested that she might need to start eating more salt but advised her to
get her blood sodium levels tested first to confirm my suspicions.
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?
We can start by telling the truth:
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.
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 are essentially salty people.
Simply put, if we eliminated all sodium from our diets, we would die.
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.9
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
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.14 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.18 The reason
why humans cannot solely live on seawater is not that our kidneys cannot handle
excreting the high salt content—it’s that in order to do so, water must leave
with it, which would eventually cause dehydration (and eventual death!). But if
we had enough access to freshwater to replace what is lost during the excretion
of that salt, humans would absolutely be able to drink seawater.
Almost without exception, salt and water regulation is a well-adapted survival mechanism for nearly all animals—and this
includes all primates, including humans.
Prehuman Primates
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 taste for fish and other aquatic creatures may have led these
prehuman primates to begin deliberately trying to catch fish by hand and
eventually using tools such as sticks, sand, and food to catch fish—which
represented a huge leap forward in cognitive development. Think of that twist
of fate: eating fish by happenstance may have enabled early primate brains to
develop the intellect to actively catch fish through the use of tools. Exactly
how they were able to obtain these salty creatures is more of a mystery, but it
is thought that they used rocks to crack shells open and tapped on bamboo to
find frogs living inside it. At least five other species, beyond orangutans,
have been found to use tools to obtain fish and other salty aquatic prey.
Thereafter, hominins—both modern and extinct humans—would have used primate
fish-catching practices.24
Early Humans
Intriguingly,
the emergence of tool-assisted fish catching in early Homo
dates to around 2.4 million years ago. Primate fish-eating habits suggest that
hominins would have also started eating aquatic plants first, then accidentally
sampled the aquatic animals clinging to their nightly feeding, and, having
acquired a taste for a newfound meat, eventually transitioned to catching fish
and other aquatic prey.25 Some
researchers assert that an early human, Paranthropus boisei,
and early Homo dug into wetlands to add vertebrates
and invertebrates to what had previously been their predominantly plant-based
diet. These aquatic animal foods yield plenty of salt and novel, high-quality
nutrients, such as docosahexaenoic acid (DHA). Similar to how these essential
fatty acids may have led to brain growth in prehuman primates, DHA allowed for
the brain to increase in size in early humans.26
The fact that DHA is important for the growth of the human brain
creates the unavoidable suggestion that aquatic foods—and the hunger for salt
that drew our ancestors to them—were an important player in how the human brain
evolved into what it is today.27
Terrestrial plants are low in DHA, which suggests that this transition to
aquatic vegetation and prey was essential to increasing our brain size.28 Imagine:
our hunger for salt may have played a role in early humans’ great leap forward.
His family was thrilled by the way salt made all their food taste better,
and none suffered any untoward health consequences as a result of greater
sodium intake. He recalled this experience when he became involved in the care
of a woman with late-stage congestive heart failure who was on the strictest
regimen of sodium restriction. “All she wanted was to taste her food. But her
doctors had banned salt from her table and her family had removed it from the
house,” he recalls. “As she was approaching the ultimate end, I finally
convinced her family to allow her some salt. They were reluctant, fearing she
would decompensate.” But recognizing her desperation and
not wanting to deny her such an earnest wish, they agreed.
Even early humans who lived far from the ocean’s brackish waters had
this hunger for salt. Data suggests that early humans roaming East Africa’s
noncoastal regions between 1.4 and 2.4 million years ago may have consumed a
diet extremely high in salt. An ancient ancestor to humans known as “Nutcracker
Man” was said to have lived on large amounts of tiger nuts.29 The fossils
of this early human, discovered in 1959 in Tanzania, feature strong jaw muscles
as well as wear and tear on molars, indicative of a diet high in tiger nuts.
Tiger nuts are extremely high in salt (up to 3,383
milligrams of sodium per 100 grams, the average amount of sodium we modern
humans eat in an entire day).30 Just a
handful (3 ounces) of these nutlike tubers would have provided an entire day’s
worth of sodium in today’s world.
Nutcracker Man did not live by nuts alone. He also survived on a diet
largely composed of grasshoppers. A close relative of the grasshopper, the
cricket contains a very good amount of sodium (about 152 milligrams of sodium
per five crickets).31 Most
likely, certain insects are so high in sodium because it allows them to move
and fly faster and thus avoid being eaten by their brethren.32 Scientists
have observed that sodium deficiency can lead to cannibalism in insects (and
probably other animals, too).33 The theory
goes that the animals instinctively know that salt is contained within blood,
interstitial fluid, skin, muscle, and other parts of their bodies. Not
surprisingly, experts believe humans have been getting protein and
micronutrients from wild insects for several millennia—and continue to do so to
this day, particularly in parts of Africa, Asia, and Mexico.34
The Case Is Clear
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.36 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.
No one truly knows how much salt our Paleolithic ancestors ate or how
much salt our human brain evolved on—but it’s probably much more than what most
experts think. Some experts believe that 45 to 60 percent
of our Paleolithic ancestors’ calories came from animal foods39 that are
naturally high in salt.
Humans Have
Always Needed Salt
If blood sodium levels drop too low, water from the blood will go into
our tissue cells in order to increase the level of sodium in the blood back to
normal, but this fluid shift can lead to cellular swelling. If the sodium level
in the blood goes up, water will be pulled out of the tissue cells and into the
blood, in order to lower sodium levels back to normal—but this can cause
cellular shrinkage. Both cellular expansion and cellular shrinkage can be
extremely harmful, which is why our body will do anything to keep a normal
sodium level in the blood and why salt intake and balance are so tightly
regulated. If our body were not able to do this, a low blood sodium level could
lead to too much water in the brain, eventually causing death.
One evolutionary adaptation that allowed us to better balance salt once
we were on land was the transformation in the production of adrenal hormones.
Lower vertebrates inhabiting salty environments produce cortisol and
corticosterone, whereas nonaquatic land-dwelling animals evolved to produce
corticosterone and aldosterone.40 Humans
then evolved to produce cortisol and aldosterone. These adrenal hormones are
critical in our fight-or-flight nervous system response (cortisol) as well as
our salt balance (cortisol and aldosterone).
Another physiological regulator of our salt status is something known
as a volume sensor, or receptor, which is found in our carotid arteries and the
aorta. These receptors sense pressure changes that trigger
signals in the brain, causing the kidneys to either retain or excrete more salt
and water, depending on body sodium stores.41 On average,
our kidneys may filter between 3.2 and 3.6 pounds of
salt (1.28 and 1.44 pounds of sodium) per day.42 This is
about 150 times the amount of salt we ingest per day. To put this into
perspective, most health agencies tell us that consuming just 6 grams of salt
(around 2,300 milligrams of sodium or 1 teaspoon of salt) is too high, yet our
kidneys filter this amount of salt every five minutes.
The salt restriction recommendations hardly make sense from a
physiological viewpoint, but seeing these numbers helps to put things further
into perspective. The amount of salt we eat per day is truly a drop in the
bucket compared to the amount that the kidneys filter on a daily basis. In
fact, the stress on our kidneys mainly comes from having to conserve salt and reabsorb all of the 3.2 to 3.6 pounds of salt that we
filter every day.43 This
reabsorption requires us to use up adenosine triphosphate (ATP), the energy
created from the food we ingest that’s utilized by our cells to facilitate many
bodily functions. Our sodium pump uses approximately 70 percent of the basal
energy expended by the kidneys,44 making a
low-salt diet an energy hog and a tremendous stress to the kidneys. This is one
way that low-salt diets can lead to weight gain, by slowly depleting our energy
stores and leading us to become more sedentary. What organism would want to
move (and sweat out precious sodium) when it has too little salt to begin with?
Similar to the way a low-salt diet depletes the energy of the kidneys,
it does the same to the heart.45 When we
restrict our salt intake, our heart rate goes up, reducing our blood and oxygen
circulation throughout our body and increasing the heart’s need for oxygen.46 Any one of
these effects, all produced by a low-salt diet, could increase our risk of
having a heart attack.
Getting enough salt is critical for so many things. Diarrhea, vomiting,
and sweating can lead to salt deficit. A salt deficit can reduce speed and
endurance as well as thermoregulation in athletes.47 Getting
enough salt creates the right fluid-sodium balance, so it prevents dehydration, low blood pressure, dizziness, falls, and
cognitive impairment. And perhaps most importantly for the fate of the human race,
salt is essential for reproduction.
Salt and Sex
One
of salt’s most intriguing properties is its importance for many facets of
reproduction—from sexual desire and procreation to gestation and lactation48—and this
connection has been known at least since the time of the ancient Greeks. In the
Aegean world, Aphrodite, the goddess of love, encourages mating and
reproduction and prevents infertility. Aphrodite is commonly depicted as having
been born from the salty sea foam and known as the “salt born.” She is thought
to symbolize the “generative” power of salt and the ancient Greeks’ belief in
the origin of mankind from salted foam.49
Greek thinker and philosopher Aristotle observed this power among the
agricultural animals of the time, stating that “sheep are in a better condition
by keeping their hydro-mineral balance under control. The animals that drink
saline water can copulate earlier. Salt must be given to them before they give
birth and during lactation.” Aristotle’s contemporaries knew that animals that
ate a lot of salt produced more milk—and salt made animals lusty and eager to mate.50
Today, farmers see these same effects among modern livestock animals.
Cutting sodium has been found to reduce birth weights and litter size.51 Reducing
the level of salt in feed for lactating sows doubles their average time from
weaning their offspring to fertility; it also reduces successful mating in
female adult pigs. And in mice, sodium deficiency has also been found to trigger
reproduction failure.
In all settings, when animals become sodium deficient, they go out of
their way to find this vital mineral. A yen for salt drives the elephants of
Kenya to walk into the pitch-black caves of Mount Elgon to lick sodium sulfate
off the cave walls. Elephants in the Gabon who are deprived of salt uproot
entire trees to get at the sodium-rich soil under the
roots. Even gorillas have been known to follow elephants to eat the salt-rich
soil and chew on rotting wood, to eat the salty microbes.52 Monkeys
that groom one another don’t do so to eat fleas, as is commonly presumed—they
do it to eat each other’s salty skin secretions.53 Many
animals participate in puddling to get salt from soil54 and will
even drink urine to obtain salt. Papilio polytes, a
type of swallowtail butterfly, has been found to drink seawater at low tide to
help meet salt requirements.55
A low-salt diet seems to act like a natural contraceptive in both
animals and humans, and in both males and females. A low-salt diet causes a
reduced sex drive; reduced likelihood of getting pregnant; reduced litter size
(in animals) and weight of infants; and increased erectile dysfunction,
fatigue, sleep problems, and age at which women become fertile.56 The
low-salt-eating Yanomamo Indians average only one live birth every four to six
years, despite being sexually active and not using contraception.57 Research
has found that women with salt-wasting kidneys due to a congenital adrenal
problem have a decreased fertility and childbirth rate.58
3- The War against Salt – and How We Demonized the Wrong White Crystal
When it comes to our current salt intake, we may be guilty as
charged—we do tend to eat more salt than the minimum amount we need to live.
For years, in order to gain support for salt restriction, many low-salt
advocates forcefully and relentlessly argued that the increased intake of salt
was paralleled by a rise in hypertension and cardiovascular disease around the
world.1 We have
been told that for millions of years humans would have consumed at most only
around 1 gram of salt (around 400 milligrams of sodium) per
day, a view that is still shared by many today—despite the clear evolutionary
evidence you read about in the last chapter.2 In fact,
if we suspend our assumptions and just look at the historical data, we see that
the exact opposite was true: as hypertension and chronic disease were on the
rise in the Western world, salt intake was already on the decline.
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.4
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.5
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
We can’t be entirely sure of the prevalence of hypertension in Europe in the 1500s to the 1800s—the blood pressure cuff was not
invented until the late 1800s, after all—but we do know that the prevalence of
hypertension in the early 1900s in the United States was estimated at 5 to 10
percent of the population.9 In 1939,
in Chicago, the prevalence of hypertension in adults was just 11 to 13 percent.
That figure then doubled to 25 percent by 1975, before finally reaching 31
percent in 2004.10 This
figure has continued to edge upward, and as of 2014, one out of every three
adults in the United States has hypertension.11
Stepping back from this data, we can generalize and say that the
prevalence of hypertension in the United States in the first half of the 1900s
was around 10 percent. However, the prevalence of hypertension is now three times as high12—despite
salt intake remaining remarkably stable over the last fifty years.13
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.
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.”18 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.21
The Kempner Rice Diet
The
third child of Walter Kempner Sr. and Lydia Rabinowitsch-Kempner, Walter
Kempner22 was raised
in pre–World War I Berlin, where he studied medicine, eventually graduating
from the University of Heidelberg. Kempner arrived in America as a refugee from
the Nazis and through good fortune began to work at Duke University. It was
there that Kempner invented his infamous Rice Diet in 1939.23
Dr. Kempner treated hundreds of patients with his Rice Diet, compiling
a large number of case reports. His analysis of his case reports suggested that
a low-salt diet, consisting mainly of rice and fruit, was effective in treating
most of his patients who had malignant hypertension, chronic kidney disease,
and even diabetes.24 Kempner
believed that salt was a “waste product” of the kidneys, and by reducing salt,
one could protect the kidneys from being overworked.25
The guidelines of Kempner’s Rice Diet might send a shiver down the
spine of any modern endocrinologist. The diet consisted of no more than 2,000
calories, 5 grams of fat, 20 grams of protein, 200 milligrams of chloride, and
150 milligrams of sodium (about 1/15 teaspoon).26 Rice of
any kind was allowed, at an average intake of 9 to 12 ounces per day. All kinds
of fruit juices and fruits were allowed with apparently no limit on their
intake, but Kempner forbade the consumption of nuts, dates,
avocados, canned or dried fruit, or fruit derivatives, and only the addition of
white sugar was allowed. (Because we all know how much nutrition white sugar
adds.)
On average, his diet contained around 100 grams of a combination of
white sugar and dextrose per day—but up to 500 grams “if necessary.” (Try to
imagine what could possibly make 125 teaspoons of added sugar per day
“necessary.”) Vegetable juices or tomato juices were not allowed, and no water
was given in the diet, with the fluid intake being limited to 700 to 1,000
milliliters of fruit juice per day. Once the Rice Diet was effective and
conditions improved, “small amounts of non-leguminous vegetables, potatoes,
lean meat or fish (all prepared without salt or fat) may be added.”27
Kempner’s case reports gained substantial media attention.28 However,
to say that his case reports were of suspect quality would be a tremendous
understatement. First of all, they were not clinical trials, so he could not
prove causation. Kempner did not have a control group with whom to compare his
patients, nor did he use adequate control periods after hospitalization. The
flaws in his research meant that his results could have been completely
spurious findings, having nothing to do with the diet. In fact, one of the most
likely reasons for the diet’s “success” was his somewhat idiosyncratic style of
monitoring his patients: Kempner was said to watch his patients “like a hawk”29—he even
admitted to whipping his patients who strayed from
the diet.30
Even back then, fellow researchers questioned whether the low-salt
aspect of his Rice Diet was the reason for its effectiveness. Indeed, one of
Kempner’s own patients with hypertension, ascites, and edema found that all
three conditions were unchanged after following a standard low-salt diet. The
patient’s blood pressure was 174/97 mmHg, but approximately two months after
being placed on the Rice Diet, his blood pressure dropped to 137/82 mmHg—not
surprisingly, a change that coincided with a 14-kilogram weight loss.31
The Rice Diet was found to dangerously deplete salt in the body,
drastically lowering plasma chloride from 97 mEq/L to 91.7 mEq/L.32 (Bear in mind that chloride levels lower than 100 mEq/L are
independently associated with higher mortality.33) According
to Kempner himself, the Rice Diet was ineffective at significantly lowering
blood pressure in 178 of 500 patients (about 36 percent). But he focused his
claims exclusively on the 322 of 500 patients (about 64 percent) in whom the
diet decreased mean arterial blood pressure by at least 20 mmHg.34 Even if we
can consider these results true, they could have been due to one of any number
of factors from the Rice Diet that had little to do with salt restriction: the
increase in the intake of potassium and fiber; the reduction in protein, fat,
trans fat, and seed oils; and the overall reduction in caloric intake and,
hence, weight loss. Yet those facets of the diet were rarely factored into the
explanation of its results.
Another detail that was rarely mentioned in the lionizing of Kempner’s
evidence was one cogent fact: Kempner’s patients had all been extremely sick at
the start of their treatment. They had an average baseline blood pressure of
199/117 mmHg, which is considered hypertensive crisis.35 This fact
alone should have disqualified the Rice Diet’s presumed effectiveness for the
general public.36 And, sure
enough—and not surprisingly—when others tested the Rice Diet, the results were
far less convincing than what Kempner was finding.
In one study of patients with essential hypertension who tried a
version of the Rice Diet, 83 percent were found to have no reduction in blood
pressure.37 Of the ten
patients whose kidney function was measured, nine had a reduced glomerular
filtration rate, a marker of kidney function; eight had reduced renal blood
flow; and in six, the maximal tubular excretory capacity was reduced. In other
words, the low-salt, low-protein diet in patients with essential hypertension seemed to worsen kidney function and
was ineffective at treating high blood pressure.
This was the opposite of what Kempner was reporting.
More troubling was a Medical Research Council (MRC) report, published
in the Lancet in 1950, indicating that a patient had
died of uremia (excess urea, or urine, in the blood due to kidney disease) on
the low-salt Rice Diet.38 The
authors argued that a kidney already damaged by hypertension might be less able
to reabsorb salt, dangerously lowering the salt levels in the blood, and that
those with renal failure might be tremendously harmed by reducing salt.
Trials continued to poke holes in Kempner’s findings, and in 1983, John
Laragh, renowned founder of the Hypertension Center at New
York–Presbyterian/Weill Cornell Medical Center, and colleagues published a
review paper citing those who had performed better-controlled studies and had
reported less-beneficial results. They found that the diet was only effective
in 20 to 40 percent of patients, compared to Kempner’s claim of 64 percent
effectiveness.39 Also, when
researchers tried to tease out the beneficial components of the diet, they
found that salt restriction (generally less than 1.15 grams per day) seemed to reverse the benefits of the Rice Diet.40 So the
primary claim about the diet was, in fact, the thing that made it less effective. With the benefit of hindsight, if we can
take away anything from Kempner’s Rice Diet, it’s that we should increase our
intake of potassium and fiber in the form of fruit and whole grains—that alone
may do the trick.
At this point, almost thirty-five years ago, Laragh and colleagues
suggested that there was no evidence that moderate salt restriction would
prevent hypertension on a population-wide scale,41 and even
in those who are considered “salt-sensitive”—those 25 to 45 percent in whom
salt restriction does slightly reduce blood pressure—there was only weak
evidence that it worked. Laragh and colleagues concluded that the weight loss
and reduction in blood pressure with the Rice Diet was actually entirely
independent of salt intake.42 They went
on to suggest that only for those in whom sodium restriction
had been proven to be “effective” should salt reduction be implemented.
Still others tested the low-salt diet and found it lacking. Arthur
Corcoran and his colleagues at Cleveland Clinic Research Division (which
Corcoran established) showed that even in patients with “severe essential hypertension,”
a low-salt diet only provided benefit in about 25 percent. In contrast,
definite harms were noted, such as azotemia (a high
level of urea, creatinine, and other nitrogen-rich waste in the blood) and
worsening kidney function. They found that most people had to get their daily
sodium intake all the way down to just 200 milligrams or
less (the equivalent of less than 1/11 teaspoon of
salt) in order to get a reduction in blood pressure, which was completely
impractical if not impossible.43
Indeed, in all of the studies done on the diet, only 28 percent of
those who attempted it could even adhere to the Rice Diet, and only 37 percent
of those who adhered to the Rice Diet showed an improvement in blood pressure.
Whenever Kempner tested his “method,” 62 percent of patients experienced an
improvement in blood pressure.44
(Presumably after being beaten into compliance!) But curiously, no other
researcher could duplicate this finding, and when tested by others, the Rice
Diet was found to cause harm.
The known consequences of salt restriction, such as low sodium and
chloride in the blood, have long been independently known to increase the risk
of death.45 And
azotemia, kidney failure, and even several deaths have occurred on the low-salt
Rice Diet.46 Other side
effects reported include lack of energy, anorexia, nausea, abnormally small
amounts of urine production (oliguria), muscle twitching and abdominal cramps,
and uremia (urea buildup in the blood), likely indicating kidney failure.
Unfortunately, both during Kempner’s time and even today, the serious risks of
low-salt diets are rarely, if ever, mentioned in any guidelines recommending
them, despite the pleas of many researchers about the weakness of the
salt–blood pressure hypothesis. “The assumption that only moderate sodium deprivation would accomplish [decreased risk of hypertension in
the general population] is even greater speculation. Furthermore, the idea that
moderate reduction in dietary salt throughout our society would be harmless is
unproved,” said Schroeder and Goldman, in a piece published in the Journal of the American Medical Association (JAMA) in 1949.47 Many
researchers remained skeptical about recommending blanket salt reduction to the
general public, and over the next several decades, others had reported much
less effectiveness of Kempner’s Rice Diet (and low-salt diets in general); salt
restriction as a means to prevent and treat hypertension generally fell out of
favor.
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.50
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).
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
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.62 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.64
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.
REVERSING THE DANGERS OF DIURETICS
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,70 but others
did not.71 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.)74
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.76
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 day81). 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.
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
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).86 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.89 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.
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.94
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.97
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.101
The Search
for the Lowest Common Denominator
By
2005, the Institute of Medicine (IOM) determined what it believed to be an
adequate intake (AI) of sodium, a minimum level at which there
would be a low probability of becoming salt deficient. The sodium AI was meant
to cover sodium losses through sweat, even in unacclimatized individuals, to
meet the needs of both healthy and moderately active people. In those who were
nine to fifty years old, the AI for sodium was listed at 1,500 milligrams per
day (and even lower levels for those younger and older). However, the AI did
not apply to individuals who were “highly active” or “workers exposed to
extreme heat stress.”102
2. Salt losses via urine, skin, and feces—without factoring in salt
losses from medications, lifestyles (caffeine or low-carb diets), or current
disease states.103
The IOM also set a tolerable upper intake level (UL) for sodium at
2,300 milligrams per day for adolescents and adults of all ages (fourteen years
and older). The UL is the highest daily nutrient intake level that is likely
not to pose risk of adverse health effects. For sodium, the UL was based on
several trials, including data from the Dietary Approaches to Stop Hypertension
(DASH)-Sodium trial.104 It was
noted in the DASH-Sodium trial and other trials evaluated by the IOM that blood
pressure was lowered when sodium intake was reduced to 2,300 milligrams per
day, and that this level of intake was the next level above the AI of 1,500
milligrams per day. Hence, the 2,300-milligram UL on sodium was based on a
surrogate marker (blood pressure), not on hard endpoints such as strokes or
heart attacks.
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.
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.110 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 1972.112
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.116
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.119
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.126
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.
That’s one Jedi-level mind trick right there.
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.132
The
American Love Affair with Sugar
Let’s
take a step back and look back at the world before sugar caught us all in its
thrall.
In 1776, the intake of refined sugar in the United States was just 4
pounds per person per year133—the
equivalent of having just over 1 teaspoon of sugar in your coffee per day and
nothing more—which increased to over 76 pounds of sugar by
the timeframe of 1909 to 1913.134 That’s
more like four frosted cupcakes per day. A similar increase in sugar intake
occurred in England. In 1700, the average intake of refined sugar in England
was just 4 pounds per person per year. That figure increased twenty-five-fold,
to 100 pounds, by 1950.135 During
this time of skyrocketing sugar intake, the intake of salt in Europe dropped by
about sevenfold, from around 70 grams per person per day in the late eighteenth
century to just 10 grams in 1950.136 The
implication is clear: the intake of sugar, not salt, has paralleled the rise of
chronic disease in Europe, and the same thing occurred in the United States.
In the United States, the intake of added sugars—table sugar and,
later, high-fructose corn syrup—reached around 100 pounds per person per year
by 1920, and stayed there until around the late 1980s, when it steadily began
increasing again, to about 120 pounds in 2002. That’s almost 150 grams of sugar
per day, or about six of those frosted cupcakes. At that point, a staggering
total of 152 pounds of total caloric sweeteners were being consumed per person
per year (the 32-pound difference coming from honey, glucose, and dextrose).137
Indeed, the army rations of the War of 1812, the Mexican War (1838),
and the Civil War (1860–1861) included over 18 grams of salt per day138—not
including the salt contained in the 20 ounces of beef, milk, beer, or rum that
was also provided to these soldiers. At the close of the Civil War, the general
meat ration for a soldier included ¾ pound of pork or bacon and 1¼ pounds of
fresh or salt beef,139 and the salt ration was around 18 grams per day. All of this
suggests that the intake of salt during the 1800s in the United States was
around 20 grams of salt per day—more than twice what we consume today.140
In general, the intake of salt in the United States and in Europe
around 1950 and onward is probably half of what was consumed in the prior
several hundred years. So it’s unlikely that a rise in salt intake parallels
the rise in chronic disease in the Western world. If anything, it has been
inversely proportional. Since household refrigeration began in the United
States (1911),141 salt
intake has been on the decline. And this would have occurred right around the
time a “toxic dose” of sugar was now being consumed in the United States.
And we can trace sugar’s effect on the country’s health status all the
way back to the 1930s. Evidence implicating sugar rather than salt as the
driver of disease can be found in 1935 in the United States, a time when the
percentage of deaths due to heart disease was only around 20 percent. However,
by 1950, heart disease was the leading cause of death in the United States,
making up around 35 percent of all deaths.142 By 1960,
that number climbed to 39 percent of all deaths (over 650,000 deaths), and
arteriosclerotic heart disease made up three-quarters of these deaths. Other
data show that between 1940 and 1954, death rates from coronary artery disease
rose by 40 percent in men and 16 percent in women143—all during
a time when salt intake, if anything, was dropping,
because of the widespread use of refrigeration after 1930.
When we step back and look at the numbers, studying the estimates of
sugar and salt consumption throughout the last several hundred years in both
Europe and the United States, it becomes abundantly
clear that sugar, not salt, is the likely dietary culprit contributing to
chronic diseases of civilization. But just as the demonization of salt will
take decades to reverse, the halo effect of unethical sugar research took (and
will continue to take) years to reveal as well.
The 1980 Dietary Guidelines for Americans accepted all recommendations
in the 1977 Dietary Goals—but not all targets. Sugar got the sweetest deal, as
it was the only dietary factor out of the six original published goals to never
receive a specific limit of intake in the Dietary Guidelines. In contrast,
salt, saturated fat, and cholesterol were all given specific stringent limits
for decades thereafter. Of particular note is dietary cholesterol, which, after
almost forty years, has now been deemed unimportant as a cause of heart
disease.144
In 1980, the Dietary Guidelines stated, “Estimates indicate that
Americans use on the average more than 130 pounds of sugars and sweeteners a
year.” However, they went on to state, “Contrary to widespread opinion, too
much sugar in your diet does not seem to cause diabetes” and “The most common
type of diabetes is seen in obese adults, and avoiding sugar, without
correcting the overweight, will not solve the problem.” The 1980 Dietary
Guidelines for Americans also stated that “there is also no convincing evidence
that sugar causes heart attacks or blood vessel diseases.”145
In 2002, added sugars were finally given their first specific limit of
intake since 1977. But the Dietary Guidelines did not give the limit—it came
from the IOM, which published a report allowing up to 25 percent of total
calories as added sugars.146 After
twenty-five years, a limit was finally placed on sugar, and
yet it was more than twice the level that was allowed compared to the last
recommendation decades earlier. Even by 2005, the Dietary Guidelines for
Americans stated that up to 72 grams of added sugars were allowed per day (over
14 percent of total calories based on 2,000 calories per day), which adds up to
58 pounds a year.147
By 2010, the Dietary Guidelines for Americans technically allowed up to
19 percent of total calories (based on 3,000 calories per day) to come from
added sugars (a stunning 143 grams per day). While the 2010 Dietary Guidelines
did not specifically state that 19 percent of calories could be consumed as
added sugars, if no solid fats are ingested, then technically this amount was
allowed.148
Fortunately, the 2015 Dietary Guidelines Advisory Committee rights
these wrongs, recommending that no more than 10 percent of calories come from
added sugars (50 grams of added sugar per 2,000 calories, adding up to about 40
pounds a year).149 The
government’s Nutrition Facts label will now include the specific number of
grams of added sugar per serving. Perhaps the American people will finally have
the information, and the guidance, they need to make the best food choices for
their health. After more than two decades, the correct
white crystal will have its bolded place of shame on the Nutrition Facts label.
Unfortunately, the wrongly accused white crystal (salt) remains in bold as
well. It’s far past time we gave salt the justice it deserves.
4 – What Really Causes Heart Disease?
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.6
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.
LOW HEART DISEASE RISK IN
HIGH-SALT-CONSUMING POPULATIONS
Sodium
intake: ~3,300 mg sodium/day
10
fatal cardiovascular events
21
nonfatal cardiovascular events
Sodium
intake: ~3,300 mg sodium/day
21
fatal cardiovascular events
48
nonfatal cardiovascular events10
*Over 90 percent of the
nuns were still alive after the thirty-year follow-up, indicating that normal
salt intake does not cause hypertension and was unlikely to cause
cardiovascular disease or premature death.
Population:
South Korea, France, Japan, Portugal, Spain, Italy, Belgium, Denmark, Canada,
Australia, Norway, Netherlands, Zimbabwe, and Switzerland11
Sodium
intake: All consume high-sodium diets
South
Korea (lowest rate of death due to coronary heart disease in the world), France
(2nd lowest rate), Japan (3rd lowest rate), Portugal (6th lowest rate), Spain
(10th lowest rate), and then Italy, Belgium, Denmark, Canada, Australia,
Norway, Netherlands, Zimbabwe, and Switzerland12
Japan
has the longest life expectancy in the world.13
Latvia,
with a salt intake about half that of Japan (7 grams versus 13 grams) has an
over tenfold higher rate of death.14
Sodium
intake: High-sodium diet
Coronary
heart disease appears to be the lowest in those who have the highest sodium
intake.
In
Korean women, the group consuming the highest amounts of sodium had a 13.5
percent lower prevalence of hypertension compared to the group consuming the
lowest amounts of sodium. “Sodium intake has quite a limited effect on
prevalence rates of hypertension or stroke.”15
The Salt–Blood Pressure
Connection
As we’ve seen, it was dead wrong.
Here’s the truth: normal blood pressure is less than 120/80 mmHg. But
reducing your salt intake to around 2,300 milligrams per day (1 teaspoon of
salt) may only lower your blood pressure by a meager 0.8/0.2 mmHg.16 So, after
enduring staggeringly bland and often debilitating salt restriction, your blood
pressure may now hover around 119/80 mmHg—a mere blip, not a significant
difference.
Plus, as you saw earlier, approximately 80 percent of people with
normal blood pressure are not even sensitive to these meager
blood-pressure-raising effects of salt; among those with prehypertension (a
precursor to high blood pressure), roughly 75 percent are not sensitive to
salt, and among those with full-blown hypertension, about 55 percent are immune
to salt’s effects on blood pressure. Indeed, even in those with hypertension
(blood pressure of 140/90 mmHg or higher), reducing salt intake may only lead
to a reduction in blood pressure of just 3.6/1.6 mmHg.17
As we’ve also seen, many people with normal blood pressure,
prehypertension, and hypertension may even get a rise
in their blood pressure if they restrict their salt intake.18 This is
because when salt intake is severely limited, the body begins to activate
rescue systems that avidly try to retain more salt and water from the diet.
These rescue operations include the renin-angiotensin aldosterone system (well
known for increasing blood pressure) and the sympathetic nervous system (well
known for increasing heart rate).19 Clearly,
this is the opposite of what you want to happen!
Another consequence of the low-salt diet is that your arteries can
become more constricted (an increase in what’s called “total peripheral
resistance”), due to the depletion of blood volume.20 To fight against this increased resistance in the smaller arteries, the
heart needs to pump harder, and the pressure of the blood coming out of the
heart would need to be even higher. Total peripheral resistance places additional
stress on the heart and arteries, leaving you more vulnerable to chronically
elevated blood pressure. In other words, low-salt diets may actually cause the very disease they are supposedly being used to
prevent and treat, hypertension.
In short, salt’s function in the body is exactly the thing it’s been
demonized for. “The ultimate physiological purpose of sodium intake is
precisely the maintenance of blood pressure,” Robert Heaney, MD, wrote in Nutrition Today. “Demonizing sodium is not only unsupported
by evidence but is counter-physiological as well, as it ignores sodium’s most
basic function in mammalian bodies.”21 Sadly,
because of false assumptions in the early twentieth century, the subsequent
overwhelming proof of salt’s innocence has been discounted. Too few people have
listened to the science, too many people have argued, and too many years have
been lost looking at the wrong end of the equation.
Why Did We
Believe the Lie for So Long?
The
public campaign against salt beginning in the late 1970s gave the impression of
a consensus among scientists that salt was bad for our health. And in the
public’s eyes, if government and health agencies were telling people salt was
bad for them, then it must be true. But unfortunately this wasn’t the case.
Indeed, as one editor of JAMA later described,
“authorities pushing the ‘eat-less-salt’ message had made a commitment to salt
education that goes way beyond the scientific facts.”22
After Ambard and Beauchard created the great salt–blood pressure myth
in 1904,23 other
early studies found increases in blood pressure—but only when giving massive amounts of sodium.24 Over
18,000 milligrams of sodium (five times a normal sodium intake) had to be given
in order for this effect to be seen.25 Other
publications reported similar results in normal patients:
sometimes consuming up to eight times a normal intake
did not produce hypertension in patients with normal blood pressure.26
Rather than admit defeat at that moment, anti-salt scientists doubled
down, arguing that those studies did not last long enough to show the
hypertensive effect of salt. So other authors decided to test high-salt diets
for longer periods of time (several weeks rather than several days) to see if
they would find increases in blood pressure. Kirkendall and colleagues studied
middle-aged men with normal blood pressure and found that changing from a
very-low-sodium diet (230 milligrams per day) to a high-sodium diet (9,430
milligrams per day) for four weeks led to no change in total body water or
blood pressure.27 Peripheral
vascular resistance actually decreased, as the salt
loading caused the blood vessels to relax. The authors concluded that there was
no change in either systolic, diastolic, or mean blood pressure. Others had
similar findings.
The bottom line was that patients with normal blood pressure had to
consume an astronomical amount of salt in order to produce even mild increases
in blood pressure. Additionally, high salt loads may actually cause the blood
vessels to relax. Belding H. Scribner, MD, from the University of Washington
School of Medicine, called our ability to handle salt amazing: “So amazing, in
fact, that as much as 80 percent of a given population can handle even the
highest habitual intakes of salt without danger of essential hypertension
developing.”28 He called
the low-salt guidelines a mistake that could “cause guilt feelings among the 70
percent to 80 percent of us who do not have to worry about salt intake.” Scribner
would go on to propose a more feasible solution compared to population-wide
salt restriction: to identify people who were salt-sensitive and restrict
sodium only in that group of the population. This at least made some logical
sense.
But the idea that everyone would benefit from salt restriction was
heavily promoted to the public by leading academics, government bodies, and
health agencies. Even today, the notion that salt raises blood pressure in
everyone is still a commonly held belief. Instead, the
opposite is true: in those who have a mix of normal blood pressure,
prehypertension, and mild hypertension, two-fifths (41 percent) have been found
to have an increase in blood pressure with salt
restriction.29 And even
in people with hypertension, more than one-third (37 percent) have been noted
to have increases in blood pressure (of up to 25 mmHg) with salt restriction.30 In other
words, about three out of five people with normal blood pressure, two out of
five people with prehypertension, and one out of three people with hypertension
may have an increase in their blood pressure when
they restrict their salt intake.
Yes, salt holds on to water in the body, to a certain extent—but this
is actually a lifesaving property, not a harmful one. Ingesting adequate amounts
of salt allows your body to maintain normal blood pressure without having to
activate an arsenal of hormones to compensate. And the idea that a high salt
intake causes overretention of water was also not supported by the literature.31 In fact,
studies consistently found that blood volume was not increased in patients with
hypertension.32 Even after
a true blood volume expansion,33 it takes
approximately seventy-five minutes for blood pressure to increase, which is
more than enough time for normal kidneys to excrete any extra salt and water to
maintain normal blood pressure.
In essence, the argument that a high salt intake would lead to volume expansion (at least in people with normal functioning kidneys)
didn’t make physiological sense. The medical field has long known that kidneys
can excrete massive amounts of salt, well beyond what we normally consume in a
day. People with normal blood pressure have been found to excrete ten times a
normal sodium intake, up to 86 grams of salt per day.34 Kirkendall
and colleagues found that in adults with normal blood pressure, even a forty-one-fold difference in the intake of sodium did not
alter total body water.35
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. Explaining to patients and
the lay public that blood pressure reductions from low-salt diets may actually
indicate low blood volume and dehydration, and could place additional hormonal
stress on the body, would require a great deal of detailed description. But the
simple equation of Salt + Increased Thirst + Water Retention = Increased Blood
Volume = Increased Blood Pressure is much easier. This simple equation just
makes “logical” sense. This idea was something that the media, medical
communities, the public, and government/health agencies could easily understand and get behind. And that’s exactly what
happened—salt was demonized as a toxic, blood-pressure-raising, addictive
substance that was being consumed in massive quantities more than ever before.
Still, as convenient and simple as this explanation was, when studies
proved that volume expansion could not be found in most people consuming
high-salt diets, regardless of their blood pressure status, the salt–blood
pressure hypothesis had to evolve in order to survive scrutiny. Rather than
low-salt advocates admitting the fallacy of the core premise—“salt bad!”—they
shifted their focus from blood volume to vascular resistance. Researchers began
to argue that the sudden blood volume expansion that comes with higher salt
intakes would lead to an increase in peripheral vascular resistance, a
constriction of the blood vessels.38
But funnily enough, subsequent studies found that higher salt intakes decrease vascular resistance, causing blood vessel
relaxation, while low-salt diets increase peripheral
vascular resistance.39 Even if
someone did get a reduction in blood pressure from a low-salt diet (again,
probably indicating harm from dehydration and low blood volume), there was an increase in peripheral vascular resistance and an increase in heart rate, which seemed to drastically
outweigh any blood-pressure-lowering benefit.40 Bjorn
Folkow, the pioneering Swedish hypertension researcher, made a compelling case
that the overall stress on the heart and arteries was from the combined effects
of heart rate and blood pressure, suggesting that salt restriction increased
the combined effects of heart rate and blood pressure.41 In other
words, low-salt diets would increase the overall stress on the heart and
arteries and hence increase the risk of hypertension and heart failure.
This newly discovered natriuretic (salt-eliminating) hormone was said
to help get rid of salt and water from the body by inhibiting the sodium
reabsorption pump in the kidney, called Na-K-ATPase. A diet high in salt was
said to lead to an increase in this hormone, causing blood vessel restriction
and hypertension. Since vasoconstriction was almost always found in patients
with hypertension,42 the
“natriuretic hormone” theory of hypertension gained a lot of attention. And you
know what happened from here: salt took all the blame.43
For many years, no one really knew what exactly the “natriuretic
hormone” was. However, today we know it as marinobufagenin, a steroid secreted
by the adrenal glands that increases the pumping action of the heart and
inhibits the sodium reabsorption pump in the kidney. However, if hypertension
were caused by marinobufagenin, and salt were blamed for causing hypertension,
then a diet high in salt should lead to increases in marinobufagenin. So what
happens when rats are given a high-salt diet? There is indeed an increase in
marinobufagenin in salt-sensitive rats, but salt-resistant rats have only “a
modest increase in marinobufagenin” after eating a salty diet.44 As we
know, salt sensitivity is not a natural condition (rats needed to be bred to
have this condition), so whatever defect causes salt sensitivity in humans was
the problem and not salt intake per se. And the other side of the hypothesis
also failed to hold up: increased marinobufagenin was supposed to lead to an
increase in peripheral vascular resistance, and in humans, eating a high-salt
diet does not cause this.45 The
“natriuretic hormone” theory of hypertension did not bear out in experiments.
Hiding in plain sight throughout this entire controversy? Insulin
resistance and diabetes, both consistently found to coincide with both salt
sensitivity and high natriuretic hormone levels. In fact, both type 1 and type
2 diabetes were associated with increased levels of marinobufagenin (the
natriuretic hormone).46 One group
found that, in diabetics, disrupted Na-K-ATPase function was associated with
insulin resistance, renal sodium retention, and the development of
hypertension.47 In other
words, whatever was causing diabetes was also impairing the
Na-K-ATPase (via increases in marinobufagenin) and causing salt-sensitive
hypertension. And the dietary substance causing diabetes was…(drumroll, please):
sugar.48
Before marinobufagenin was determined to be the natriuretic hormone, it
was found to be significantly increased in the urine of patients with type 1
diabetes.49
So the inhibition of N-K-ATPase (caused by marinobufagenin) was
seemingly caused by diabetes. And consuming high amounts of sugar, not salt,
was consistently linked with an increased risk of diabetes.50 Diets high
in sugar were found to increase the diagnosis of diabetes or prediabetes, even
when calories were held constant.51 Thus, by
increasing marinobufagenin, a diet high in sugar was the likely culprit causing
hypertension as well as kidney damage and an increased risk of stroke.52
The idea that sugar could be causing salt-sensitive hypertension was
considered nutritional blasphemy. That is, until 1988, when Ottavio Giampietro
and colleagues proposed a mechanism for how diabetes causes hypertension.53
At the time, it was well known that people who had diabetes were also
likely to have high blood pressure.54 And
Giampietro and his fellow authors knew that diabetics receiving insulin had
increases in body sodium,55 likely
caused by high insulin levels in the blood, which were known to stimulate the
reabsorption of sodium by the kidneys.56 (In other
words, rather than excreting the normal amount of salt in their urine, diabetics
would hold on to that salt in their bodies.) Additionally, insulin-dependent
diabetics were found to have high circulating levels of growth hormone,57 which also
increases sodium reabsorption.58 Giampietro
and colleagues were one of the first groups to conclude that diabetes was a
state of sodium retention and decreased Na-K-ATPase activity in the heart,
peripheral nerves, blood-brain barrier, and red blood cells;59 they
surmised that the sodium pump became insulin resistant in those who were
diabetic, as insulin was found to stimulate its activity.60 Thus, the
idea that diabetes (or high insulin levels) was the culprit
for “salt-sensitive” hypertension can be traced back as early as the late
1980s.
Interestingly, sodium in the cell was found to be higher in obese
people with high blood pressure compared to those who were lean.61 In
essence, whatever causes obesity may also be increasing sodium levels in the
cell.
In the 1980s, the idea that hypertension was a metabolic disorder, and
in particular a state of insulin resistance, was finally beginning to gain
support by many scientists.62 Indeed,
hypertension was often found to cluster in patients with high levels of
glucose, insulin, and obesity.63 And up to
80 percent of people with essential hypertension had been found to have insulin
resistance.64 Another
group of authors publishing in the New England Journal of
Medicine concluded that “essential hypertension is an insulin-resistant
state.”65
Separately, John Yudkin had shown that sugar was found to increase fasting
insulin levels in humans and nonhuman primates.66 At the
same time, low-salt diets were found to cause insulin-resistant blood vessels,
leading to increased vasoconstriction, the same problem found in patients with
hypertension.67 Thus, it’s
not a huge leap to say that, even without the help of sugar, low-salt diets were
probably contributing to hypertension by causing insulin resistance.
But still, old dogma dies hard, and even with this convincing new line
of research, the consensus was that around 90 percent of people with high blood
pressure had “essential hypertension”—high blood pressure without any known
cause. These people were believed to be simply “genetically predestined” to
develop hypertension—genetically susceptible to salt, not sugar.68 Those same
people were found to have increased insulin resistance, and their degree of
insulin resistance was also associated with increased mean arterial pressure.69 Having a
family history of hypertension was found to more than double the risk of
insulin resistance (45 percent prevalence versus 20 percent in those without a
family history of hypertension). However, this created a chicken-or-egg
conundrum—was it hypertension causing insulin resistance, or
vice versa? In essence, those who are born to hypertensive parents have a
higher degree of insulin resistance, which likely leads to higher blood
pressure later in life. The authors also concluded that disturbances in these
patients’ ability to metabolize carbohydrates effectively could be detected
well before they developed high blood pressure,70 suggesting
that insulin resistance came first, with hypertension developing later.
Whatever caused the insulin resistance would then cause hypertension.
These results were repeatedly confirmed in later studies:71 children
of parents with high blood pressure showed a tendency to develop insulin
resistance and high levels of circulating insulin.72
Studies also showed that prehypertension and hypertension clustered
with obesity and insulin resistance.73 And
reports began to show that salt sensitivity was common in those with obesity
and hyperinsulinemia.74 But again those
old dictums held sway—obesity was considered a state of “caloric imbalance,”
whereas the idea that an elevated insulin level (from overconsuming sugar)
could cause weight gain was not an accepted theory.
However, studies from the late 1980s up until the mid-2000s started to
suggest that obesity was a state of hormonal imbalance, marked in particular by
high levels of insulin, and that treating high insulin levels may treat high
blood pressure. Indeed, one twelve-month study published in 2007 showed that
when insulin levels were reduced as a result of lifestyle changes plus
metformin (a diabetes medication), salt-sensitive blood pressure was
effectively eliminated.75 The
authors suggested that the metabolic defects that appeared alongside obesity
(such as insulin resistance and the activation of the sympathetic nervous
system) were causing salt-sensitive hypertension, and that fixing those metabolic
abnormalities corrected the salt sensitivity. Another 1989 study found that
obese teenagers who lost 8 percent of their starting weight were able to
correct their salt-sensitive blood pressure.76 Animal
studies extended these findings, with one showing that giving rats metformin
prevented salt-induced hypertension.77 Another found that eating more salt improved
the blood-pressure-lowering effects of metformin.78
Even weight loss itself had been found to produce large reductions in
blood pressure—even when sodium intake was not reduced.79 One group
of authors studied twenty-five obese patients in the UCLA Risk Factor Obesity
Control Program who were randomized to eat a normal sodium intake of 2,760
milligrams per day or a low sodium intake of 920 milligrams per day while also
losing weight. Both groups’ blood pressure fell equally with weight loss. The
results of the study were clear: drop the pounds, and the blood pressure would
follow without having to drastically cut salt intake.
There was one final line of evidence implicating sugar as the cause of
salt-sensitive hypertension, and that was cortisol. Local cortisol excess was
known to lead to hypertension in those with Cushing’s syndrome, chronic renal
failure, and essential hypertension. And cortisol-induced hypertension was
likely being confused with salt-sensitive hypertension, because as cortisol
increased in the body, so did sodium, blood volume, and blood pressure. High
cortisol levels were also implicated as a cause of high insulin levels, as an
excess of cortisol (as seen in Cushing’s syndrome) leads to abdominal obesity,
glucose intolerance, hyperglycemia, hyperlipidemia, hypertension, and
atherosclerosis. Undiagnosed local cortisol excess was causing hypertension—and
high-salt diets continued to take the blame. It was also known that salt could
raise blood pressure in animals when they were given injections of
corticosteroids.80 But if the
high cortisol levels were lowered, then the hypertensive effect of salt would
go away.
And so the big question: What causes high cortisol levels? And yes, you’ve guessed it: sugar can raise cortisol levels and hence cause
salt-sensitive hypertension.81 John
Yudkin had shown this in 1974, when feeding sugar to rats increased levels of
corticosterone (the equivalent to cortisol in humans) by 300 percent.82 This was
found even before insulin levels were increased, implying that elevated
cortisol may actually cause insulin resistance.
Dr. George A. Perera had also written about how corticosteroids may be
the underlying cause of hypertension. He showed that adrenocorticotropin
hormone (ACTH), the hormone that precedes the release of cortisol and aldosterone
from the adrenal gland, could increase blood pressure.83 But it
wasn’t until half a century later that fructose in the brain was found to
stimulate ACTH release, and thereby increase the secretion of cortisol.84
Importantly, it was thought that fructose levels would be too low in the body
for this to matter to the brain. We’ve since discovered, however, that fructose
can be formed in the brain from glucose, particularly in states of insulin
resistance.85
Dr. Perera also showed that low-salt diets could be dangerous in
someone lacking corticosteroids. Perera wrote that reducing salt intake in a
patient with Addison’s disease (in which the adrenal glands produce inadequate
levels of cortisol and aldosterone) led to large drops in blood pressure as
well as low sodium levels in the blood and severe weakness. However, when
corticosteroids were supplemented, the blood sodium returned to normal and
blood pressure rebounded. Thus, it was obvious that glucocorticoids and
mineralocorticoids determined the effects that dietary salt had on blood
pressure and not salt intake per se.86 And it was
sugar that was found to increase glucocorticoids and hence cause people to have
salt-sensitive blood pressure.
All signs have long pointed directly toward sugar—but it took us so
long to see it. Part of the problem was the stubborn resistance of researchers
clinging to their long-held beliefs. Another part of the problem was the
willful influence of the sugar industry, deflecting attention away from the
clearly guilty suspect. And the convincing evidence
disproving the salt–blood pressure theory can be seen simply by stepping back
and looking at large-scale studies of whole populations. And in those studies,
the findings are irrefutable.
Salt Intake
and Blood Pressure: Population Studies
Regardless, a large body of data kept poking holes in the idea that
salt was the cause of hypertension of acculturation. For one, numerous
populations that ate a high-salt diet lacked hypertension, whereas the same
could not be said for sugar. Consider the high salt intake of these various
populations and their blood pressure, shown in the list that starts on this page.
One of the strongest arguments supporting the notion that salt causes
hypertension and cardiovascular disease had always been from Japan. The
Japanese were known to eat lots of salt, and while in general they had low
rates of heart disease, they had a high rate of cardiovascular conditions, such
as stroke and hypertension. Indeed, people living in Akita, Japan, were known
for having a very high rate of hypertension and death due to stroke, and they
ate a lot of salt (around 27 grams of salt per day, with a maximum intake
between 50 and 61 grams) coming from miso soup, soy sauce, seasonings, and
vegetables/pickles. Salt was just one of several possible causes of their
cardiovascular disease. Researchers suggested that the high rate of stroke in
Japan (particularly in Akita) was due to other factors besides salt, such as
“an unbalanced diet consisting of polished rice and deficiencies in the dietary
life.” Others have noted “gluttony over rice,” “life stress such as overwork of
farmers,” “vitamin C deficiency in the diet,” “the
quantity of silicic acid in drinking water and food,” “cadmium in the
intestines of widely eaten river fish of Japan,” and the “sulfur/carbonate
ratio of river water” as possible contributors to the high rate of death from
stroke.87 And
cadmium is a likely suspect. It is estimated to contribute to 17 percent of the
stroke cases in Japan.88 Also, the
low intake of saturated fat in Japan was linked to the higher rate of death due
to stroke.89
Still, the Akita stroke rates are striking when compared with the
stroke rates in Aomori, Japan, an area where the population tended to consume
around 15.2 grams of salt per day. In fact, the rate of death due to stroke was
more than twice as high in Akita as in Aomori. The average blood pressure in
Aomori was fairly low (131.4/78.6 mmHg) and the incidence of death from stroke
was only moderate,90 with 139.2
deaths from stroke per 100,000 in those thirty to fifty-nine years old. In
Akita, this number was 218.6. What was happening here?
POPULATIONS THAT CONSUME AMPLE AMOUNTS OF SALT IN WHICH HYPERTENSION IS
VIRTUALLY ABSENT
Sodium
intake: ~3,300 mg sodium/day
Not a
single nun with a diastolic blood pressure over 90 mmHg.91
Sodium
intake: ~3,300 mg sodium/day
Population:
The Kuna Indians (off the coast of Panama)
Sodium
intake: ~3,450 mg sodium/day (the same amount of sodium consumed in the United
States today)
Blood
pressure: Only 2 percent known to have hypertension. Blood pressure did not
increase with age.92
Population:
Seventh-Day Adventist vegetarians and omnivores and Mormon omnivores93
Sodium
intake: ~3,600 mg sodium/day
Adventist
vegetarians—blood pressure: 114/67 mmHg in men and 108.6/ 66.6 mmHg in women
Adventist
omnivores—blood pressure: 121.9/72 mmHg in men and 110/66 mmHg in women
Mormon
omnivores—blood pressure: 122.2/73.2 in men and 117.2/74.5 mmHg in women
Population:
Java (part of Indonesia)
Sodium
intake: ~3,600 mg sodium/day
Blood
pressure: 124/73 mmHg in men and 128/75 mmHg in women94
Sodium
intake: ~3,600 mg sodium/day
Blood
pressure: 120/75 mmHg in men and 118/77 mmHg in women95
Population:
Taiwan (agricultural population)
Sodium
intake: ~4,000 mg sodium/day
Blood
pressure: 128/83 mmHg in men96
Sodium
intake: ~4,000 to 5,000 mg sodium/day during the wet season (around five months
out of the year);97 ~3,500 to 4,000
mg sodium/day during the dry season
Population:
Inhabitants of Kotyang, Nepal
Sodium
intake: ~ 4,600 mg sodium/day
Blood
pressure: No cases of hypertension in the men. Blood pressure did not increase
with age. In the women, hypertension was extremely rare (1.4 percent). The
authors concluded, “In the present study, no significant increase in systolic
blood pressure with age was found in men living in Kotyang, and no hypertensive
men and very few hypertensive women were detected in Kotyang in spite of taking
on the average 12 g/day of salt.”99
The intake of
sugar was less than 1 gram/day in Kotyang. However, in another village in Nepal
(Bhadrakali) there was a greater intake of sugar (25.5 grams/day in Bhadrakali
men and 16.3 grams in Bhadrakali women). And the prevalence of hypertension was
10.9 percent in men and 4.9 percent in women.
Sodium
intake: 5,600 mg sodium/day
Blood
pressure: 133/81 mmHg100
Population:
South India (consume less salt than North Indians yet have higher blood
pressure)
Sodium
intake: 3,200 mg sodium/day
Blood
pressure: 141/88 mmHg101
Population:
Apple-eating zones of Aomori, Japan (low prevalence of diastolic hypertension)
Sodium
intake: ~6,000 mg sodium/day
Blood
pressure: 131.4/78.6 mmHg102
Population:
Okayuma, Japan (in the summer)
Sodium
intake: ~6,000 mg sodium/day
Blood
pressure: 122/75 mmHg in men and 122/72 in women103
Sodium
intake: ~7,600 mg sodium/day
Blood
pressure: 128/79 mmHg in men104
Population:
Buddhist farmers in Thailand
Sodium
intake: ~8,000 mg sodium/day
Blood
pressure: No rise in blood pressure with age105
Researchers suspected another factor at work: potassium. In a study of
1,110 adults in Aomori, Japan, an increase in apple intake was associated with
lower blood pressure. Apples are a good source of potassium. Men’s systolic
blood pressure tended to be over 150 mmHg when they ate no apples per day, but
it dropped to less than 140 mmHg when they ate three apples per day.
Researchers believed that the potassium in the apples was key here. This
blood-pressure-lowering effect of apples was also confirmed in a clinical trial
of thirty-eight middle-aged men and women in Akita,106 and again
in a study of Japanese patients with essential hypertension—who, despite eating
approximately 15 grams of salt per day, found that their blood pressure dropped
down to normal when they increased their dietary potassium intake from
approximately 3 grams to 7 grams.107 Who knew
there was so much truth to the old adage about an apple a day? The problem in
Akita is not the salt, but that the diet there is otherwise deficient in
potassium.
This effect was also seen in Seventh-Day Adventist vegetarians,
Seventh-Day Adventist omnivores, and Mormon omnivores.108 The daily
intake of sodium in these groups was between 3,500 and 3,700 milligrams,
slightly higher than what the average person in the United States consumes.
However, the average blood pressure in the three groups was totally normal.
Importantly, the potassium intake was between 3,000 and 3,600 milligrams per
day (almost twice as high as the average potassium intake in America)—providing
additional evidence that potassium plays a critical role in regulation of blood
pressure.
These population studies give us real-world proof that higher salt
intake can be healthy—indeed, way healthier than salt restriction. But they
also help us start to tease out the complexity of the factors leading to high
blood pressure and stroke. Perhaps we need to shine attention on the fact that
the average intake of potassium in the United States is about half that
compared to what the groups studied here consumed—mostly due to lower fruit and
vegetable consumption.109 The real
lesson for all of us might be that, rather than look for ways to cut salt, we
could seek out ways to eat more potassium-rich plant-based foods, such as leafy
greens, squash, mushrooms, and avocados. And guess what helps us to do that?
Eating more salt!
How Low-Salt May Have Created the High Blood Pressure Epidemic
At the same time, data continued to mount showing that sugar increased
both blood pressure and heart rate, but it wasn’t discovered until decades
later that a diet high in sugar increased the risk of cardiovascular death
threefold compared to a diet low in sugar. Yudkin was able to show over and
over again that numerous abnormalities found in patients with coronary heart
disease (elevated lipids, insulin, and uric acid and abnormal platelet
function) could be caused by just a few weeks on a high-sugar diet.110 But still,
despite Yudkin’s efforts, and even to this day, sugar has not been given the
clear responsibility for our epidemic of cardiovascular disease. In the eyes of
the public and most of the medical profession, that blame
somehow—astoundingly—still lies at the feet of salt.
The Centers for Disease Control and Prevention (CDC) recently asked the
Institute of Medicine (IOM) to reevaluate the evidence relating to sodium
intake and cardiovascular risk, and its 2013 report found that there was no
benefit for restricting sodium intake below 2,300 milligrams per day. In fact,
it found that there may be adverse health outcomes.111
Nevertheless, inexplicably, the original 2004/2005 IOM upper limit on sodium of
2,300 milligrams per day was allowed to stand and “remains the basis for
federal salt policy today.”112 Even today,
the leading health agencies cannot agree on what amount of salt we should be
consuming—yet that still hasn’t stopped
the low-salt dogma. And the frightening conclusion to this entire controversy
may end up being that a low-salt diet has contributed to, rather than helped
prevent, the rising levels of heart disease in this country.
Reducing salt has been found to accelerate hardening of the arteries
and raise cholesterol and triglycerides in animals.113 Salt
restriction in humans with hypertension also increases plasma lipoproteins and
inflammatory markers.114 In people
with chronic high blood pressure, cutting salt increased low-density
lipoprotein (LDL; “bad” cholesterol) levels in the blood.115 But other
studies found that restoring higher levels of salt (going from 2 grams of salt
per day to 20 grams per day for five days) significantly lowered
plasma total cholesterol, esterified cholesterol, beta-lipoprotein, low-density
lipoprotein, and uric acid in people with hypertension.116 Even the
famous DASH-Sodium trial—the foundation of the most well-known low-salt
diet—found that salt restriction increased triglycerides, LDL, and the
total-cholesterol-to-high-density-lipoprotein ratio (TC:HDL).117
Even in people who had normal weight and regular blood pressure,
low-salt diets have been found to compromise kidney function, decrease
high-density lipoprotein (HDL; “good” cholesterol), and reduce adiponectin, a
substance released by fat cells thought to improve insulin sensitivity.118 A Cochrane
meta-analysis of almost 170 studies found that low-sodium interventions lowered
blood pressure only minimally while significantly raising levels of kidney
hormones, stress hormones, and unhealthy triglycerides. The authors of the
Cochrane analysis (which is usually seen as the gold standard of research
reviews) concluded that low-salt diets might lead to an overall negative effect
on health based on increases in hormones, “bad” cholesterol, and triglycerides.119
Another health risk, increased blood viscosity—“thickening” of the blood—has been thought to occur during salt restriction.120 Increased
blood viscosity, often noted in obese patients, is thought to contribute to an
increased risk of thrombotic vascular events, such as blood clots and deep vein
thrombosis.121 Salt
restriction also increases fasting norepinephrine, a substance that increases
heart rate. The heart receives blood supply during relaxation, whereas every
other organ gets blood when the heart is contracting. So the quicker one’s
heart pumps means the less time the heart is relaxed to receive blood and,
hence, oxygen. This is one reason why low-salt diets122 have been
implicated in increasing the risk of heart attacks: by reducing blood flow to
the heart. The increase in norepinephrine on low-salt diets may even produce
cardiac hypertrophy, overgrowth of the heart, which can lead to heart failure.123
Speaking for many a frustrated salt proponent, Weder and Egan concluded
in one of their papers that “the net cardiovascular risk benefit of an average
blood pressure reduction of only 1.1 mmHg could well be more than offset by the
rises in cholesterol, insulin, norepinephrine and hematocrit resulting from
salt restriction.”124 By
increasing angiotensin-II and aldosterone, low-salt diets could actually cause
overgrowth of the heart and kidneys, which could lead to heart failure and
kidney disease—the very diseases we have been told high-salt diets cause.
Weder and Egan concluded, “The potentially adverse impact of dietary
salt restriction on the risk factor profile for cardiovascular disease suggests
that further studies are necessary before a reduction in dietary salt intake
can be prescribed for the general population.”125
This was in 1991, over twenty-five years ago.
In 1995, Michael Alderman and coauthors openly suggested that low-salt
diets may increase the risk of cardiovascular events.126 They
reported a more than fourfold increased risk of myocardial infarction in men
who ate the lowest amounts of salt compared to the highest-salt-intake group.
Large-scale studies continued to emphasize these same findings. Two
large prospective European studies, which included almost four thousand patients without prior cardiovascular disease, found a more
than fivefold increase in mortality with a low sodium intake versus the highest
sodium intake.127 The
Prospective Urban Rural Epidemiology (PURE) study examined over 100,000 people
in seventeen countries and found that the lowest risk of death or
cardiovascular events was in those consuming between 3,000 and 6,000 milligrams
of sodium per day.128 The group
consuming less than 3,000 milligrams of sodium per day had the greatest risk.
Graudal and colleagues performed a meta-analysis of almost 275,000 patients129 and found
that consuming between 2,645 and 4,945 milligrams of sodium per day was
associated with the lowest risk of death and cardiovascular disease events.
After adjusting for other confounding factors, only the group consuming less
than 2,645 milligrams per day had a significant increase in all-cause
mortality; this was not found in those consuming more than 4,945 milligrams of
sodium per day.
There’s no denying that we are in the midst of a nationwide obesity
epidemic that threatens our collective health, well-being, and longevity: 69
percent of adults in the United States are now overweight or obese.1 Obesity
began to rise in the 1950s; it spiked around 1980, and the rate doubled from
1980 to 2000. Conventional wisdom blames obesity on an imbalance between our
consumption of calories and our expenditure of energy—eating more calories than
we burn through various activities, in other words. This is why we’re often
told to eat less and move more. As you may know from
personal experience, this strategy doesn’t work for everyone—or even most
people.
Increasingly, alternative theories of obesity have focused on the
quality of the calories we consume and how they affect us physiologically, as
Gary Taubes illustrated in his book Good Calories, Bad
Calories. Plenty of circumstantial evidence supports these contentions.
For one thing, the surge in our growing girth has paralleled our increased
intake of refined carbohydrates, sugar, and high-fructose corn syrup
(particularly in liquid form). The sugar industry would have us believe that as
long as we hit the gym to work off those calories, no harm would be done. But
new research suggests that our increasingly sedentary lifestyle may actually be
driven by these dietary factors, too.2 (The
potato comes before the couch.)
Given that sugar has finally been getting its due as Public Health
Enemy #1, it’s no surprise that sugar triggers an internal chain of events that
negatively affects our waistlines and our health. But what we’re just starting
to realize is how a low salt intake can produce similar physiological effects.
Consuming too little salt can set into motion an unfortunate cascade of changes
that result in insulin resistance, an increase in sugar cravings, an
out-of-control appetite, and what’s been dubbed “internal starvation” (aka
“hidden cellular semistarvation”), thereby promoting weight gain.3 Someone
who is overweight literally may be starving on the inside.
When you start restricting your salt intake, your body will do anything
to try to hold on to it. Unfortunately, one of the body’s defense mechanisms is
to increase insulin levels. It does this by creating a state of insulin
resistance. When insulin resistance kicks in, the body is less able to shuttle
glucose into cells, and it needs to secrete more insulin in order to control
blood glucose levels. Also, remember that when a person’s intake of dietary
salt is on the paltry side, hormones that compensate to help the body retain
salt (such as renin, angiotensin, and aldosterone) are released in greater
amounts. Well, these hormones end up increasing fat absorption, too. In
essence, compared to someone who hasn’t slashed his or her salt intake, a
low-salt diet may cause you to absorb twice as much fat for every gram you
consume.4
This chronically elevated insulin level keeps stored fat and proteins
locked away, making them unavailable to the cells that need them. When your
insulin levels are elevated, the only macronutrient you can
efficiently utilize for energy is carbohydrate. In effect, high insulin levels
basically force you to eat more carbs because you can’t readily get energy from
anything else. Then, consuming high levels of refined carbs triggers greater
insulin release, and the cycle repeats and reinforces itself, endlessly
perpetuating the problem of high insulin levels—which, in turn, perpetuates
obesity.5
Plus, low-salt diets increase the risk of overall dehydration (and
hence cellular dehydration), and that’s a problem because generally
well-hydrated cells function much more efficiently and consume less energy than
dehydrated cells do.6 The less
energy that’s available in your body, the greater the state of internal
starvation, and the more calories you’re likely to consume. Are you starting to
see how low-salt diets can cause weight gain?
Even if these shifts don’t lead to the accumulation of extra pounds,
the result is the same: these physiological changes cause someone to become
“metabolically overweight” or obese, even if it’s not reflected as a higher
number on the scale or as a body mass index (BMI) in the overweight or obese
category. In other words, you can be “thin on the outside and fat on the
inside” (what’s often referred to as TOFI—aka “skinny fat”). You may be TOFI if
your body weight is normal but you have a disproportionate amount of visceral
fat, adipose tissue stored in your abdomen, where it is most harmful. In other
words, your weight could remain within the normal range, but you could still
have a dangerous buildup of fat in and around your organs as well as insulin
resistance and metabolic syndrome, a cluster of conditions such as a large
waistline, elevated fasting blood sugar, high blood
pressure, high triglycerides, and low HDL cholesterol that raise your risk of
developing heart disease, diabetes, and stroke.
With internal starvation, insulin resistance essentially degrades your
body’s fat metabolism system, encouraging you to overeat to compensate for all
the calories that are being vectored into your fat cells and locked down there.
This can make you feel like you’re starving inside while you may be gaining
weight at the same time. Moreover, because your body cannot access its stored
energy, exercise becomes highly unappealing. Instead, your brain and body swing
into calorie-conservation mode and you seek relative stillness, rather than
energy-expenditure mode, because you’re literally starving for usable energy.
The likely result: weight gain and further body fat accumulation, another
continuous cycle that perpetuates this unfortunate state of internal affairs.7
The concept of internal starvation was first theorized right around the
time that the Salt Wars began—although it would be decades until the idea
caught on. “Hypothalamic obesity,” a phrase created in 1900 by French
neurologist M. J. Babinski, is a condition that results from damage to the
hypothalamus (the part of the brain that controls satiety and hunger), thus
leading to metabolic changes, overeating, rapid, unrelenting weight gain, and
insulin resistance.8 The late
Stephen Walter Ranson, MD, who was the director of the Institute of Neurology
at Northwestern University, is often credited as being one of the first to
suggest in the 1940s that obesity is a condition of “hidden cellular
semistarvation.” Ranson believed this state was triggered by a shortage of
nutrients, which then forces the body to increase its food intake, reduce its
energy expenditure through less physical activity, or pursue a combination of
the two measures (again causing weight gain).9 Twenty years
later, Edwin Astwood, MD, an endocrinologist and physiologist at Tufts
University, coined the term “internal starvation” to describe the same
phenomenon.
By any name, it’s a paradoxical effect that can make you wonder whether
obesity leads to overeating and being sedentary, or the other way around.
Increasingly, this conundrum is being addressed and studied
by obesity experts and endocrinologists alike. Maybe we don’t get fat because
we eat too much—we eat too much because something has made us fat.
Interestingly, there’s also mounting evidence that your mother’s salt
intake while you were in the womb can affect your risk of experiencing internal
starvation once you’re alive and kicking. Specifically, if your mother consumed
a low-salt diet during pregnancy, you may be born into a state of internal
starvation, with more fat around your organs, abnormal leptin levels, and
insulin resistance.10 A low salt
intake during pregnancy may essentially program obesity in a mother’s offspring
from day one, according to research in animals. That’s a powerful trickle-down
effect, indeed!
The Salty Truth
We
know that low salt intake leads to insulin resistance and increases insulin
levels, and insulin resistance causes glucose to build up in the blood instead
of being absorbed by the cells for energy, triggering a long, problematic chain
of physiological events—excessive hunger, overeating, greater fat storage in
your fat cells, and an internal energy crisis. In someone who is healthy and
lean, a normal fasting insulin level is generally 5 uIU/mL or less, whereas a
level just twice as high (10 uIU/mL) likely indicates insulin resistance.11 Low-sodium
diets may increase the fasting insulin level from 10 to 50 percent, which could
throw someone from a healthy level to one that’s trending toward diabetes.12 One review
looked at the harms of low-salt diets and reported that in studies of just one-
or two-week duration, low-salt diets have an insulin-raising effect in obese
patients with high blood pressure.13 The review
found that even moderate salt restriction (2 grams of salt per day) could increase
insulin response to an oral glucose tolerance test in patients with high blood
pressure.14
Restricting sodium to around 460 milligrams per day (about ⅕ teaspoon of salt)
for one week has been found to increase fasting insulin, insulin
response to an oral glucose tolerance test, fasting triacylglycerol, plasma
fatty acids, and aldosterone and renin levels.15
We know that higher insulin levels will lead to greater fat storage,
even if your overall caloric intake remains the same—and now we see that this
higher fatty acid concentration in the blood may also increase damage to the
arteries and blood vessels.16 When salt
restriction reduces blood circulation, less blood flows to the liver,
interfering with the liver’s ability to break down insulin—a possible mechanism
explaining how low-salt diets raise insulin levels.
In contrast, higher-salt diets keep looking better and better. We’ve
heard previously that eating more salt enhances the dilation of the blood
vessels, especially in salt-resistant patients, an effect that sticks around
for at least several months in clinical studies. Restricting your salt intake
can do the opposite—constrict your blood vessels and decrease your muscles’
ability to absorb glucose, which may lead to chronic high insulin and—you
guessed it—increased fat storage.17 So many
pathways all lead to the same place: increased body fat.
Eighteen studies, including around four hundred patients, have looked
at the effects of sodium restriction on fasting plasma insulin concentrations.18 In one study
of 147 people with normal weight and blood pressure, salt restriction caused
increases in insulin, uric acid, LDL, and total cholesterol levels.19 Fasting
insulin was higher in twenty-two of the twenty-seven groups (thirteen
statistically significant), unchanged in two, and lower in three (not
statistically significant). Egan and colleagues found that low-salt diets
increase both fasting and postglucose insulin by about 25 percent compared to
high-salt diets, an effect that has been duplicated and confirmed—that is, proven—in many later studies and meta-analyses of
randomized controlled trials.20 Even those
few people whose blood pressure might go down on low-salt diets—the
“salt-sensitive” among us—experience significant increases in insulin.21
One of the mechanisms that could be at work here is salt’s ability to
actually improve our cells’ ability to use glucose.
Animal studies indicate that salt restriction worsens the body’s ability to use
glucose correctly while also increasing body weight, body fat, and fatty acid
levels. A high salt intake likely increases the glucose transporter GLUT4 in
insulin-sensitive tissues and thus allows greater glucose disposal.22 Indeed,
high-salt diets have been found to increase GLUT4 protein in both fat tissue
and muscle. This is a good thing, because it allows your body to pull more
glucose out of the bloodstream, reducing insulin levels and minimizing the
damage that high glucose levels would have on the blood vessels. While a
low-salt diet has been shown to impair insulin signaling, a high-salt diet has
been proven to enhance insulin signaling.23
Salt-restriction studies in humans have found adverse effects on glucose and
lipid metabolism.24 One animal
study even found that a low-salt diet increased body weight, belly fat, and
blood glucose and plasma insulin levels, while it induced insulin resistance in
the liver and muscle tissue.25
Low-salt diets have also been found to increase liver fatty acid
synthesis, which can contribute to nonalcoholic fatty liver disease (NAFLD),
commonly known as “fatty liver,” as well as organ fat storage, compared to a
normal salt intake. Researchers found that the activity of brown adipose
tissue—the “good fat” that burns calories—was reduced on a low-salt diet,
indicating that low-salt diets may lower our basal metabolic rate, and possibly
contribute to accelerated aging.26
Worse, many obese patients begin their weight-loss programs by trying
to cut their carbohydrate intake. Cutting carbs causes you to become a “salt
waster,” excreting more salt than you would on a more balanced diet, especially
when you hit ketosis (near 50 grams of carbohydrates per day or less). Thus, if
you are going to cut your carbohydrate intake, you want to increase your salt
intake to match the additional salt loss by the kidneys and to help prevent the
subsequent rise in insulin levels to compensate for this loss. Sadly, most
doctors will pair recommendations to lose weight with recommendations to reduce
salt at the same time. But it appears that most people need an additional 2
grams of sodium per day compared to their normal sodium
intake during the first week of carbohydrate restriction, and around an additional
1 gram of sodium per day during the second week to match increased salt losses.
Indeed, we’re finding that increasing your salt intake, even above
what’s generally considered a normal intake, may help improve your insulin
sensitivity. One clinical trial found that compared to consumption of about
3,000 milligrams of sodium per day, those who consumed around 6,000 milligrams
of sodium per day significantly lowered their glucose response to a 75-gram
oral glucose tolerance test. Moreover, the researchers found that when diabetic
patients were placed on the higher-sodium diet, their insulin response
improved. The authors were quite emphatic and suggested that some people even
supplement with sodium, stating that “an abundant sodium intake may improve glucose
tolerance and insulin resistance, especially in diabetic, salt-sensitive, or
medicated essential hypertensive subjects.”27
We know that low-salt diets seem to cause your fat cells to become
resistant to the effects of insulin,28 which in
turn increases the level of glucose in the blood and causes oxidative stress,
inflammation, and damage to your arteries, as well as further insulin
resistance. It’s a vicious cycle of internal starvation. Doctors have known for
decades that giving people diuretics, which help the body get rid of salt, can
also promote insulin resistance and diabetes. Well, when you restrict your salt
intake, you are essentially deriving the same detrimental physiological effects
as if you were placed on a diuretic medication.29
• Insulin resistance and
higher insulin levels are likely physiological adaptations to salt restriction.
• The elevation in
insulin levels makes us fatter and shifts us further into internal starvation.
The Sugar Connection
As
important as it is to increase salt to prevent internal starvation, it’s even
more important to avoid sugar. We all know that calories from sugar are
especially detrimental when it comes to our ability to manage our weight and
overall health. This is partly because a greater intake of sugar calories
stimulates more insulin resistance and more fat storage than other types of
calories do, even when the total calorie intake remains the same.30
Excessive consumption of fructose can cause too much fat to accumulate
in the liver, which causes this vital organ to become resistant to insulin,
thereby setting you up for overall insulin resistance throughout your body.31 A high
fructose intake can also decrease the adipose tissue’s fat-storing capacity,
slamming that fat into and around organs like your heart, pancreas, and liver.
(Indeed, by overconsuming fructose you hit the liver with fat storage from two
different directions.) This is harmful to your health on so many levels because
it causes chronic inflammation and oxidative stress, among other detrimental
effects.32 What’s
more, letting your sweet tooth get the upper hand on your diet can also damage
mitochondria, the power source in your cells, which leads to a decrease in ATP
that in turn increases your hunger and leaves you with no
energy for exercise.33 Those high
glucose levels in the blood even pull water out of the cells, causing cellular
dehydration. The water that was essentially stolen from your cells and pushed
out into your blood—a phenomenon that has traditionally been blamed on salt, by
the way—leads to a lower salt level in your blood.
In essence, a high-sugar diet increases your need for salt by diluting
its level in your blood.34 And yet
this is one more way to illustrate how more salt can help us: eating enough
salt to satisfy our salt cravings may just be the key to kicking our sugar
cravings for good.
6 – Crystal Rehab: Using Salt Cravings to Kick Sugar Addiction
Salt is one of our five innate taste sensations, and with good reason:
besides making food taste good, we’ve seen how vital salt is to our health. Fortunately,
the human body has a built-in system—a “salt thermostat”—that helps us get just
the right amount. Our salt thermostat signals the brain to seek more salt when
we need more to meet our physiological needs, as well as to stop when we have
enough to fulfill our biological functions. This built-in system helps regulate
our internal fluid-salt-electrolyte balance and resets it when necessary—and
it’s all taken care of automatically, without any effort on our part.
Luckily for us, relearning how to listen to one has the power to help heal us from the other. It’s time to set the record straight about
the health-protecting, lifesaving nature of salt cravings—and drop the guilt
for good.
Is Salt Addictive?
When Salt Became a Spice
M.
Lapicque, who studied the salt habits of native Africans of the Angoni
district,1 was first
credited in 1896 with proposing the idea that salt was a condiment, similar to
pepper, curry powder, paprika (capsicum), and other flavoring agents, its main
purpose being a “gustatory stimulus.”2 This idea
stems from the fact that when salt is introduced to low-salt-eating natives,
their salt intake increases. Anti-salt evangelist Graham MacGregor was one of
the biggest promoters of the idea that “the ‘need’ for salt is a habit [a mild
form of addiction] that can be changed by gradual reduction in the salt content
of the food consumed.”3 And other
low-salt advocates similarly believed—and still do believe—that salt is mildly
addictive. For example, fathers of the 1977 low-salt recommendations, George
Meneely and Harold Battarbee, were highly influential in promoting the idea
that salt is addictive. These authors believed that the intake of salt was
“induced” from its “noxious effects beginning in childhood, when habits of
excess salt consumption are acquired at the family table, and are perpetuated
by continuing habit.”4
This idea actually stemmed from our old pal Lewis Dahl, who, like
Meneely and Battarbee, viewed salt as “a condiment, not a requirement.”5 Lewis Dahl
suggested that salt intake was induced because of its ubiquity in the food
supply. He suggested that if salt was provided in lower amounts, we would adapt
and consume less, and if given more salt, we would rapidly become accustomed to
it and begin eating a diet higher in salt. Meneely and Battarbee followed
Dahl’s lead and suggested that “salt appetite is induced rather than innate and
that like salt intake, appetite for salt bears no necessary relation to
requirement.” So, in essence, the idea that salt is addictive can be traced
back to those few low-salt advocates who brought us the low-salt guidelines to
begin with—another commonly held belief that comes from their “expert opinion”
rather than sound science.
Our “hunger” for salt bears the most physiological resemblance to our
thirst for water—how much we take in is controlled by how much we need. In summer, we drink more water because we lose more in our
sweat; in winter, our water intake goes down.6 We adjust
water intake by listening to our thirst. Salt consumption works exactly the
same way. Indeed, numerous experiments have found that animals who are
deficient in salt will increase their intake once it’s available—which is why
animals are drawn to a salt lick.7 The same
happens in humans who have been depleted of salt (such as athletes on a hot day
or someone receiving dialysis).8
So how did this myth get started? Some experts used population data to
suggest that salt intake will increase when it is introduced to societies that
do not use a lot of salt. Norman K. Hollenberg of Harvard Medical School termed
it a “habituation” that can develop with salt intake, similar to what happens
with alcohol, tobacco, and coffee, all of which are habit-forming. However,
this increased intake does not mean salt is habit-forming—it’s actually
evidence that if enough salt is available, people will consume more, but only
up to a physiologically determined set point, one that provides ideal health and
longevity. Indeed, when salt is freely accessible, people across numerous
populations tend to eat an amount that stays within a remarkably narrow range,
generally between 3 and 4 grams of sodium per day.9 When salt
is freely available, even animals consume an amount almost exactly proportional
to humans’ instinctive intake.10 This
consistency supports the idea of an evolutionary “salt set point” that resides
in both humans and animals. Our salt intake is unconsciously controlled by our
internal salt thermostat.
What may look from the outside like salt “addiction” may actually be a
reflection of the flux in salt storage. Interestingly, salt can be stored in
the skin—similar to the way a camel stores fat in its hump, but distributed
widely and invisibly—via a mechanism that appears to be controlled by certain
hormones that are produced within the body. Some
have proposed that aldosterone increases those salt stores in the skin, whereas
cortisol may deplete those stores.11 (Recall
that aldosterone also helps the body retain salt during salt depletion.) When
we aren’t eating enough salt, aldosterone increases, which in turn stores salt
in the skin. People who have consumed low-salt diets their entire lives, such
as those in primitive societies, automatically switch over to eating more salt
once it’s introduced, and the higher salt intake may cause the body to lose
some of its salt stores in the skin. The reduced amount of salt in the skin may
be a signal to continue to eat the salt in the range of 8 to 10 grams per day.
In essence, the fact that certain low-salt-eating people begin to consume more
salt once it’s introduced may have nothing to do with salt being addictive—and
everything to do with human physiology. They’re simply eating more because
those hidden salt stores in the body have gone down because of the increased
salt supply in their environment.
Certain individuals have “less desire” for salt after reducing their
intake, a phenomenon that has been proposed as proof that low-salt diets are
ideal.12 But this
theory has never been proven to be true; even if some people eat less salt upon
its restriction, this is undoubtedly a conscious choice. In fact, even if there
is a reduction in the desire for salt with salt restriction, this is due to the
kidneys shutting off salt excretion (the kidneys try to hold on to every
filtered milligram of sodium on low-salt diets). Furthermore, only a small
percentage (around 25 percent) of the population can even drive their salt
intake down to what most guidelines recommend.13 The body
seems to “fight” salt restriction with all its might
because of the additional stress placed on it by salt restriction. Those who
seem to be consuming extremely high amounts of salt (putting salt on every meal
they eat) may unconsciously be protecting their optimum blood volume.14 So the
next time you find yourself looking at someone with those “judgy eyes” across
the dinner table or at a restaurant as they sprinkle loads of salt on their
food, you should instead think to yourself, “That person’s body is telling them
they need more salt.”
The Dark
Side of Low-Salt Eating
The
body has a very elegant way of ensuring that you replace any lost salt: by
making your brain’s reward system hypersensitive and allowing it to receive
more pleasure from eating salt. This “sensitization” occurs during salt
depletion, giving you a greater craving for salt so you seek it out, and then
helping you experience increased reward when you eat a lot of it.15 Salt
depletion simply makes us like salt better.16 This
survival mechanism developed over 100 million years of evolution and has
ensured the survival of almost every single species since then.17 If our body
could not enhance the brain’s craving and reward for salt during states of
deficit, our species (as well as others) would have become extinct long ago.
However, there is a downside to this enhanced reward in the brain when
we restrict our salt intake: the same sensitization that drives you to seek out
and consume more salt could also prime your brain for other addictions. By
turning up the volume on your reward circuitry, your brain may experience
greater pleasure when consuming other dietary substances that trigger the
brain’s reward system. This priming could create problems with addictive
substances, especially refined sugar and drugs of abuse, increasing their
addictive potential.18
It’s not too much salt that creates “salt addiction.” It’s salt
restriction, which increases our risk of salt depletion, that can produce
changes in the reward center of the brain. Restricting salt leads to structural
modifications in the nucleus accumbens that cause the brain to get a greater
reward or “high” from salt. These modifications resemble the changes that occur
in people who have become addicted to drugs of abuse, and this sensitization
can be hijacked by other substances of abuse.19
Sounds amazing, doesn’t it? That an enhanced “hunger for salt,” born
during times of salt depletion, may “cross over” and enhance our reward from
refined sugar and drugs of abuse? But the evidence in the literature strongly
supports this notion. For example, sodium depletion has been found to
cross-sensitize with amphetamine, a drug also known to cross-sensitize with
cocaine.20
Cross-sensitization is a phenomenon that generally only occurs between drugs of
abuse, in which the use of one drug leads to enhanced effects (and increased
abuse potential) of the other.21 In this
case, sodium depletion itself is acting like a
substance of abuse, increasing the reward and abuse potential of other
substances of abuse. Indeed, this shared brain pathway was shown in a 2009
study from the University of Florida College of Medicine in Gainesville.
Investigators were looking into the Salted Food Addiction Hypothesis, which
proposes that salty food acts in the brain like an opioid drug, stimulating our
brain’s receptors and producing pleasurable reward sensations and cravings when
salty food isn’t available.22 The
researchers found that salty food has a slight appetite-stimulating effect in
people who are dependent on opiates, but not in nonaddicts. This point
underscores the shared pathways in the brain and really highlights how
dangerous salt restriction can be: by making the brain’s addictive pathways
more sensitive, salt restriction likely also makes people more susceptible to
dangerous addictive drugs and food addiction.
Restriction-induced periods of enhanced salt cravings do not seem to
lead to prolonged overconsumption—they seem to last only until the salt depletion has been corrected. And once it is corrected, inhibitory
signals will turn off the “liking” for salt and turn on an “aversion” signal.23 It has
been postulated that a high salt intake during times of repletion causes the
“salt receptors on the tongue to ‘flip’ from positive to
negative…quite unlike the response of the other four basic taste sensors and
thereby tends to decrease intake of salty foods.”24 (Behold
the salt thermostat at work!)
We live in a society where substances of abuse are readily accessible.
Almost thirty thousand people in the United States die every year from
overdosing on prescription opioids, cocaine, and heroin.25 Given the
very real death toll of this staggering epidemic, if salt depletions and low
salt intakes increase the potential to abuse addictive substances, we need to
seriously ask ourselves: Do the hypothetical and largely disproven “benefits”
of restricting our salt intake really outweigh the proven, multiple,
life-threatening risks? Or is it time to hold our public health officials
accountable for their willful disregard of decades of scientific evidence, and
protect future generations from these needless risks?
From Cradle
to Grave: How Our Salt Thermostat Gets Derailed
Let’s say your mother consumed too little salt during pregnancy,
thinking she was doing the right thing for herself and her baby. As a fetus, your body would develop in a salt-deprived state, and the
dopamine receptors in the reward center of your brain would become highly
sensitized to salt, causing you to get amplified gratification from eating
salt. Studies have noted that a low salt intake in pregnant mothers may cause
offspring to eat and crave more salt throughout childhood and adulthood.26 The
increase in salt appetite seems to help ensure the survival of offspring during
further sudden dehydration events (such as dramatic sweat loss on a hot day).
Unfortunately, it may also predispose you to addiction to substances of abuse.
This adaptation started out well. Fessler introduced the idea that
there is a prenatal “early calibration system” for salt preference. He believed
that “complex neurophysiological machinery” was responsible for creating our
innate set points for salt intake, and they helped us maintain homeostasis
later in life. These set points might have helped save our ancestors from
dangerous bouts of dehydration from diarrhea and vomiting due to intestinal
infections. Then, natural selection would ensure that this adaptation would be
passed on to future generations.27
As evolution continued, however, this adaptation would eventually make
us a bit more vulnerable in modern life. Because salt depletion early in life
(in utero or shortly after birth) seems to predispose offspring to become drawn
to eating higher levels of salt, they will probably also have an increased risk
of becoming addicted to drugs of abuse as well as refined sugar due to chronic
activation of the brain’s reward system.28
When it comes to the intake of salt, your body knows best. Eating the
level of salt that your body drives you to consume, rather than trying to
consciously restrict your salt intake, will help ensure that you avoid harms during salt depletions, and by doing so may help you
prevent problems with sugar and other drugs of abuse.
Salt and Anxiety
A
2011 study from the University of Haifa in Israel suggests that a high salt
intake may help buffer the effects of stress, serving as an adaptive
coping mechanism for dealing with psychological and emotional adversity. As
part of the same line of study, the researchers also found that decreased
consumption of sodium-rich foods caused anxiety in subjects when they were
presented with mental challenges.29 Similarly,
researchers at the University of Iowa found that when rats are deficient in
sodium chloride (table salt), they shy away from normally enjoyable activities,
suggesting that salt has a positive effect on mood.30 Low-salt
diets can cause tremendous sacrifice and general misery for those who attempt
to follow them. Pines and colleagues have even suggested that low-salt diets
may induce serious anxiety, hypochondriasis, and invalidism.31 In other
words, people feel anxious and ill on low-salt diets.
Some people may turn to sugar to help them cope. The increased
psychological anxiety from consuming diets low in salt may lead to sugar
cravings, as sugar triggers neurochemical release in the brain that may help
people temporarily “manage” their anxiety.32 It’s
commonly believed that consuming sugar has a positive effect on mood, but it’s
a fleeting lift at best. If people opt to reach for sugar rather than salt,
they may find themselves becoming dependent on sugar as a short-term stress
fix. The negative effect of that coping mechanism would only be heightened on a
low-salt diet, leading to a perpetual cycle of “medicating with sugar”—and,
eventually, sugar addiction.
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.34
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.
People can also develop a tolerance to sugar so that they need more and
more of it to satisfy their sweet tooth. And those who are hooked on sugar can
experience mood changes and bingeing behavior—as well as withdrawal symptoms
when they’re suddenly cut off from or go too long without consuming sugar. As
they withdraw from sugar, people may even have ADHD-like symptoms (from a
depletion of dopamine in the brain), such as being unable to concentrate or think straight, or experience shakiness, jitteriness, sweating (from
low blood sugar, a result of physiological withdrawal and dependence), and
anxiety.
Do any of these symptoms sound familiar?
While this emotional dependence can be a hard habit to break, the body
can develop a state of physical dependence. People with insulin resistance
release an excessive amount of insulin when they eat sugar, causing large drops
in blood sugar levels, which can lead to shakiness, jitteriness, sweating,
palpitations, and anxiety—nudging them back toward the sugar to “cure” their
ills. If indulged regularly, this could create a vicious cycle of continued
sugar intake (and true sugar dependence) in order to treat the low blood sugar
levels. As many as 110 million Americans have some form of insulin resistance,37 so much of
the population is not only at risk for type 2 diabetes but is likely also at
risk for sugar addiction.
Addiction to sugar may even be more intense than addiction to other
drugs of abuse. Studies have found that when rats are addicted to cocaine, if
they’re given a choice between cocaine and sugar, they will opt for the sugar
instead, likely because the reward from sugar surpasses that of even cocaine.38 Some of
the best proof we have of sugar’s true addictive power is how that addiction
can be treated. Drugs that are designed to block the brain’s opiate receptors
and are used to treat opiate addiction (in those hooked on
heroin and morphine) may also help with dependence on sugar. (See the table
that follows for the shared features between addictive drugs and sugar, and the
list following that for a possible effective strategy that the U.S. Food and
Drug Administration [FDA] should consider approving for the treatment of sugar
addiction.) People don’t get strung out on sugar like they can on illicit
drugs—sugar doesn’t distort your perception of reality and although they may
feel like it, nobody is literally going to kill for a
cookie—but they can certainly experience pronounced withdrawal effects.39
Shared Features between Addictive Drugs and Sugar 40
|
Neurochemical/Behavioral
Effects |
Addictive
Drugs |
Sugar |
|
Withdrawal upon removal |
+++ |
+ |
|
Withdrawal from an opiate-antagonist |
+++ |
+ |
|
Reward upon consumption (persistent and intense release of opioids
and dopamine after administration, leading to behavioral reinforcement) |
++ |
+++ |
|
Increase in dopamine D1 receptor binding |
NCD |
NCD |
|
Decrease in D2 receptor binding |
NCD |
NCD |
|
Decrease in D2 receptor mRNA in the nucleus accumbens |
NCD |
NCD |
|
Increase in p-opioid receptor binding |
NCD |
NCD |
|
Dopamine/acetylcholine imbalance upon naloxone withdrawal |
NCD |
NCD |
|
Dependence on endogenously released opioids |
+++ |
++ |
|
Sensitization to stimuli acting upon D1 and p-opioid receptors
(likely leads to addiction) |
++ |
++ |
|
Dependence due to a low dopamine state in the brain |
+++ |
++ |
+ moderate,
++ strong, +++ very strong, NCD no comparative data Note: These ratings do not
necessarily indicate the exact strength of effect; rather, they are meant as a
general comparison.
A POSSIBLE TREATMENT STRATEGY
FOR SEVERE SUGAR ADDICTION
Induction
treatment of sugar addiction
Maintenance
treatment of sugar addiction (generally day 3)
As we talked about previously, excess consumption of refined sugar,
particularly of fructose-derived sweeteners such as sucrose and high-fructose
corn syrup, can also trigger resistance to the satiety hormone leptin, throwing
your appetite and your body’s fat-regulation system out of whack.41 Normally,
leptin, which is released by our fat cells, crosses the blood-brain barrier and
binds to receptors in the appetite-regulating center of the brain, helping
regulate your calorie intake over the long haul. Leptin tells you to stop
eating and to increase your physical activity when appropriate; it also
activates the central nervous system, stimulating fatty tissue to burn fat for
energy. So there’s a harmful double whammy that occurs when someone becomes
leptin resistant. The brain believes the body is starving, triggering continued
hunger and calorie intake—most often in the form of those fast-acting carbs
because, remember, these are the only macronutrients your cells can burn
efficiently while insulin levels are raised and your body
is in “internal starvation.”42 A
consistently high sugar intake will diminish your appetite for nourishing
foods, and the changes that occur in the brain during this overconsumption of
refined sugar can lead to sugar dependence, sparking intense cravings and
bingeing, and then withdrawal symptoms when you don’t consume sugar on a
regular basis.43 And all of
these mechanisms become even more pronounced in the absence of sufficient salt.
7 – How Much Salt Do You Really Need?
As with many things in life, there’s an optimal range of salt
consumption. That ideal varies somewhat from one person to another. Advocates
of salt restriction don’t consider how much sodium we need to thrive; they focus only on our minimum requirement in order
to survive. So how do you make sure you get enough—but not too much?
• Hyperaldosteronism (an aldosterone disorder that involves increased
secretion of the salt-retaining hormone called aldosterone)
• Liddle
syndrome (an inherited form of high blood pressure that causes excess
reabsorption of sodium in the kidneys)
• Overconsumption of sugar leads to specific kidney problems that cause
salt wasting.
• Our java-junkie habits
and our dependence on energy drinks, teas, and other caffeinated beverages put
us at risk for salt depletion because caffeine acts as a natural diuretic,
flushing water and salt from our kidneys.
• Intense exercise causes
us to lose considerable salt and water in sweat.
How Much
Salt Do We Really Need?
The optimal amount of salt can differ widely from person to person,
depending on your unique situation. Here are a few important definitions to better understand terminology that will be discussed in
this chapter.
Sodium Deficit: A simple
way of knowing if someone has a sodium deficit (assuming they are healthy) is
when they ingest sodium but none (or much less than what is consumed) is
excreted in the urine.1
The Salt Thermostat: The
salt set point is controlled by the salt thermostat of the body. The salt
thermostat is a metaphor for a complex, interconnected set of sensors in your
brain that work together to ensure the optimal sodium stores in the body, trying
to avoid having to activate the salt-retaining hormones of your
renin-angiotensin-aldosterone system. Your brain would really, really prefer that you simply eat more salt rather than
having to hoard it or scavenge it from
vulnerable parts of your body. These self-protective mechanisms help the body
tightly control salt intake, causing you to crave salt when you need it. So
when you crave salt, remember: that’s your salt thermostat telling you that
your body’s sodium content is too low and that you need to eat more salt until
you’ve reached the salt set point, the proper amount of sodium storage in the
body.
Sodium
balance can be maintained at the salt set point (consuming around 3,000
milligrams of sodium) but can also occur after about four to five days of salt
restriction (generally after consuming around 300 milligrams of sodium or less
per day). This is because it takes four to five days for your kidneys to slowly
turn off the salt spilling out of them. However, after four to five days, your
body finally shuts the sink off, so that you can maintain sodium balance by
consuming as little as 300 milligrams of sodium per day (but that’s only if you
have healthy kidneys). Once you are in sodium balance, sodium excretion is
slightly lower than intake because of nonkidney salt losses (such as from sweat
and feces).2 During
sodium balance, if you take in more sodium than needed, most if not all sodium
will be excreted. However, the ability of a healthy person to maintain sodium
balance on a low-sodium diet (but not below 300 milligrams of sodium per day)
does not mean that a low sodium intake is ideal or provides optimal health and
longevity! In fact, being in sodium balance on a low-sodium diet requires the
activation of certain rescue systems or salt-retaining hormones, which have
been consistently found to induce harm. Salt-retaining hormones can harm the
body’s organs and may cause hypertension and other health consequences by
causing enlargement as well as stiffening (fibrosis) of the heart and blood
vessels.3 This may
be why low-salt diets are associated with greater cardiovascular risk and
premature mortality. In general, a low salt intake places an individual at
greater risk of salt deficit during sodium depletion. And there is no easy way
of telling if someone has appropriate salt stores.
When you consume less sodium, your kidneys generally excrete less in
order to maintain normal sodium balance and normal extracellular fluid volume.
But if there is any problem with your kidneys’ ability to retain sodium, you
can become deficient in sodium rather quickly. (See the preceding story of my
elderly family member; because of her damaged kidneys, she probably can’t
maintain sodium balance on a low-salt diet.) For example, during a hemorrhage,
the kidneys almost immediately shut down sodium excretion to maintain normal
blood volume.4 And if
your kidneys were unable to do this (for example, in patients who have
tubulointerstitial damage in their kidneys from overconsuming refined sugar for
decades), a bleeding event could be disastrous, particularly if the intake of
salt is being restricted.
A phenomenal experiment published in the late 1950s looked at what
would happen in someone who was in sodium balance while on a low-sodium diet if
they experienced a sudden salt deficit, perhaps from gardening for hours on a
hot day, a new prescription to control elevated blood pressure such as a
diuretic, shock from trauma, burns, vomiting, or a bad bout of diarrhea. To
simulate a sudden salt deficit, the patient was given a diuretic and lost 2,300
milligrams of sodium in the urine; the experiment found that after the patient
ate salt again, there was no sodium excretion until the entire 2,300 milligrams
of sodium was regained. This shows that the body can be in balance on a low-salt diet, but if something were to cause salt loss,
the body would avidly retain salt until it reached sodium balance again. But if
your kidneys are damaged and you are unable to hold on to extra salt, then you
are in big trouble. In other words, when life throws you a salt-depleting
curveball, the last thing you want is to be following
the AHA advice to consume less than 1,500 milligrams of sodium per day. On the
other hand, salt losses in people eating a normal-salt diet are much less
likely to place them into salt deficit and cause subsequent harm. In essence,
maintaining a normal sodium intake (3 to 4 grams) versus a low sodium intake
(less than 2.3 grams) decreases your chances of becoming deficient if
salt-depleting events occur. Experts believe we evolved with these sodium
storage mechanisms to endure these salt-depleting events. The systems work best
when we operate well above the minimal sodium intake (which, you’ll recall, is
just 300 milligrams per day) to maintain balance.5
In 1936, McCance performed what may be one of the most important
studies to determine the ideal total body sodium content. Experimenting on himself, he was able to cause a net loss of 17.4 grams
of sodium in his body, mostly through induced sweating.6 McCance’s
urine became “virtually free of sodium” (less than 23 milligrams per day). When
he began sodium repletion, consuming around 11.5 grams of sodium over the next
two days, the urinary sodium excretion still remained at 23 milligrams per
day—in essence, his body was still regaining all the salt he was consuming,
indicating true salt deficit. The next day, he consumed 5,382 milligrams of
sodium, bringing his three-day sodium intake to 16.836 grams (or 96.6 percent
of what was lost) and, even then, only 368 milligrams of sodium was excreted in
his urine. Remember, a normal sodium intake is about 3,400 milligrams per day,
and we excrete all the sodium we take in every day under normal circumstances,
so if you were to consume 5,382 milligrams of sodium, about 5,000 milligrams of
sodium would be excreted in the urine, and the rest would come out in your
sweat and stool for the day. But McCance’s body was holding on to almost all of
his sodium.
Sadly, governments and guidelines do not seem to give enough credence
to the important fact that low-salt diets put stress on our bodies. Let’s
consider a few of the situations in which consuming a higher-salt diet could
protect you from dire health concerns.
You May
Need More Salt to Prevent Dehydration
You
may be asking yourself, what typically causes dehydration? Does it happen
often? What are the symptoms? We all say, “I feel dehydrated” when we are
parched, but is that true dehydration? When you are parched, that is just one
of the body’s mechanisms to drive you to drink more water, and no one can say
with certainty that a parched mouth indicates dehydration. Dehydration is
typically caused by numerous factors, mainly by not consuming enough water, but
it is also caused by exercise and not eating enough salt. The best measurement
of dehydration is by looking at sodium levels in the blood; if they are high,
then that is a good indication that you are dehydrated. Sodium levels increase in the blood for a few reasons, but mainly because with
dehydration comes low blood volume, which increases the sodium concentration in
the blood.
Symptoms That May Indicate a Greater Need For Salt7
Decreased
skin turgor (the skin remains “tented” when it is pinched)
Decreased
urinary sodium excretion relative to intake
Dry
axilla (armpit or underarm) and tongue
Postural
tachycardia/dizziness/hypotension (occurs after rising from a seated or
reclined position)
Syncope
(loss of consciousness from low blood pressure)
During states of dehydration, our kidneys step up their sodium
reabsorption—an effect known as the dehydration reaction. Sodium helps manage
how hydrated we are by controlling the movement of water into and out of our
cells. When we’re dehydrated, the sodium level in the blood increases because
it’s hard at work, drawing water out of the cells and into the blood, where
it’s needed. That’s why highly concentrated sodium in the blood is almost
always a sign of dehydration.8 But that
level of sodium isn’t dangerous in and of itself—it’s actually helping us!
A low sodium intake reduces urine volume,9 which can
reduce our ability to clear metabolic wastes from the body
and increases the risk of urinary tract infections. We rely on frequent urine
flow in the urinary tract to get rid of bacteria; producing urine is our body’s
way of “flushing out the system.” Eating a low-salt diet may also reduce the
total amount of water in our body, leading to dehydration and problems with the
cardiovascular and central nervous systems, thermoregulation, metabolic
abnormalities, and performance issues (particularly in military and sports
settings). This can increase the risk of fainting, vomiting, circulatory
collapse, heatstroke, and even death.
You May
Need More Salt to Help Manage Shock (Burns, Trauma, and Hemorrhage)
Salt
helps the body withstand accidents and other kinds of traumatic events. Besides
excessive bleeding (hemorrhage), we experience a loss of fluids in states of
shock from burns or trauma.10 This
“loss” of body fluid happens without any water actually leaving the body, as
injured regions draw fluid to speed the healing process, making that fluid unavailable
to other areas. And since sodium is the main determinant of body fluid status,
patients experiencing these forms of shock require greater amounts of salt. In
fact, evidence suggests that a loss of salt is actually more dangerous than a
loss of water,11 because it
decreases the body’s ability to circulate blood around the body and reduces
blood volume out of the heart more than water loss does. Salt depletion, even
in untraumatized animals, can lead to a form of peripheral vascular collapse
that looks like traumatic shock. This doesn’t happen with water depletion.
You May
Need More Salt to Counter Low Sodium Levels
Low
sodium levels in the blood is called hyponatremia, and it’s the most common
electrolyte abnormality.12
Approximately 65 percent of cases of hyponatremia in the ER
are caused by gastrointestinal disorders.13 When
people seek medical treatment in an outpatient setting, 4 to 7 percent have
hyponatremia; in the hospital, the rate can be as high as 42 percent (but is
generally around 15 to 30 percent).14 In the
elderly, hyponatremia is over 31 times as prevalent
as hypernatremia (high sodium levels in the blood)15 and is
associated with an increased risk of death, length of hospital stay, falls,
rhabdomyolysis (rapid breakdown of muscle), bone fractures, and increased
healthcare costs.16 Even mild
hyponatremia puts you at a higher risk of death due to cardiovascular events
and increased risk of falls, bone fractures, and osteoporosis.17
Medications such as selective serotonin reuptake inhibitors (SSRIs) can
cause hyponatremia by triggering an oversecretion of antidiuretic hormone,
leading to water retention. Small-cell lung cancer, malnutrition, and
infections such as tuberculosis and pneumonia have the same effect.18
Hyponatremia can also be caused by numerous other diseases: liver cirrhosis,
pneumonia, and acquired immune deficiency syndrome (AIDS), to name just a few.19 In
addition to all the terrible symptoms that come along with hyponatremia—such as
anorexia, cramping, nausea, vomiting, headache, irritability, disorientation,
confusion, weakness, lethargy, and bone fractures—people with lower than 125
mEq/L can experience seizures, coma, permanent brain damage, respiratory
arrest, and even death. One problem with chronic hyponatremia is that
neurological symptoms may not be present until the serum
sodium drops to 125 mEq/L or less, because of adaptive mechanisms in the
brain—so someone could be walking around with low sodium levels in the blood
and not even know it.20
Hypothyroidism, which becomes more common as people age, can cause
salt-wasting kidney problems, as thyroid hormones are important in the
functioning of Na-K-ATPase, which helps reabsorb salt at the kidney tubules.21 Osmotic
laxatives such as polyethylene glycol (for example, Miralax) may lead to salt
wasting and volume depletion.22
Hyponatremia can even be a complication of undergoing a colonoscopy, as the
“bowel prep” induces massive diarrhea and salt loss.23
Many common medications that increase the risk of bleeding (such as
nonsteroidal anti-inflammatory drugs [NSAIDs], aspirin, antiplatelets, and oral
anticoagulants, to name just a few) also increase the risk of salt loss via
blood. Indeed, it’s been estimated that 16,500 people in the United States die
every year from NSAID-induced gastrointestinal bleeding.24 A
higher-salt diet may have been able to help. Since it is not always apparent
when someone has a gastrointestinal bleed, following the low-salt advice would
not be advisable for someone taking medication that increases the risk of
bleeding. (Sadly, many of these individuals probably never even knew they had a
bleed until it was too late.)
You May Need
More Salt When You Sweat
Sweating helps the body maintain normal body temperature (aka thermoregulation) to prevent heatstroke—it’s our body’s way of cooling
off. Having enough salt in the body to be able to adequately sweat is of vital
importance in thermoregulation. The amount of sodium in our sweat generally
ranges between 40 and 60 mEq/L, and we sweat out 1 to 1½ liters per hour in
moderate climates and 2 to 3 liters per hour in hot climates.25 So, on
average you will sweat out around 1,437 milligrams of sodium per hour when
exercising in moderate climates and around 2,875 milligrams of sodium per hour
when exercising in hot climates. Depending on exercise intensity and ambient
temperature, you could easily lose more than an entire day’s worth of salt intake
in just one hour of exercise. In hot climates like India, you could lose up to
14,720 milligrams of sodium per day.26 How would
consuming just 1,500 milligrams of sodium per day (or even 2,300 milligrams of
sodium) help you survive these conditions, let alone improve your health?
In one study by Mao and colleagues, one hour of soccer practice in
temperature between 89.6°F and 98.6°F with 50 percent relative humidity caused
players to lose 1,896 milligrams of sodium from sweating. One player actually
lost almost 6,000 milligrams of sodium in sweat during the one-hour game.
Importantly, soccer players also lost on average 52 micrograms of iodine in their
sweat (and one player lost 100 micrograms); this amount of iodine loss is over
one-third the recommended daily intake (150 micrograms per day). Almost half of
the players were found to have a Grade 1 goiter, compared to 1 percent of the
sedentary control subjects. It’s very likely that because of continued iodine
losses in sweat and not enough iodized salt intake, the players had developed
goiters, which are a sign of severe thyroid problems. This happened despite the
fact that the estimated iodine intake of soccer players, in general, met
guideline recommendations (100 to 300 micrograms of iodine per day).27 Bottom
line: when you exercise, your body needs more salt and iodine than when you
don’t—and some people may need more than others.28
The average nonathletic adult excretes up to about 600 milligrams of
sodium and about 22 micrograms of iodine in their average daily sweat. The average athlete, who sweats 3 to 5 liters per day, can
lose between 111 and 185 micrograms of iodine in sweat, for a total iodine loss
between 195 and 270 micrograms per day (when combined with loss from sweat,
urine, and feces). Even consuming up to 340 micrograms of iodine per day, which
is more than double the current recommended daily allowance (150 micrograms per
day), could still lead to goiter and hypothyroidism in certain athletes. And
it’s not just athletes: iodine losses during the summer correlate with an
increased prevalence of goiter among school-age children.29
(Especially during the hotter months, you can ensure that your family gets
sufficient iodine by seeking out more foods rich in iodine, such as seaweed,
cranberries, and yogurt.)
Goiters aren’t the only risk. Depletion of body sodium can lead to
symptoms comparable to overtraining syndrome, even before we can detect lower
levels of sodium in the blood. Salt depletion can cause the body to work harder
than normal, pushing you into training overload prematurely. Your physical
strength starts to falter and your sympathetic nervous system gets so exhausted
that your blood pressure drops and you’re at risk of fainting. Part of the
reason sodium depletion may lead to impaired muscular strength and energy
metabolism is that it raises the acidity of our cells.30
People who aren’t in the best shape may take longer to finish athletic
competitions, and that extended time exercising may increase risk of
hyponatremia.31 The
consequences of excessive losses of salt (and other minerals) in sweat during
exercise can include dehydration, tremors, muscular weakness, and even cardiac
arrhythmias.32 In one
report, a reduced sodium intake during high-intensity exercise increased cramps
and muscle fatigue; reduced endurance performance; and caused general fatigue,
joint pain, sleeping disorders, circulatory impairments, and distinct thirst.
But these symptoms were vastly improved when people increased their sodium
intake—even when they worked out harder, their symptoms of overtraining were
eliminated.33
The “thirst” that we experience during bouts of exercise, particularly
among endurance athletes, may actually be for the replacement of salt, not water. If we increase salt intake, we may find we have
less “thirst.”34 Tap water
has a sodium content of only 1 to 3 mmol/L,35 whereas
sweat contains 20 to 80 mmol of sodium per liter. Basically, your sweat is
seven to eighty times as concentrated in sodium as tap water—so you should be
hydrating with something that contains much more salt than just plain tap
water.
Athletes who struggle with arthritis could experience relief with extra
salt. Here’s why: cartilage cells (chondrocytes) contain sodium/hydrogen
(Na/H)-antiporter systems. When you don’t have enough sodium in your cartilage
cells, acid (hydrogen, H+) can build up. And that’s not good for your cartilage
or your joints. In osteoarthritis and rheumatoid arthritis, the excess fluid
that surrounds inflamed cartilage cells can dilute the sodium level in those
areas, which may lead to further pain.36 Thus,
low-salt diets may worsen cartilage health in both those with and without
autoimmune diseases, decreasing their ability to protect joints and increasing
joint pain, especially during exercise. Thus, low-salt diets can be a triple
whammy for runners—they lose salt from their sweat, from
the fluid surrounding their cartilage cells, and even from within the cartilage
cells themselves.
What to Do for
Exercise
The
answer is simple: Consume more salt before and during exercise. It may help
your body cool off faster.37 Adding
2,300 milligrams of sodium (1 teaspoon of salt) per liter of water has been
found to reduce total fluid loss during exercise.38 In the
largest field-based study, the prevalence of hyponatremia in triathlon
finishers was 18 percent, most likely caused by overhydration.39 But that
doesn’t mean you can or should prevent hyponatremia by drinking less water.
Rather, drink the same amount, but add the appropriate level of salt to
whatever liquids you are drinking.
If you are on a long endurance run, you may want to carry a small pouch
of salt along with a plastic ½-teaspoon measuring spoon. After each hour of
exercise, simply scoop out the dose of salt recommended in the list
“Recommendations for Salt Dosing Prior to and During Exercise” (see this page), based on
ambient temperature, and consume. Replacing the amount of salt that is lost through
sweat helps your body’s thirst mechanism. Your body will tell you how much
water to drink, and it will do this more accurately, when you consume the
appropriate amount of salt—which will also reduce your risk of overhydration.
POSSIBLE BENEFITS OF DOSING YOURSELF WITH SALT PRIOR TO AND DURING
EXERCISE
Decreased
risk of iodine deficiency (if using iodized salt)
Improved kidney function (improving the
ability to excrete more water, which decreases the risk of dilutional
hyponatremia, making the kidneys less sensitive to the effects of antidiuretic
hormone [reducing the risk of overretention of water and subsequent hyponatremia])40
HOW TO CONSUME YOUR DOSE OF
SALT PRIOR TO AND DURING EXERCISE
Eat
three large dill pickles (or five large olives) washed down with some
pickle/olive juice
Dissolve
a chicken bouillon cube(s) in warm water and consume
Dissolve
½ teaspoon of salt in 1 liter of water (tastes like sweat, not recommended)
RECOMMENDATIONS FOR SALT DOSING PRIOR TO AND DURING EXERCISE
Exercising
in moderate climates (below 80°F)
Consume
½ teaspoon of salt prior to exercise and every hour thereafter
Exercising
in hot climates (80°F to 89°F)
Consume
½ to 1 teaspoon of salt prior to exercise and every hour thereafter
Exercising
in very hot climates (90°F or above)
Consume
1 to 2 teaspoons of salt prior to exercise and every hour thereafter
Note: Patients who are exercising or performing activities that lead to
excessive sweating and who are also on salt-depleting medications such as
diuretics (such as hydrochlorothiazide or furosemide), angiotensin-converting
enzyme inhibitors (such as ramipril or lisinopril), or
mineralocorticoid receptor antagonists (such as spironolactone or eplerenone)
may need to use even more salt than what has been recommended in the preceding
list “Recommendations for Salt Dosing Prior to and During Exercise.”
While
the health benefits of heat and sweating from saunas, sun baths, tanning beds,
and Jacuzzis have been debated for years, one issue beyond debate is the
increased risk of tissue sodium depletion. It may also be a good idea to
consume salt prior to thermal-induced dehydration. Follow the salt dose
recommendations in the “Recommendations for Salt Dosing Prior to and During
Exercise” list on this page before
hitting the sauna.
You May
Need More Salt When Pregnant or Lactating
Earlier
in the book, I talked about how lower salt intake has a proven link with lower
reproductive success. Indeed, a low-salt diet seems to act like a natural
contraceptive in both men and women, causing reduced sex drive; reduced
likelihood of getting pregnant; reduced litter size (in animals) and weight of
infants; and increased erectile dysfunction, fatigue, sleep problems, and age
at which women become fertile.41 We can see
the importance of salt in fertility in the low incidence of pregnancy among the
low-salt-eating Yanomamo Indians, who average only one live birth every four to
six years, despite being sexually active and not using contraception.42 Women with
congenital adrenal hyperplasia (specifically those with salt-wasting
nephropathies) have a decreased fertility and childbirth rate.43
A mother’s salt status not only determines her ability to get pregnant
but may control the future health of her infants. Because salt is so important for numerous functions in the body, a depletion of salt
from either a lack of dietary intake (following the low-salt recommendations)
or salt loss (think of nausea and vomiting during pregnancy) not only may
worsen the health of the mother but can impair the health of the growing child
even into adulthood. Pregnancy and lactation place increased nutritional
demands on the mother in order to supply the baby with enough nutrients for
proper growth and development44—and salt is
one of those nutrients. Salt restriction in pregnant or lactating mothers seems
to increase the vulnerability of their children to multiple hazardous outcomes.
For example, in animals, low salt intake during pregnancy and/or
lactation leads to increased fat mass, insulin resistance, and raised levels of
“bad” cholesterol and triglycerides in the offspring, which may carry over into
adulthood.45 More
worrisome is that a low-salt diet in pregnancy has also been found to cause
hypertension and kidney disease in adult offspring.46 All of
this suggests that low salt intake during pregnancy may program our children to
develop abnormal lipids, diabetes, obesity, hypertension, and chronic kidney
disease—the very diseases we believe a low-salt diet will prevent!
Sadly, the increased physiological need for salt during pregnancy
conflicts with population-wide low-salt advice, which has been entrenched into
our minds by government and health agencies. The American Heart Association,
for example, recommends that all Americans reduce their daily sodium intake to
less than 1,500 milligrams, and women of childbearing years or who are pregnant
or lactating do not appear to be exempt from this advice. Even the World Health
Organization (WHO) recommends that pregnant and lactating women restrict their
sodium intake to less than 2 grams per day.47 But these
recommendations may have unintended consequences. Health agencies and
government bodies seem to have forgotten that dietary iodine requirements
increase by 50 percent or more during pregnancy and lactation,48 and that
iodized salt has been an important way to prevent iodine deficiency for
decades. Indeed, the WHO recommends that pregnant and lactating women consume
250 micrograms of iodine per day.49 However,
even if all maternal dietary salt intake during pregnancy/lactation comes from
iodized salt, the Recommended Nutrient Intake (RNI) for iodine (250 micrograms
per day) will still not be met by following these low-salt recommendations! And
we can’t assume that pregnant and lactating women know to eat enough
high-iodine foods every day to make up the difference.
Considering that iodine deficiency during pregnancy is the leading cause
of mental retardation, health agencies may want to rethink their low-salt
advice during this critical time in human development. An iodine deficiency in
pregnancy or lactation can also lead to impaired motor function and growth as
well as hypothyroidism, and even perinatal and infant death.50 Moreover,
national data indicates that weaning babies may not have adequate iodine intake
and thus may benefit from a greater iodized salt intake.51
Indeed, what we currently think is an “adequate” iodine intake in
pregnancy may actually be insufficient, as data suggests that over 36 percent
of pregnant women develop hypothyroidism (or thyroid insufficiency), even among
pregnant women with “adequate” iodine status in the first trimester.52
Importantly, iodine deficiency is still a significant health problem worldwide
that affects both industrialized and developing nations, with fifty-four
countries still considered iodine deficient.53 This is
perhaps why the Council for Responsible Nutrition (CRN) recently recommended
that dietary supplements should include at least 150 micrograms of iodine in
all supplements intended for pregnant and lactating women in the United States.54 But until
then, telling pregnant and lactating women to consciously restrict their salt
intake increases their risk for iodine deficiency and may be a decidedly
harmful recommendation.
One myth that persists is that too much salt during pregnancy can lead
to preeclampsia, a dangerous condition characterized by hypertension that can
endanger both mother and child and lead to premature birth, among other
complications. Over fifty years ago, a study published in the Lancet of more than two thousand pregnant women found that
a low-salt diet, as compared to a high-salt diet, caused more miscarriages, premature babies (born prior to 34 weeks gestation),
stillbirths, perinatal and neonatal deaths, edema, preeclampsia (previously
known as toxemia), and bleeding.55 And since
there was less preeclampsia in those on the high-salt diet, it was decided
later that cases of preeclampsia would be treated with extra dietary salt.
Between the end of May and the end of September 1957, twenty-eight women were
diagnosed with what was then known as “toxemia of pregnancy.” Eight were not
given extra salt, while the other twenty were advised to ingest more dietary
salt. All of the twenty women treated with extra salt improved, and all gave
birth to healthy, full-term babies. An account of the study said, “the larger
the dose of salt taken, the quicker and more complete was the recovery. The
extra dose of salt had to be taken up to the time of delivery; otherwise the
symptoms of toxemia recurred.” In other words, giving more salt treated preeclampsia rather than causing or worsening it (a
common misconception). Consider this account from the researcher (from the
study published in the Lancet):
Sixteen patients were advised to measure out each morning four heaped
teaspoonfuls of table salt and to see that by night they had taken all of it.
It was calculated that they took about 200–300 grams of salt
daily [emphasis added]. The larger the amount taken the quicker was the
recovery. They found it easiest to take the bulk of this salt in orange-juice,
lemonade, or lime-juice, the remainder being put on their food. They were
visited daily until all symptoms had disappeared. All of them recovered
completely and continued well on at least three heaped teaspoonfuls of table
salt a day. None of them had an infarcted placenta, and all gave birth to live
full-term infants.56
severe backache, some
[complained] of irritation of the skin of arms, legs, or abdomen, and some of
weariness and stiffness in the limbs. Others complained of falling because
their legs suddenly gave way under them. Sometimes this was so severe that they
were afraid of going out of their houses or of crossing the road, in case they
fell. These symptoms did not develop in the group given salt, and if they were
present at the first examination they disappeared as soon as the women took
more salt.57
In other words, low-salt diets in pregnancy seem to lead to muscle
weakness, particularly in the legs, which was treated by giving more salt. The
authors concluded that extra salt in the diet seemed to be “essential for the
health of a pregnant woman, her fetus, and the placenta.”58 Because of
the risks involved, ethics boards would not likely approve this kind of study
today. With these kinds of results in only two small randomized controlled
trials testing a low-salt versus a normal-salt diet in just a few hundred
pregnant women, we may want to give strong reconsideration to the practice of
recommending low-salt diets in pregnant women.59
Another paper described the experience of a pregnant woman with
elevated blood pressure and evidence of low aldosterone levels who was given 20
grams of salt per day, which led to a decrease in systolic and diastolic blood
pressure of 16 and 12 mmHg, respectively. The authors concluded that low blood
volume during pregnancy might be due to a reduced ability to produce
aldosterone and that pregnant women would probably benefit from salt
supplementation.60 Another
study confirmed these findings, saying they “support the importance of salt in
normal pregnancy, a critical issue given the passionate campaigns to lower salt
intake in the general population.” The researchers suggested that salt could be
a “cheap and easy intervention,” particularly in areas with lower resources, to
help avoid dangerous pregnancy conditions such as preeclampsia.61 The
possible harms of a low-salt diet in pregnancy or those trying
to become pregnant are summarized in the list that follows.
Consuming more salt may even help prevent pregnant women with normal
blood pressure from transitioning into hypertension/preeclampsia, as low plasma
volume is a risk factor for developing hypertension in these women.62 In fact,
blood volume has consistently been found to be reduced in preeclampsia, and its
improvement may be why salt is so helpful for treating preeclampsia in
pregnancy.63
THE POSSIBLE HARMS OF A LOW-SALT DIET IN PREGNANCY OR THOSE TRYING TO
BECOME PREGNANT
Reduced
chance of becoming pregnant
Increased
chance of a miscarriage
Increased
risk of premature delivery
Increased
risk of infant mortality
Increased
risk of bleeding in the mother
Increased
risk of preeclampsia
You May
Need More Salt for Energy and Muscle Health
One
side effect of low-salt diets that is seen in almost every population is
reduced energy and increased fatigue. Consider the findings of the Trial of
Antihypertensive Interventions and Management (TAIM), a multicenter,
randomized, placebo-controlled clinical trial that evaluated nine different
combinations of diet and medications for the treatment of mild hypertension.64 The
average change in sodium intake in the TAIM Study was from 3,128 milligrams per
day at baseline down to 2,484 milligrams per day after six months. This
reduction of over 600 milligrams per day was found to cause worsening
fatigue, sleep disturbances, and erectile dysfunction.65 In other
words, salt restriction drastically reduces the quality of life. Moreover, as
much as they tried, only 25 percent of people were able to reduce their sodium
intake to below 1,610 milligrams per day.66 Compared
with the control group, twice the number of people on the low-sodium diet
complained of fatigue, with more than one out of three patients having an
increase in fatigue symptoms.67
Among patients with chronic fatigue syndrome, 61 percent have reported
that they “usually or always tried to avoid salt and salty foods,”68 presumably
because they believe it is healthy for them to do so. But this may be a
decidedly unhealthy decision.69 Low-salt
diets may lead to weaker muscles and increase or worsen chronic fatigue
syndrome, and may be particularly harmful in people with conditions that share
chronic fatigue syndrome’s symptoms of hypotension, dizziness,
light-headedness, and syncope (temporary loss of consciousness), such as
Parkinson’s disease.70
You Need
More Salt When High-Sugar Diets Lead to Salt Wasting
Not
only do high glucose levels in the blood deplete the body of sodium through
increased excretion; they can also lower the blood sodium level overall. High
glucose in the blood is known to reduce blood sodium levels as it pulls water
out of the cells and into the blood.71 Those with
poorly controlled diabetes and high levels of sugar in their blood may be at
risk of sodium depletion as high glucose levels can cause
this osmotic diuresis, as well as salt wasting and hyponatremia.72 A list
follows that covers the twenty-two ways sugar causes salt depletion.
All of this suggests that once glucose levels are chronically elevated,
giving someone more salt may actually improve health—and may even be
lifesaving. In one study of patients with insulin resistance, researchers found
that giving around 6,000 milligrams of sodium per day as compared to 3,000
milligrams of sodium per day ameliorated their insulin resistance.73 With over
50 percent of adults in the United States now considered diabetic or
prediabetic, low-salt diets may be causing harm to over half the adult
population.74
TWENTY-TWO WAYS SUGAR CAUSES SALT DEPLETION
1. Sugar ➔ damages
intestinal cells ➔ celiac disease/Crohn’s
disease/ulcerative colitis ➔ decreased absorption of
salt via the intestines75
2. Sugar
➔ fructose malabsorption ➔
irritable bowel syndrome ➔ diarrhea ➔ increased salt excretion76
3. Sugar
➔ Candida albicans ➔ irritable bowel syndrome ➔
diarrhea ➔ salt wasting from gastrointestinal tract77
4. Sugar
➔ damages the reabsorptive capacity of the kidneys
(tubulointerstitial damage) ➔ salt-wasting kidneys78
5. Sugar
➔ damages kidneys ➔ reduced
glomerular filtration rate ➔ preferential retention
of water ➔ low sodium and chloride levels in the
blood79
6. Sugar
➔ damages the juxtaglomerular cells (atrophy of the
juxtaglomerular apparatus) and kidney tubules ➔
decreased renin production (low-renin hypertension) ➔
decreased aldosterone (and decreased response of the kidney tubules to
aldosterone) ➔ increased sodium excretion ➔ sodium wasting80
7. Sugar
➔ diabetic dysautonomia (malfunction of the autonomic
nervous system) ➔ decreased conversion of pro-renin
to renin by the kidney ➔ low renin ➔ low aldosterone ➔ sodium
wasting81
8. Sugar
➔ damages the heart ➔
congestive heart failure ➔ preferential retention of
water to maintain cardiac output ➔ risk of low blood
levels of sodium and chloride82
9. Sugar
➔ damages the liver ➔ fatty
liver ➔ liver cirrhosis ➔
overretention of water ➔ low blood levels of sodium
and chloride83
10. Sugar ➔ increases blood glucose
levels ➔ increased need for water in the blood to
prevent hyperglycemia ➔ low blood levels of sodium
and chloride84
11. Sugar
➔ hyperglycemia ➔ osmotic
diuresis (polyuria/natriuresis) ➔ hypovolemic
hyponatremia (sodium elimination via urine when glucose levels are
uncontrolled)85 (For every
100 mg/dL increase in plasma glucose above 150 mg/dL, serum sodium will drop by
approximately 2.4 mEq/L.86 Patients
with diabetes who have uncontrolled glucose levels have a higher risk for
hyponatremia.)87
12. Sugar
➔ diabetic ketoacidosis ➔
ketones promote sodium elimination ➔ renal sodium
wasting88
13. Sugar
➔ diabetes ➔ diabetic
medications (sodium-glucose cotransporter 2 [SGLT2] inhibitors, acarbose,
metformin, sulfonylureas) ➔ increased sodium
elimination and/or risk of hyponatremia (from reduced insulin levels, reduced
absorption and increased elimination of sodium, increased secretion of
antidiuretic hormone)89
14. Sugar
➔ diabetes ➔ reabsorption
of hypotonic fluids due to delayed gastric emptying ➔
low blood levels of sodium and chloride90
17. Sugar
➔ inflammation, oxidative stress, cellular damage,
high insulin levels ➔ cancer ➔
low sodium levels in the blood91 ➔ certain anticancer medications (cisplatin) ➔ salt-wasting nephropathy92
18. Sugar
➔ obesity ➔ bariatric
surgery ➔ reduced absorption of salt ➔ risk of salt depletion93
19. Sugar
➔ Candida albicans ➔ proteins in Candida albicans
can bind to thyroxine ➔ allergic response to Candida albicans cross-reacts with thyroxine ➔ autoimmune thyroiditis ➔
hypothyroidism ➔ salt depletion94
20. Sugar
➔ Candida albicans ➔ reduced lactase activity in the small intestine ➔ lactose intolerance ➔ diarrhea ➔ increased salt excretion95
(Importantly, sugar compounds are required for Candida
to bind to intestinal mucosal membranes, and thus sugar is required for Candida to cause lactose intolerance.)96
21. Sugar
➔ Candida albicans ➔ immunologic response ➔
cross-allergy to gluten ➔ celiac disease ➔ damage to intestinal microvilli ➔
reduced salt absorption97
22. Sugar
➔ one-kidney renal artery stenosis ➔ renal ischemia ➔ high renin ➔ high angiotensin-II (leads to high antidiuretic hormone
[ADH]) ➔ thirst and water retention ➔ hyponatremia ➔ increased blood
pressure ➔ pressure natriuresis through the normal
kidney ➔ volume depletion ➔
further ADH release ➔ hyponatremic-hypertensive
syndrome98
You May Need More Salt for
Kidney Disease
As we
age, our levels of renin and aldosterone are reduced, and with them, our
kidneys’ ability to retain salt, increasing our risk of salt deficit.99 People
with chronic renal insufficiency—kidneys that do not function at their optimal
level—cannot maintain the optimal level of sodium in their body, even when they
follow a normal or average sodium intake. One study found deficits in excess of
5,750 to 6,900 milligrams of sodium after only three or four days when sodium
intake was reduced to 690 to 920 milligrams of sodium per day.
One sign that you may have salt-wasting kidney disease is if more
sodium comes out in your urine than the amount you are eating. If you have salt-wasting
kidney disease, you may require more than 6 to 7 grams of sodium per day to
maintain stable kidney function. If you cut your sodium to 1,610 to 2,300
milligrams of sodium per day, you could promptly become severely ill because of
low blood volume and compromised kidney function.100 In essence,
following the low-salt advice (less than 2,300 milligrams of sodium per day)
may lead to kidney failure, circulatory collapse, and even death in patients
with salt-wasting kidney disease. People who have chronically elevated
aldosterone levels when they eat a normal salt intake, or up to tenfold higher
aldosterone levels when you’re on a low-sodium diet, may be showing signs of
salt-wasting kidney disease.
The sodium pumps of the kidney not only help to remove potassium but
also function to reabsorb sodium. Structural damage or changes to the kidneys
can reduce the sodium pumps’ ability to absorb sodium and excrete potassium. If
this is the case, inappropriately high blood potassium can indicate damage to
the sodium pumps and can be easier to detect than sodium loss via the kidney.101
As our kidneys age, their ability to excrete water decreases,
predisposing the elderly to hyponatremia.102
Additionally, as we age, the risk of metabolic acidosis increases, which is
considered a side effect of eating a Western diet.103 The extra
acid (hydrogen ions) then needs to be secreted via the urine, increasing the
risk of renal tubular acidosis and decreasing the kidneys’
ability to retain sodium.104 The
kidneys of patients with hypertension may overretain water or reabsorb
insufficient amounts of salt (sodium chloride) or both.105 This means
that patients with hypertension or certain kidney diseases may need more salt,
to balance not only the high amounts of retained water but also the loss of
salt via the kidneys.
A reduction in the intake of sodium has been found to impair kidney
function and reduce kidney plasma flow and filtration rate.106 Even in
uncomplicated hypertension, low-salt diets can cause marked decreases in serum
sodium and chloride107 and even
induce shock due to sudden falls in blood pressure.108 In people
whose kidney function has taken a hit and who also have low blood pressure,
increasing their intake of salt can show immediate improvements in symptoms of
shock.109 One group
of authors concluded that the benefits of low-salt diets for hypertension were
unproven but warned that “strict low sodium diets are unpalatable, require
extensive environmental and psychological adjustments, and carry the occasional
risks of inanition and—particularly in the presence of renal damage—of
collapse, uremia and even death.”110
Low-salt diets can also reduce our kidneys’ filtration rate, which can
increase our body’s retention of nitrogen—and may even lead to death in
patients with uremia, a condition of fluid, hormone, and electrolyte imbalance
in which toxic by-products build up in the blood. In fact, one group of authors
noted the harms of salt deprivation: “significant nitrogen retention, and death
in uremia has been reported in at least two hypertensive patients on this
regimen.”111 Many
commonly prescribed medications, including those that lower heart rate
(atenolol, for example) or prevent stroke in patients with atrial fibrillation
(such as dabigatran) are cleared by the kidneys. If individuals start lowering
their salt intake while on medications that are cleared by the kidneys, this
could reduce that clearance, increasing the concentration of these drugs in the
blood and hence increasing the risk for serious side effects (and even possibly
death). Of course, low-salt guidelines do not make any mention of this
important side effect to the kidneys upon sodium
restriction, so clinicians and patients are generally unaware of this risk.
Our kidneys’ ability to dilute our urine decreases as we progress
further into kidney disease.112 And since
patients with chronic kidney disease have a reduction in kidney filtration
rate, we start to retain water, increasing the risk of both dangerously
increased blood volume and hyponatremia. As the kidneys’ primary function is to
reabsorb all sodium that gets filtered, a reduction in glomerular filtration
does not seem to cause sodium retention (as we reabsorb about 99 percent of the
sodium that is filtered by the kidneys; the other 1 percent comes from our
diet). Even if there is a true overretention of sodium by the kidneys, the
liver can signal the intestine to reduce sodium absorption, and both the liver
and gastrointestinal systems can signal the kidneys to reabsorb less sodium.113
Additionally, the body can shunt extra salt into the skin and organs and
possibly even into the cartilage/bone.114 All of
these secondary mechanisms suggest that the human body is well adapted to
handle salt overload—but not salt deficit.
Sodium restriction is particularly harmful in chronic kidney disease
because hyponatremia is extremely common (13.5 percent). In fact, more than one
out of four chronic kidney disease patients (26 percent) will experience at
least one episode of hyponatremia during a five-year period, whereas the rate
of hypernatremia is less than one in fourteen people (7 percent). The
prevalence of hyponatremia seems to go down slightly with advancing kidney
disease but is still much more prevalent than hypernatremia. Hyponatremia is
twenty to thirty times as prevalent as hypernatremia in chronic kidney disease
stages 1 and 2, five to seven times as prevalent in stage 3, and about four
times as prevalent in stages 4 and 5.115
Interestingly, the impact of hyponatremia on mortality has a similar
magnitude no matter what stage of chronic kidney disease, whereas the magnitude
of mortality with hypernatremia is less pronounced when it becomes more
prevalent (during later stages of kidney disease). This indicates that while
high sodium levels in the blood may
become slightly more prevalent in later stages of kidney disease (stages 4 and
5), they are not as harmful. This may be because the body has ample time to
adapt to the high blood sodium levels, which does not seem to occur with low
sodium levels in the blood.116
In one study, hyponatremia and hypernatremia both predicted increased
mortality, with the lowest risk of mortality found at a serum sodium level of
140 to 144 mEq/L.117 Other
experts have defined the optimal range of blood sodium as between 139 and 143
mEq/L.118 If your
blood sodium level is not in this optimal range, you may need to eat more (or
less) salt. The risks of dying with serum sodium levels greater than 145 mEq/L
(hypernatremia) and between 130 and 135.9 mEq/L (hyponatremia) do not seem to
significantly differ from one another in patients with chronic kidney disease.
However, once blood sodium levels fall below 130 mEq/L, the risk of death is
almost twofold compared to just 1.3-fold with a blood sodium level greater than
145 mEq/L).
In summary, hyponatremia is extremely common in chronic kidney disease,
especially when compared to hypernatremia. Restricting sodium in patients with
chronic kidney disease is not necessarily a good idea and may lead to adverse
health outcomes. If anything, patients with chronic kidney disease may benefit
from eating more salt. Even hemodialysis patients (who generally lack an
ability to excrete salt in between dialysis sessions) may actually benefit from
eating more salt, as hyponatremia increases the risk of mortality in these
patients as well.119 Low
dietary sodium intake is also associated with an increase in the risk of death
in peritoneal dialysis,120 and
hyponatremia is a complication in peritoneal dialysis.121
Low-salt diets may also make sugar more harmful to the kidneys, as they
can lead to dehydration, which activates the “polyol pathway” in the kidneys
that causes us to form more fructose from glucose, metabolize fructose more
quickly, and increases our oxidative stress and damage to our kidneys.122 And,
again, all of this can lead to salt-wasting kidneys. In essence, if you choose
a low salt intake on top of a high-sugar diet, you have the perfect formula for
causing kidneys that can no longer hold on to salt.123 That’s why
low-salt diets are potentially extremely harmful in those
consuming diets high in sugar, especially in patients with diabetes.124
You May
Need More Salt if You Have Inflammatory Bowel Disease
The
surgical removal of the small intestine can lead to intestinal failure, “short
bowel syndrome,” and reduce a person’s ability to absorb salt.125 However,
the intestine can also fail because of inflammation, ischemia, or motility disorders.
The primary task of the colon, besides moving fecal material out of the body,
is to absorb salt and water. Patients with inflammatory bowel disease (Crohn’s
and ulcerative colitis) have significant problems absorbing salt in the
intestine and colon, respectively, which leads to excreting more salt and lower
blood sodium levels, even in moments of remission.126 People who
have had part of their colon removed (during treatment for colon cancer, for
example) are also at risk of developing sodium and water depletion.127 In fact,
any damage to the intestinal mucosa, such as celiac disease, will reduce the
absorption of salt—and increase the risks of following a low-salt diet.
You May Need More Salt on
Low-Carbohydrate Diets
Patients
eating low-carbohydrate diets will need more salt (especially during the first
two weeks of the diet) compared to someone who has higher levels of insulin
(someone eating over 50 grams of carbohydrates per day). Higher levels of ketones,
greater release of glucagon, and lower levels of insulin, all of which occur on
a low-carb diet, increase our excretion of sodium.128
When dietary carbohydrate is restricted to 50 grams per day, the same
excretion of sodium that occurs during starvation occurs with this level of
carb restriction.129 In one
study of normal healthy patients, despite eating more than 100 grams of protein
and 1,500 to 2,000 calories per day, their elimination of carbohydrates caused
a significant sodium depletion of about 4.7 to 5.6 grams in just three days. The
sodium depletion that was previously attributed to the lack of calories during
fasting turned out to be the result of carbohydrate restriction.130 Another
study of obese subjects showed that 4,266 milligrams of sodium was depleted
from the body in just seven days on a low-carbohydrate (40 grams per day) diet.131
Eliminating carbohydrate intake in healthy patients, down to 0 grams per day
(as found in one fasting/starvation study) for ten days was found to deplete
18.72 grams of sodium from the body, just from losses via the urine.132 In another
study of forty obese patients, people lost an average of 8 to 19 grams of
sodium over ten days.133 Another
fasting study of seven obese females found that they went through their sodium
excretion in five- to six-day cycles, losing between 18.6 and 57.3 grams of
sodium over a period of thirty days.134 It’s clear
that low-carbohydrate diets (as well as prolonged fasting) can cause a dramatic
reduction in total body sodium content (and hence a greater risk of sodium
deficit). The losses of sodium in the urine on low-carb diets seem to dissipate
after about two weeks as the body makes its adjustment. However, compared to
when they followed a previous diet that was higher in carbohydrates,
individuals following low-carb diets keep losing more salt in the urine because
of the reduction in insulin levels. They may experience
symptoms such as dizziness, fatigue, and carb cravings, which could be greatly
improved by upping their salt intake.
ADDING SALT TO A LOW-CARB DIET
Dr. E. S. Garnett and colleagues performed a metabolic ward study in
which seven obese females were placed on total-starvation diets (consuming only
115 milligrams of sodium per day). These authors found that while exchangeable
sodium (the sodium that can move into and out of the extracellular fluid) fell
during the first week of starvation, it progressively rose to prestarvation
levels despite continued fasting and sodium restriction.135 This
occurred despite a large negative sodium balance, indicating that stored sodium
(from either bone, skin, or organs) was being pulled into the exchangeable
sodium space. These findings suggest that prolonged fasting on top of a low
sodium intake pulls sodium from body stores (such as bone) to replenish the
exchangeable sodium space. In essence, prolonged fasting, especially on top of
a low sodium intake, may put patients at risk of osteoporosis, as sodium is an
important component in bone formation and seems to be depleted while fasting.
We really cannot rely on blood sodium levels to know if someone is
deficient in salt because the body maintains a normal blood sodium level at the expense of sodium depletion in other parts of the body.
Despite starting with different levels of total body sodium, almost all
patients stop losing sodium once they hit around 69 grams of total body sodium.
In fact, 63 to 69 grams of total body sodium may indicate a minimal
level of total body sodium required for humans to survive. Importantly, in one
study, a patient who started with 151 grams of total body sodium lost 82 grams
of sodium during total starvation, whereas the others patients lost much less.
This study suggests that certain individuals function at a higher total body
sodium content compared to others and, therefore, some are at less risk of salt
deficit. That means some individuals are likely more susceptible to the harms
of low-salt diets compared to others—and we need to determine just who those
people are before we issue blanket recommendations about salt intake.136
You May
Need More Salt to Prevent Iodine Deficiency
Iodization
of salt has been an important public health victory for eliminating goiter
around the world. In one study, 133 people were tested to see if salt
restriction was related to iodine deficiency.137 Half the
subjects were placed on a normal-sodium diet and half were placed on a
reduced-sodium-intake diet, and then twenty-four-hour sodium and iodide
excretions were measured. The results indicated that those in the
salt-restricted group consumed just 1.9 grams of sodium per day, and 50 percent
of the patients excreted 100 micrograms or less of iodide per day at eight
months. In other words, more than half of the subjects restricting their salt
intake were probably not getting the daily recommended iodine intake—and these
subjects were consuming more sodium than what is
currently recommended by the American Heart Association (1.9 grams per day
versus less than 1.5 grams per day, respectively) and meeting the WHO
recommendations (less than 2 grams of sodium per day). However, only 25 percent
of patients eating the normal-sodium diet excreted 100 micrograms or less of
iodide per day at eight months. In essence, compared to people who do not restrict their salt intake, those who follow the low-salt
advice may be twice as likely to not get the recommended daily amount of
iodine.
In order to prevent goiter, one needs to consume 50 to 70 micrograms of
iodine per day. Based on twenty-four-hour urinary iodide levels, 15 percent of
people in the low-salt group were at risk of goiter compared to 10 percent of
the control group—suggesting there’s a 50 percent increased risk for developing
goiter when on a low-salt diet (around 1.9 grams of sodium) versus a
normal-salt diet. The risk is certainly higher in those who aren’t eating foods
naturally high in iodine. Importantly, approximately 50 percent of the
individuals in this study ate seafood at least once a week, so this study may
underestimate the risk of iodine deficiency in developing goiter for those who
do not regularly eat the same amount of seafood. Interestingly, around the time
of this study (1983–1984), iodophors were still being heavily used as cleaning
agents in the dairy industry, which ensured that dairy products provided more
iodine.138 Thus,
current populations, who consume dairy products without the same levels of
iodophors, may be at even greater risk for iodine deficiency and goiters than
the study group.
You May Need
More Salt to Fight Infections
Our
host-defense system may be driven by salt, which may activate other
antimicrobial defense systems. Without salt, we wouldn’t be able to effectively
get rid of pathogens from the skin, as a hypertonic environment increases the
production of nitric oxide, helping to eliminate pathogens.139 This may
be why salt excretion is substantially reduced in patients who have a fever and
infection, in order to help combat the microbial invaders. Eating enough salt
can ensure adequate salt deposits in our skin, which can help encourage
protective macrophages to help attack bacterial infections. The authors of one
study concluded, “Our findings suggest that edema formation in infection is not
only characterized by water retention and swelling but also creates a microenvironment of high sodium concentration.” The
researchers found that in mice fed a high-salt diet, their “sodium reservoir”
was particularly powerful in fighting off L. major
bacterial infections, with salt serving an antimicrobial barrier function in
the skin.
Eating a normal-salt diet may help us ward off skin infections. As we
enter the days of antibiotic resistance, skin infections can potentially be
lethal if they become systemic. Even scarier: low-salt diets may predispose us
to a greater risk of complications, or even death, from methicillin-resistant Staphylococcus aureus (MRSA) and other skin infections or
flesh-eating bacteria. MRSA is often treated with a medication called
Bactrim/Septra (a combination of trimethoprim and sulfamethoxazole), which can
cause kidney damage and metabolic acidosis that can also lead to salt wasting.
Sulfamethoxazole causes increased sodium excretion by the kidneys, so patients
receiving high doses of this medication may be at risk of sodium depletion.140 Additionally,
since salt is so important for fighting skin infection, a higher-salt diet may
help diabetic patients heal their skin ulcers (a common complication). In
essence, patients with diabetes may need even more salt to help prevent and
treat skin ulcers. But the skin isn’t the only organ that salt helps fight off
infection. High concentrations of salt in lymphatic organs (lymph nodes,
spleen, thymus) and inflamed tissue may help the body fight off infections.141 A
high-salt diet may also help in sepsis, as hypertonic saline increases T-cell
function,142 and may
help in other systemic infections, such as human immunodeficiency virus (HIV)
or other dangerous viruses such as Ebola or hepatitis.
Infections come via our food supply as well. Over one million cases of
food poisoning in the United States happen every year (almost five hundred
being fatal), and “low-salt” versions of packaged food products may have higher
microbial counts than normal-salt versions, increasing the risk of food
poisoning.143 Hence,
low-salt packaged foods may increase the risk of food-borne illness.
Additionally, when you have food poisoning, you lose a lot of salt in your
vomit and diarrhea. Basically, low-salt diets may increase
the risk of death in the over one million food poisoning cases just in the
United States every year.
One study in Australia estimated that decreasing microbial growth rates
by modest amounts can have a large effect on the risk of listeriosis from
processed meats. The study authors said that “reducing the growth rate of L. monocytogenes by 50 percent decreased the risk of
illness in the population by 80 to 90 percent.”144 This
suggests that even a small increase in growth rate resulting from a decrease in
salt without adequate adjustment of other preservative factors could
considerably increase the risk to the susceptible population.
All of this indicates that lowering the salt content of food, in the
effort to meet unscientific low-salt guidelines, may increase the risk of
food-borne illness and the degree of food wastage. “One manufacturer producing
reduced salt bacon has already used this technique; when the salt content of
bacon was reduced from 3.5 percent to 2.3 percent, the shelf-life was reduced
from 56 days to 28 days.”145 Lowering
the salt content of packaged foods may also require higher use of suspect
preservatives, such as phosphates, nitrates, and nitrites, in order to maintain
microbial stability, which are likely more detrimental to our health compared
to salt.146
YOU MAY ALSO NEED MORE SALT FOR…
• Autism: Autism is a complex disorder, with
many likely causes and genetic links. However, one theory holds that autism
could be a disorder of overhydration, with low sodium levels in the blood
depleting certain essential brain nutrients, such as taurine and glutamine.147 This may be one reason why children
with autistic disorders tend to have salt cravings. Children with autism may
benefit from consuming more salt, whereas low-salt diets may actually worsen
their condition. Oral rehydration salts may also be of benefit in autism.148
• Caffeine: Caffeinated beverages, acting like natural
diuretics, can increase water and salt loss from our kidneys. Coffee and tea
are now the second and third most commonly consumed beverages around the
world—not to mention other caffeinated drinks such as sodas and energy/sports
drinks that flood the market. We are now more than ever a salt-excreting
society, because of our caffeine addiction.
• Certain
conditions: Hypotonic hyponatremia can be found in severe polydipsia
(frequent among schizophrenic patients) or “beer drinker’s hyponatremia” (also
known as “beer potomania syndrome”—people who overconsume beer basically give
themselves dilutional hyponatremia). Certain types of renal tubular acidosis
and metabolic alkalosis cause hyponatremia, whereby the increased bicarbonate
in the urine forces sodium to flow out of the kidneys.149 Cerebral
salt-wasting syndrome (from subarachnoid hemorrhage) can also cause low sodium
levels in the blood. Euvolemic hyponatremia can be caused by hypothyroidism,
primary adrenal insufficiency, and hypopituitarism with secondary adrenal
insufficiency. Autoimmune Addison’s disease (or other adrenal insufficiency
disorders, such as adrenal fatigue) can also lead to hyponatremia.150
Hyponatremia can also be caused by cortisol deficiency.151
• Nicotine:
Those using forms of tobacco that contain nicotine (cigarettes, cigars, pipe
and chewing tobacco) have an increased risk of low blood sodium levels due to
nicotine’s ability to increase water retention (via an increased production of
antidiuretic hormone).152
Because of the many chronic disease states and medications that cause
salt depletion in the Western world, we are now at a much greater risk of salt
deficit than even primitive societies that eat very little salt. Thankfully,
now that we recognize this, we can do something about it—and, in so doing, we
can help ourselves prevent or even reverse many of today’s most debilitating
conditions. It’s time for the Salt Fix. In the next chapter, I’ll walk you
through a step-by-step plan to help correct the salt balance in your body,
reconnect with your innate salt thermostat, choose the best sources of
high-quality salt for your situation, and help you drop the salt guilt, so you
can get back to enjoying the vitality, energy, and delicious savory
satisfaction that salt can bring.
8 – The Salt Fix: Give Your Body What It Really Needs
You’ve seen the evidence: your body needs more salt! Luckily, reversing
your salt deficit is straightforward: simply by giving in to your innate,
natural cravings, you can naturally guide yourself back to the ideal amount of
salt your body needs to operate at its best. You’ve been taught to ignore those
cravings and disregard your body’s salt thermostat, so it can take a bit of
time and experimentation to reset those internal protective mechanisms.
Thankfully, just a few adjustments to your current diet and lifestyle can have
significant, wide-ranging effects on your health.
There’s no downside to this program. You’ll enjoy more energy, fewer
infections, improved sexual and athletic performance, and a faster metabolism. Your body will have increased immunity, better
cellular function, and much less stress on critical organs. All you need to do
is eat delicious foods with zero added calories! What could be better? Here’s
how to do it.
Step 1:
Visit Your Doctor to Test for Internal Starvation
• If you eat or drink something that’s high in added sugars (generally
more than 20 grams) and you become shaky, jittery, or sweaty afterward, that
may mean that your body is oversecreting insulin and causing your blood sugar
to crash.
If this sounds like you, here’s what to do:
Generally, a fasting insulin level of 5 uIU/mL or less is optimal; if
it’s higher than that, you’ll probably store more fat than someone who has a
lower fasting insulin level, even if both of you consume the same number and types of calories. To put this number in perspective,
less-developed societies typically have a fasting insulin level of 3 to 5
uIU/mL; by contrast, in the United States the average fasting insulin is around
9 to 11 uIU/mL (though it has wavered a bit through the years).1
Reevaluate your medications. If the tests detect high insulin, you’ll want to work with your
physician to lower it. The first step is for your doctor to assess whether a
medication you’re taking could be causing insulin resistance/high insulin
levels. Many common drugs—including the SSRI antidepressants, certain
antipsychotic medications, diuretics and beta-blockers for hypertension, and
more—may worsen insulin resistance. For each of these underlying health
conditions, there may be other drugs or better options within the same class
that can effectively treat what ails you without promoting high insulin levels.
Depending on your fasting insulin and blood sugar levels, you may also want to
discuss whether you’d benefit from taking an insulin-sensitizing medication (such
as metformin, acarbose, or pioglitazone). The table on this page provides
alternative medications that may help to prevent or reverse insulin resistance.
Consider Medication Swaps to Prevent (or
Reverse) Insulin Resistance
Current Medication
|
Suggested Alternative
|
Diuretics
|
|
Hydrochlorothiazide
|
Indapamide
|
Statins
|
|
Atorvastatin, Simvastatin,
Rosuvastatin
|
Livalo or Pravastatin
|
Anti-diabetic medications
|
|
Glyburide, Glipizide,
Glimeperide, Insulin, Repaglinide
|
Acorbase, Metmorfin, Pioglitazone
|
Angiotensin-converting enzyme (ACE)
inhibitors
|
|
Enalapril or Lisinopril
|
Perindopril
|
Step 2:
Replace Simple Sugars with Real Salt
• The full amount of salt you crave, enough
to fulfill your body’s needs and please your taste buds, without going
overboard (no more than around 6,000 milligrams of sodium per day for someone
who isn’t wasting salt from their kidneys or not able to absorb salt well); and
When patients come into the doctor’s office with high blood pressure,
the first recommendation that many doctors make is to reduce salt—but I believe
so many lives could be saved if we urged patients to enjoy
plentiful salt and cut way back on their sugar instead. Allowing yourself to
eat as much salt as you crave can help you kick your sweet tooth.
Never drink your sugar.
To cut sugar from your diet, the first place to
start is by dropping any source of liquid-added or free sugars, such as soda,
fruit juices (even 100 percent real fruit juice), smoothies, sweetened iced
teas, energy drinks, sports drinks, and lattes/mocha drinks—even the teaspoons
of sugar you add to your coffee. Liquid sugar is the worst because it’s most
rapidly absorbed and therefore leads to worse metabolic consequences than solid
sources. The 40 grams of sugar you can drink in literally seconds from one can
of soda floods you with a huge sugar load. All that sugar can override the
body’s ability to metabolize it, so cutting back on these sweet liquids (or,
ideally, forgoing them entirely) helps you make the most impactful difference
for your body in this one change. (Artificial sweeteners aren’t the answer,
either; read on for more about that.)
Root out hidden sugars.
Once you’ve cut out the obvious sources of added sugar, start to avoid added
sugars such as high-fructose corn syrup and sucrose in other processed foods.
Research has found that simply reducing your intake of added fructose lowers
chronically high levels of insulin and reduces insulin resistance—so this is an
essential change to make.
Stay vigilant with “healthy” sugars. Some forms of sugar are touted as being “healthier” than others, and
there actually is some truth to that, but it’s truer to say that some sugars
are more harmful than others. Physiologically
speaking, fructose and glucose are metabolized differently in the body, so
sugars that contain fructose are not the same as those that contain pure
glucose. Despite their different flavors, textures, and colors, the nutritional
value of most forms of sugar is quite comparable, though molasses contains
trace amounts of calcium, iron, and potassium, and honey is highest in
antioxidant and antibacterial properties. And while a given amount of any type
of sugar has the same number of calories (16 per teaspoon), the calories
from fructose are much more harmful.3
Avoid fake sugars entirely. Most sugar substitutes aren’t necessarily the answer. Basically,
artificial sweeteners confuse your body: when sugar doesn’t accompany the sweet
taste of sugar substitutes, your appetite kicks into overdrive so that your
body can get the sugar it thinks it deserves. This may cause you to seek out
real sugar in your diet, and you may even end up
consuming more of the sweet stuff. Additionally, any carbohydrate that comes
along with diet drinks (burger bun, fries, etc.) may be absorbed more easily,
spiking your glucose levels and leading to worse health outcomes.
Resist the “sugar” in savory carbs. Then cut way back on refined carbs such as white bread, white rice,
white pasta, and even starchy vegetables such as white potatoes. (See
“Guilt-Free Potatoes” on this page for the
sole exception.) Other strategies include eating a healthy carbohydrate in
small amounts, such as one slice of Ezekiel (sprouted grain) bread dipped in
extra-virgin olive oil. This flourless bread provides the “sugar fix,” and the
olive oil provides additional satiety as well as healthy phenolic compounds.
One piece of Ezekiel bread contains only 14 grams of carbohydrates (3 grams of
which are fiber, providing a net effective carb content of just 11 grams per
piece). Moreover, Ezekiel bread seems to cause less of a blood sugar spike
compared to other more refined breads, and it is also organic (so it doesn’t
contain artificial preservatives or vegetable oils). It also contains other
types of healthy substances (such as barley, lentils, and organic sesame seeds,
depending on which Ezekiel bread you buy—the sesame seed version is my
favorite!). Keeping Ezekiel bread in the refrigerator and then toasting it
enhances its flavor, and dipping it in extra-virgin olive oil provides a great
satiating healthy snack without causing the damage that a rapidly absorbed
sugary snack would. Make sure to spice up the olive oil with some good garlic
salt, spices, and perhaps a dash of pepper before dipping.
SALT HELPS LOW-CARB EATERS
THRIVE
CONSIDER SUGAR-TAMING
SUPPLEMENTS
• L-carnitine has been found to improve fatty liver, may help with
weight/fat loss, and may help reduce hunger.4 Supplementing with 1,000
milligrams of L-carnitine two to three times daily (taken on an empty stomach)
for a few months may be helpful.
• Glycine, which is the
smallest of the amino acids, has also been found to help mitigate some of the
metabolic harms of sugar. Consuming 5 grams of glycine (preferably in powder
form mixed with water) three times daily thirty to forty-five minutes prior to
meals may help reduce high blood pressure, improve fatty liver disease, and
drop a few extra pounds of fat.5
• If your dietary intake
of iodine is not adequate (not eating foods high in iodine such as cranberries,
seaweed [as in sushi wrappers], or yogurt), supplementing with iodine may be
the next best choice. Pure Encapsulations (www.pureencapsulations.com) hires a
third-party company to regulate their supplements. This may be a good option,
although only healthcare professionals are allowed to purchase and sell its
products.6
Note: if you have diabetes or prediabetes or are on any medication that
may cause blood sugars to drop, make sure your doctor is aware that you plan on
cutting back on consuming refined sugars and carbohydrates, especially if you
take insulin. While there is debate if there is a true need (requirement) for
dietary carbohydrates, this does not mean that there cannot be consequences
when cutting your intake (like hypoglycemia, also known as low blood sugar), so
make sure your doctor is in the loop.
Step 3:
Focus on Whole, Salty Foods
Also, don’t forget that for most people your body constantly tells you
to consume 3,000 to 5,000 milligrams of sodium per day, so if you avoid salt in
your meals, this will likely cause you to consume more food throughout the day
to get the amount of salt your body craves. Your body will eventually drive you
to get more salt until you’ve hit that
3,000-to-5,000-milligrams-of-sodium mark—so if you consume low-salt versions of
foods, you may end up eating two to three times as much because your body is
still “hungry” for salt. Which may obviously mean more pounds in your near
future, so try to avoid low-salt versions unless your body is telling you it
has had enough.
Seek out alternative iodine sources. To emulate these salt-rich cuisines, aim to eat whole foods that can
help you get your iodine needs covered, such as dairy, eggs, seafood, sushi,
seaweed, cranberries, and potatoes that have been undercooked and cooled (see this page for
preparation information). Stick as close to nature as possible, such as fish
from the ocean rather than farmed, and dairy/eggs from grass-fed and free-range
sources.
Incorporate salts into every meal. For breakfast, start with some organic
salted nuts—especially helpful if you drink coffee, to replace what is lost in
the urine. For lunch, create your own homemade dressing with extra-virgin olive
oil (preferably organic), organic garlic salt, pepper, and herbs—mix well and you
have created a healthy dressing. Take this delicious salt-enhanced dressing and
pour it over bitter greens or salads. You can even use this dressing as a
dipping sauce for your meats. Other good options for lunch include organic
salted cured meats with aged cheeses (preferably from free-range or pastured
animals) with organic pickles or olives as a side. For dinner, if you’re in the
mood for some grass-fed meat, use olive oil to coat both sides, sprinkle
liberal amounts of organic garlic salt on both sides with a dash of pepper, and
sear each side over medium-high heat; then drop the temperature down to medium
to avoid overcharring your meat.
In particular, ocean fish that consume algae and have a high omega-3
fatty acid and salt content—such as salmon, mackerel, tuna, and sardines—will
promote satiety and fat loss. If your hunger is in a state of overdrive due to
internal starvation and high insulin levels, consuming healthy fats and lean
proteins—in fatty fish, nuts, grass-fed beef, organic cheeses, olives, and the
like—will help promote feelings of fullness and improve insulin sensitivity and
leptin resistance.7 And adding
salt to healthy but generally less palatable foods (such as Brussels sprouts,
cabbage, and turnips) will allow you to eat more of them.
Diversify flavors to wean yourself from sugar. Once you start consuming more real foods and fewer items with added
sugars, your palate will grow accustomed to foods that are less sweet; you
really will be retraining your
taste buds, in the right direction this time! And before you know it, foods
with even modest amounts of added sugar that used to taste good to you will
taste too sweet—that’s a very good thing! The key is to learn to consciously
make healthy whole-food choices; pair ingredients smartly and use herbs and
spices strategically. And when you’re not craving salt but you need some extra
flavor, add additional spices and herbs instead of sugar.
One
theory that’s been gaining traction in recent years is the notion that an
imbalance between bad and good bacteria in the gastrointestinal system—your
“gut microbiome”—may play a role in setting the stage for obesity. Simply put,
consuming lots of sugar may promote the growth of harmful gut bacteria and Candida albicans (a type of yeast), microorganisms that can
impede the absorption of nutrients by your cells, another form of internal
starvation.8
Step 4: Add in Naturally
Higher-Nutrient Salt
Type of salt: Redmond Real Salt
Purity issues: Apparently this salt does
not contain anticaking agents, and it seems to lack the radioactive elements
found in Himalayan salt. There also appears to be less subjection to
environmental pollutants compared to salt obtained from modern oceans.9
Harvesting: Mined from an ancient seabed in
Redmond, Utah.10
Nutrient profile: Provides eighty-two vital
trace minerals but in rather low quantities. Celtic sea salt is touted for
having the highest magnesium content of all the salts, but it may provide only
around 40 milligrams of magnesium per day. Other trace minerals in an entire
day’s worth of Celtic sea salt include just 17 milligrams of calcium, 9
milligrams of potassium, and only 6 micrograms of iodine. To sum it up, the
actual amount of almost all of these trace minerals (except perhaps the
magnesium content) is so minimal that the added benefit may not be worth the
added cost.11
Purity issues: This salt is supposedly not
subjected to refinement or bleaching processes, and there are no additives in
it; however, it is harvested from modern-day seas, which means it may contain
traces of toxic metals such as mercury. However, it is said that Makai Pure
Deep Sea Salt from the Selina Naturally Celtic Sea Salt collection is taken
from the deep sea (2,000 feet below the ocean’s surface). This part of the
ocean supposedly does not mix with other parts of the ocean (because of the
deep cold ocean currents) and hence that particular Celtic sea salt may
possibly contain less contamination.12
Harvesting: Comes from a modern ocean and
gets evaporated in ponds off the shores of France (hence, it is not subjected
to very high heat as is regular table salt).13
Type of salt: Himalayan (pink)
salt
Qualities: Pinkish in color; crystalized or
chunky in texture; earthy flavor
Nutrient profile: Contains eighty-four
minerals and trace elements and may have the most potassium of any of the sea salts (about three times as much potassium as Redmond Real Salt).
To be fair, however, even if your total salt intake came from Himalayan salt,
this would only provide around 28 to 32 milligrams of potassium (only a
fraction of the daily recommended amount—4,700 milligrams).14 To put
this in perspective, 1 cup of black beans provides 2,877 milligrams of
potassium. Himalayan salt is the most expensive of all the popular salt
varieties.
Purity issues: It is generally mined by
hand and hand-washed after being collected from unspoiled underground sources;
hence, it is probably less contaminated by toxic metals but may have other
radioactive elements such as radium, uranium, polonium, plutonium (although the
concentrations are less than 0.001 part per million).15
Harvesting: Mined in different parts of
Pakistan. Comes from an ancient dried-up ocean.16
Type of salt: Himalayan black
salt (kala namak)
Harvesting: It appears kala namak can be
produced in numerous ways, either from natural halite (rock salt) of the
Himalayan salt ranges (mined in Bangladesh, India, Nepal, and Pakistan) and the
North Indian salt lakes (Sambhar Salt Lake or Didwana as well as the Mustang
District of Nepal), or synthetically created by
combining sodium chloride with sodium sulfate, sodium bisulfate, and ferric
sulfate (apparently this is the most common way of production nowadays).17
Type of salt: Black and red
Hawaiian sea salts*
Qualities: Hawaiian black lava salt is
actually not a volcanic salt deep within the earth.
It is made up of Pacific white sea salt crystals mixed with activated charcoal
from burned-up coconut shells.18 The
activated charcoal supposedly provides antioxidants, has detoxifying
properties, and may be good for digestion.19 Hawaiian
black lava salt is said to have a nutty or smoky flavor. Hawaiian red Alaea
salt is also made up of white sea salt crystals, but it is infused with
volcanic red clay (rich in iron oxides). Hawaiian red Alaea salt is said to
have a sweet flavor.20 These salts
come as fine or coarse crystals that may be damp.
Purity issues: The Pacific Ocean near
Hawaii may be less contaminated than other parts of the ocean. The Hawaii Kai
Corporation website provides the authentic Hawaiian salt from Molokai
(supposedly the most isolated island, and because of this the salt here may
have the least contamination from pollution). The sea salt harvested by the
Hawaii Kai Corporation is “apparently under the supervision of certified salt
masters, who are members of the Salt Masters Guild of Hawaii, an association
formed with the goal of reinvigorating the thousand-year tradition of salt
making as practiced by the ancient Hawaiian culture.”22 However,
you can get other good Hawaiian salts from the other islands.23 Beware of
imitation salts that are “produced by mechanically mixing a cheap, highly
refined California sea salt (about 99.8 percent pure sodium chloride) with
alaea clay from China or Hawaii. Typically the darker the red color, the higher
the quality of alaea clay used to make it.”24
Harvesting: Solar-evaporated Pacific sea
salt.25
Type of salt: Table salt (aka
sodium chloride)
Qualities: Fine white crystals
Harvesting: Mined throughout various parts
of the world.26
* Also
known as Hawaiian black lava salt and Hawaiian red Alaea salt. However, pink,
green, white, and gray Hawaiian sea salts are also available, but they are not
as popular or as traditional to the islands as the black and red salts.21
|
|
Iodized Table Salt |
Redmond Real Salt |
Celtic Sea Salt |
Hawaiian Sea Salts |
Himalayan (Pink) Salt |
|
Iodine |
450 mcg |
178 mcg |
6 mcg |
Little to none |
<100-250 mcg |
|
Calcium |
0 mg |
45 mg* |
17 mg |
11-14 mg |
37 mg |
|
Magnesium |
0 mg |
8 mg |
40 mg |
30-35 mg |
1,4 mg |
|
Potassium |
0 mg |
9 mg |
9 mg |
18 mg |
28-32
mg* |
* Indicate
the salt with the highest content of that mineral.
As discussed earlier, the actual amounts of additional trace minerals
provided by the sea salts are fairly minimal, except for the iodine (and
perhaps calcium) contained in Redmond Real Salt and perhaps the magnesium
content in Celtic sea salt and Hawaiian sea salts. If you are not obtaining an
adequate intake of iodine, using Redmond Real Salt may provide some advantages.
If your diet lacks calcium or magnesium, Redmond Real Salt and Celtic Sea Salt,
respectively, may provide some additional health benefits compared to plain
table salt. However, eating real foods will provide at least ten times the
amount of these trace minerals.
Perhaps the most significant difference between table salt and the
popular sea salts listed here is in the processing. Table salt is said to be
bleached (to make it pure white) and treated with high heat (around 1,200°F)
and anticaking agents (so the salt doesn’t clump together).27 However,
the sea salts seem to lack this type of processing, which may provide a higher
level of reassurance regarding their safety.
The best salt (in my opinion) would be Redmond Real Salt for five main
reasons:
1. It seems to be the cheapest of the popular sea salts.
2. It provides a
meaningful amount of iodine.
3. It may have the least
contamination (as it comes from an ancient
dead sea, whereas Celtic sea salt, for example, comes from a modern ocean).
4. It seems to have fewer
radioactive elements compared to Himalayan salt.
Vegans are particularly at risk of iodine deficiency, as some of the
most common food sources containing substantial amounts of iodine include
dairy, eggs, shellfish/seafood, and sushi (vegans can obtain iodine from
seaweed, cranberries, and baked potatoes). For example, it is estimated that
one sushi roll contains around 92 micrograms of iodine, mostly from the seaweed
(according to Food Standards Australia New Zealand).28
Sometimes
people who are avoiding salt on recommendations from their doctor turn to salt
substitutes. But they aren’t necessarily the answer, either. For one thing,
many salt substitutes contain potassium and chloride (such as AlsoSalt)29 instead of
sodium chloride, and people with kidney problems often have trouble processing potassium
chloride or getting rid of the excess. If you have chronic kidney disease or
you take certain antihypertensive medications (such as ACE inhibitors or
potassium-sparing diuretics), the extra buildup of potassium could lead to
potassium overload (a condition called hyperkalemia), which can be fatal if
it’s not treated promptly. Go for the healthiest option: real salt!
Step 5: Let
Salt Fuel Your Exercise
If you’ve been sedentary for a time, a good starting point is to
increase your level of physical activity (under your doctor’s supervision) with
modest moderate forms of exercise such as going for a twenty-minute brisk walk
or bike ride. But please don’t stop there—also implement weight training,
because lifting weights or doing resistance exercises (using resistance bands,
weight machines, or your own body weight) is one of the best ways to help with
insulin resistance. While aerobic exercise helps your body use insulin better
and decreases storage of visceral (abdominal) fat, resistance training makes
your body more sensitive to insulin and helps your muscles take up more glucose
(sugar) from the blood, thereby lowering blood sugar. Even simply exercising
before or right after you eat something with higher
carbohydrate levels can help reduce any resulting swings in your blood sugar
and insulin release.
Start slow and low, and build from there. Begin with walking and slowly
increase to jogging and then running; start with light weights, and slowly
increase to heavier weight lifting. In one 2012 study, researchers from the
University of Verona in Italy found that after forty people with type 2
diabetes did aerobic training or resistance training for four months, both
groups improved their insulin sensitivity and reduced their abdominal fat.30 Meanwhile,
a 2012 study from the Norwegian University of Science and Technology in
Trondheim found that both maximal resistance training and endurance resistance
training led to decreased insulin resistance in people who were at risk for
developing type 2 diabetes. Interestingly, the maximal approach, which uses
heavy loads to increase muscle power and force, led to a greater increase in
the muscles’ capacity for taking up glucose (sugar) from the blood, whereas the
endurance type of resistance training brought greater insulin sensitivity.31 One way or
another, with increased exercise, your body will become better at soaking up
sugar from your blood, and the carbohydrates you do eat will be less damaging
as a result.
Even if you’re not at peak fitness level yet, eating enough salt is a
great way to increase your energy levels, which will help you want to exercise,
one of the best things you can do for improving internal starvation. Best of
all, when you stop restricting your salt intake, your insulin levels can start
to drop toward the normal range, and your body will start to access its stored
energy—in other words, you’ll burn more fat! Your body will also use the
calories you consume from food for energy, rather than immediately hoarding
those calories as fat. More importantly, your salt-retaining hormones will go
down, improving the sensitivity of your fat cells to insulin. Because of this,
your fat cells can begin to absorb any extra fat and glucose—exactly where it’s
supposed to go, rather than being driven into your belly and internal organs. Your
brain will become more sensitive to leptin, your natural appetite controls will
return, and you’ll have enough energy to exercise and feel good. Ultimately, by
rebooting your internal salt thermostat—and achieving your long-lost normal
salt intake—you’ll help restore your vim and vigor, avoid reentering a state of
internal starvation, turn up your slogging metabolism, and regain control of
your weight. You will finally shift away from being “thin on the outside and
fat on the inside” and move toward being “thin on the outside as well as the
inside”! And best of all, you’ll be able to kick that toxic sugar habit, once
and for all.
SALT SAVED MY EXERCISE PROGRAM
Not bad for a little dash of salt, huh?
Epilogue : Reach fot the Right White Crystal
After reading this book, hopefully you’re wise to the dietary deception
that’s been perpetrated on us all, and you have a sense of the tremendous
effect the Salt Wars have had on our bodies and our health for over four
decades. Rather than denying yourself the pleasures of this essential mineral,
now is the time to welcome salt back to the table and embrace it as something
that could help your body feel and function better. We need to move past the
outdated, disproven salt–blood pressure hypothesis and consider what salt has
done for us throughout human evolution. We need to remember:
Salt restriction raises heart rate. Any dehydration-related blood pressure reduction you may get from salt
restriction is going to be offset by the larger increase in heart rate. So
while you may see a 2 percent reduction in your blood pressure, most people
have a 10 percent increase in heart rate. This increase in heart rate is
probably more harmful than the small drop in blood pressure, increasing the
amount of stress on your heart and arteries, potentially leading to
hypertension, heart failure, and cardiovascular events.
* Start eating real food and salting to taste.
* Talk to your friends and family about the ideas
in this book.
* Discuss the ideas in this book with your medical
caregivers.
* Stop eating refined sugar, which is the true
hypertension culprit.
* Stop telling your patients that they should
consciously restrict their salt intake; their bodies know better than any
guidelines when it comes to salt intake.
* Educate yourself on the contraindications of the
low-salt guidelines, and discuss these conflicts with your colleagues and
hospital or practice administrators.
* Become a vocal advocate for removing low-salt
recommendations among your peers in the medical community.
* Discuss the ideas in this book with colleagues
and experts. Challenge those who rest on “received knowledge” to back up their
assumptions with evidence and high-quality studies.
* Join the growing chorus of voices urging the FDA
to remove its voluntary sodium reduction policy aimed at food manufacturers.
* Petition New York City lawmakers to remove
warnings about “high-salt” foods in restaurants, ballparks, and movie theaters
(i.e., a saltshaker outlined in an ominous black triangle).
Meanwhile, we should all focus on limiting our intake of the more
harmful white crystal—sugar—for the sake of our waistlines, our health, and our
longevity. Even if consuming lots of sugar doesn’t lead to obesity for you,
your sweet tooth could be silently and stealthily killing you by triggering
chronic inflammation in your body, wreaking havoc with your hormones, causing
oxidative stress, and triggering other forms of
coronary or inflammatory damage that can increase your risk of having a heart
attack or stroke, developing high blood pressure or type 2 diabetes, or getting
Alzheimer’s disease, fatty liver disease, or certain forms of cancer. Nothing good ever comes from consuming loads of sugar.
100-YEAR
TIME LINE COVERING THE IMPORTANT HISTORICAL EVENTS RELATING TO SALT AND SUGAR
1904 and 1905—Ambard and Beauchard are
given credit for launching the salt–blood pressure hypothesis and the belief
that hypertension is caused by a retention of salt.1
1907—Lowenstein did not confirm the benefit
of a low-salt diet for hypertension.2
1920s—Beginning of the Salt Wars in the
United States.3
1920/1922—Allen, Scherrill, and coworkers
promote the idea that salt increases blood pressure in those with and without
kidney disease.4
1929—Berger and Fineberg conclude that
low-salt diets (less than 1 gram of salt per day) are ineffective for treating
hypertension in almost three out of four patients with essential hypertension.5
1930–1944—Low-salt diets slowly fall out of
favor for the treatment of hypertension.6
1944–1948—Kempner shows benefit of his Rice
Diet (which was, among other things, low in salt).7
1945—Grollman is credited for confirming
that it was the low-salt part of Kempner’s Rice Diet that lowered blood
pressure.8 However,
the study actually showed that not all patients benefited, others experienced
harm (one patient actually died), and another patient experienced circulatory
collapse (which was fixed by providing salt to the patient).9
1950s—Lewis Dahl and
George Meneely begin to suggest that salt is important in hypertension and
chronic disease.10
1950s—The beginning of a debate, largely
between the ideas of Ancel Keys and John Yudkin, regarding saturated fat versus
sugar as a cause of heart disease.11
1960—Lewis Dahl publishes a famous paper
correlating higher sodium intake with a higher prevalence of hypertension in
only five populations.12 This graph
is very similar to the evidence Ancel Keys used to demonize dietary fat as a
cause of coronary heart disease back in 1953.13
1961—Keys’s “diet-heart hypothesis” is
accepted by the American Heart Association. The idea of too much saturated fat,
not sugar, is embraced as the dietary culprit causing heart disease.14
Consequentially, the AHA recommends restriction of animal fats and an increase
in the intake of vegetable oils to reduce the risk of heart disease.
1966—Hall and Hall show that sugar has a
hypertensive effect in rats.15
1972—The New England
Journal of Medicine publishes a paper by John Laragh and colleagues,
which states, “Plasma renin activity emerges as a potential risk factor for
patients with essential hypertension.” Additionally, the study showed that a
lower sodium intake correlated with higher plasma renin activity.16
1974—Richard A. Ahrens publishes a review
paper suggesting that sugar is a driver of hypertension and heart disease.17
1974—The Food and Nutrition Board indicates
that there is little direct evidence that hypertension is produced in people
with normal blood pressure on a normal-sodium diet.18
1975—Alexander Walker writes that there is
no definitive data that a high-sugar diet is a driver of heart disease or
hypertension. His research seemed to have partial grants from the sugar
industry.19
1976—Edward Freis and Meneely and Battarbee
publish influential review papers on the harms of salt.20
1977—The Dietary Goals recommend that all
Americans restrict their salt intake to 3 grams per day.21
1978—A. E. Harper publishes a critique of
the 1977 Dietary Goals showing that the evidence for low-salt diets in
hypertensive patients was inappropriately
extrapolated to the general public and that a 3-gram daily salt intake was
unrealistic and unattainable.22
1979—F. Olaf Simpson publishes a review
paper that is skeptical of the benefits derived from a low-salt diet.23
1980—J. D. Swales publishes a review paper
concluding that it was premature to recommend population-wide sodium reduction.24
1980—Preuss and Preuss show that sugar
(without a high salt intake) increases blood pressure in rats with normal
kidney function.25
1981—Yamori shows that as long as the Na/K
ratio is less than 6 (despite a high sodium intake) in the Japanese, then the
mean blood pressure is not hypertensive.26
1982—Time
magazine releases its issue titled “Salt: A New Villain?”27
1983—Tessio Rebello and colleagues may have
been the first to show that sugar significantly raises blood pressure in
humans.28 This was
after we had vilified salt as the main dietary culprit causing hypertension.
1983—Robert E. Hodges and Tessio Rebello
publish a review paper showing that sugar increases blood pressure in both
animals and humans.29
1985—Boon and Aronson’s review paper
concludes that the amount of salt that needs to be restricted to obtain a
measurable effect on blood pressure was intolerable for most patients.30
1988—Intersalt shows that when the four
primitive societies were removed (leaving a total of forty-eight populations),
a higher sodium intake did not correlate with a higher median blood pressure or
prevalence of hypertension. Importantly, “body mass index had strong,
significant independent relations with blood pressure in individual subjects.”31
1989—Harriet P. Dustan states that there is
no relation between blood pressure and salt depletion/salt loading, and that
“salt-dependent hypertension” is not strictly controlled by salt intake but
rather is probably controlled by aldosterone, norepinephrine, and epinephrine.32
1991—The first meta-analysis (which
included nonrandomized and randomized trials) looking at sodium restriction and
blood pressure is published.33 Based only
on reductions in blood pressure, the authors concluded, “Salt reduction by 100
mmol/24h would reduce mortality from ischaemic heart disease
by an estimated 30 percent in the long term,” and “A 50 mmol/24 h reduction in
sodium intake would reduce the incidence of stroke by a fifth and that of
ischaemic heart disease by a sixth.”
1993—The Fifth Report of the Joint National
Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure (JNC 5) cites the recently published 1991 meta-analysis to support
sodium reduction.34
1995—Michael Alderman and colleagues
publish a paper showing that “low urinary sodium is associated with greater
risk of myocardial infarction among treated hypertensive men.”35
1998—Niels Graudal publishes a
meta-analysis of strictly randomized trials testing a low-sodium diet. The
results found minimal reductions in blood pressure, whereas low-density
lipoprotein (LDL) cholesterol, total cholesterol, noradrenaline, renin, and
aldosterone were increased with a low-sodium diet. Their conclusion was, “These
results do not support a general recommendation to reduce sodium intake.”36
2001—The DASH-Sodium trial is published.
This is a thirty-day randomized study that shows that reducing sodium intake
may provide blood-pressure-lowering benefits.37 However,
it provided little benefit in those who had normal blood pressure and in those
without hypertension who were forty-five years old and younger.38
Additionally, there were increases in triglycerides, low-density lipoprotein
(LDL), and total-cholesterol-to-high-density-lipoprotein (TC:HDL) ratio in
those on the control diet when they restricted their salt intake.39
2002—Raben and colleagues show that a diet
high in sugar significantly increases blood pressure in humans.40
2008—Brown and colleagues show that sugar
raises blood pressure, heart rate, and cardiac output in humans, and that sugar
increases blood pressure variability and myocardial oxygen demand.41 These
authors also show that sugar’s antihypertensive effect occurs after its
ingestion.
2010—Perez-Pozo and colleagues show that a
high-sugar diet significantly increases twenty-four-hour ambulatory blood
pressure in just a few weeks.42
2011—Stolarz-Skrzypek
and colleagues publish a prospective population study concluding, “Lower sodium
excretion was associated with higher cardiovascular disease mortality.”43
2014—Malik and colleagues publish a
systematic review of twelve studies (cross-sectional and prospective cohort)
encompassing over 400,000 participants, showing that sugar-sweetened beverage
intake is significantly associated with higher blood pressure and an increased
incidence of hypertension.44
2014—Te Morenga and colleagues publish a
meta-analysis of randomized controlled trials showing that a high-sugar diet
significantly increases blood pressure versus a lower-sugar diet (the effect is
around twice that found with altering sodium intake).45
2014—Adler and colleagues publish the most
up-to-date Cochrane meta-analysis of randomized controlled trials indicating
minimal reductions in blood pressure with a low-sodium diet and no significant
reductions in all-cause mortality or mortality due to cardiovascular disease.46
2014—Graudal and colleagues publish a
meta-analysis of twenty-three cohort studies and two follow-up studies of
randomized controlled trials in 274,683 patients concluding that “compared with
usual sodium intake, low- and excessive-sodium diets are associated with
increased mortality.”47
2015—Dietary Guidelines for Americans
removed the severe limit on sodium intake (i.e., 1,500 milligrams per day), but
the 2,300-milligram sodium limit remains.48
2016—Low sodium intakes are associated with
an increased risk of cardiovascular events and death in those with or without
hypertension, whereas high sodium intakes are associated with these harms only
in hypertensive patients from a pooled analysis of four studies.49
2016—Patients without hypertension have no
significant reduction in blood pressure with sodium restriction based on a
meta-analysis of clinical studies.50
TIME LINE COVERING THE RECOMMENDATIONS FOR SODIUM INTAKE
1977—1st Edition of the
Dietary Goals: set an upper intake of sodium at 1.2 grams (3 grams of
salt).51
1977—2nd Edition of the
Dietary Goals: set an upper intake of sodium at 2 grams (5 grams of salt).52
1980—Dietary Guidelines
for Americans: “use less table salt,” avoid
“pickled foods, salted nuts,” “do not add salt to baby food,” we “eat much more
sodium than we need,” and “the major hazard of excessive sodium is for persons who have high blood pressure.”53
1985—Dietary Guidelines for
Americans: “avoid too much sodium.”54
1990—Dietary Guidelines for Americans: “use salt or
sodium only in moderation.”55
1995—Dietary Guidelines for Americans: Daily Value for
sodium is 2,400 milligrams per day (6 grams of salt).56
2000—Dietary Guidelines for Americans: “Healthy
children and adults need to consume only small amounts of salt to meet their sodium
needs—less than ¼ teaspoon of salt daily.”57
2005—Institute of
Medicine (IOM): introduces an adequate intake
(AI) of 1,500 milligrams and upper level (UL) of
intake of 2,300 milligrams for sodium.58
2005—Dietary Guidelines for
Americans: All Americans should
consume less than 2,300 milligrams of sodium (about 1 teaspoon of salt) per day59 (based on the IOM report). “Individuals with hypertension, blacks, and middle-aged and older
adults. Aim to consume no more than 1,500 mg of sodium per day.”
2010—Dietary Guidelines for
Americans: “Reduce daily sodium intake to less than 2,300 mg and further reduce
intake to 1,500 mg among persons who are 51 and older and those of any age who are African American or have
hypertension, diabetes, or chronic kidney disease.”60
2015—Dietary
Guidelines for Americans: remove the severe sodium restriction
recommendation (i.e., 1,500 mg of sodium per day) but keep the recommendation
that all Americans should restrict their sodium intake to less than 2,300 mg
per day.61
TIME LINE COVERING THE RECOMMENDATIONS FOR SUGAR INTAKE
1977—Dietary Goals 1st edition: 15 percent
added sugars62
1977—Dietary Goals 2nd edition: 10 percent
refined and processed sugars63
1980—Dietary
Guidelines for Americans: “Contrary to widespread opinion, too much sugar in your diet does not seem
to cause diabetes.” And “avoid excessive sugars.”64
1985—Dietary
Guidelines for Americans: “Avoid too much sugar” and “contrary
to widespread belief, too much sugar in your diet does not cause diabetes.”65
1990—Dietary
Guidelines for Americans: “Use sugar only in moderation” and “Diets high in sugar have not been shown to cause diabetes.”66
1995—Dietary
Guidelines for Americans: “Choose a diet moderate in
sugars.” It’s as if the guidelines want us to eat added sugar.67
2000—Dietary
Guidelines for Americans: “Choose beverages and foods
to moderate your intake of sugars.” This is the first time that the
Dietary Guidelines no longer state that “sugar doesn’t cause diabetes” or that
“there’s no proof sugar causes diabetes.”68
2002—Institute of
Medicine (IOM): allows for 25 percent of total calories to come from
added sugars.69
2005—Dietary
Guidelines for Americans: 267 calories of “discretionary” calories
(coming from added sugars and/or solid fat) are allowed; this would be only 67 grams of added sugars (267/4 calories per gram of sugar
= 67). However, it states that up to 72 grams of added sugars are allowed.70 (“If fat
is decreased to 22 percent of calories, then 18 teaspoons [72 g] of added
sugars is allowed.”)
2010—Dietary
Guidelines for Americans: technically up to 19
percent of total calories can be ingested from added sugars if someone
consumes 3,000 calories per day (the guidelines don’t specifically state this,
but if no solid fats are ingested, then 19 percent of calories from added
sugars may be consumed).71
2015—Dietary
Guidelines for Americans: finally recommends that added sugars should
make up no more than 10 percent of total calories.72
DRUGS
THAT CAN INCREASE NEED FOR SALT
Hypovolemic
hyponatremia can be caused by thiazide and loop diuretics, sodium-glucose
cotransporter 2 (SGLT2) inhibitors (like dapagliflozin) used to treat diabetes,
salt-wasting nephropathies such as renal tubular acidosis, polycystic kidney
disease and obstructive uropathy, medications like cyclosporine and cisplatin,1 or
conditions like sepsis.2 Other
medications that can cause hyponatremia include oxcarbazepine, trimethoprim,
antipsychotics, antidepressants, NSAIDs, cyclophosphamide, carbamazepine,
vincristine and vinblastine, thiothixene, thioridazine, other phenothiazines,
haloperidol, amitriptyline, other tricyclic antidepressants, monoamine oxidase
inhibitors, bromocriptine, clofibrate, general anesthesia, narcotics, opiates,
ecstasy, sulfonylureas, and amiodarone.3
SALT
CONTENT OF FAVORITE FOODS
|
Food |
Sodium Content |
|
Frozen dinners |
Up to 1,800 mg
per meal |
|
Canned soups and
vegetables |
Up to 1,300 mg
per serving |
|
Cottage cheese |
~1,000 mg per cup |
|
Spaghetti sauce |
Up to 1,000 mg
per cup |
|
Sandwiches |
Up to 900 mg per
sandwich |
|
Pickles |
Up to 785 mg per
pickle |
|
Instant beef
noodle soup |
757 mg per packet |
|
Roasted and
salted pumpkin seeds |
Up to 711 mg per
ounce |
|
Hot dog |
Up to 700 mg per
hot dog |
|
Tomato juice |
Up to 700 mg per
8 ounces |
|
Teriyaki sauce |
690 mg per
tablespoon |
|
Roquefort cheese |
507 mg per ounce |
|
480 mg per ounce |
|
|
Bagel |
~460 mg per bagel |
|
Veggie burger |
400–500 mg per
patty |
|
Soy sauce |
409 mg per
teaspoon |
|
American cheese |
400 mg per ounce |
|
Salad dressing |
Up to 300 mg per
2 tablespoons |
|
Capers |
255 mg per
tablespoon |
|
6-inch tortilla |
~200 mg |
|
Cereal |
180 to 300 mg per
serving |
|
Cured bacon |
175 mg per slice |
|
Ketchup |
150 mg per
tablespoon |
|
Spinach |
125 mg per cup |
|
Sweet relish |
122 mg per
tablespoon |
|
Beets |
65 mg per beet |
|
Celery |
50 mg per large
stalk of celery |
|
Carrot |
50 mg per large
carrot |
References: http://www.health.com/health/gallery/#cottage-cheese-1;
https://www.healthaliciousness.com/articles/what-foods-high-sodium.php;
http://www.everydayhealth.com/heart-health-pictures/10-sneaky-sodium-bombs.aspx#02;
http://www.webmd.com/diet/ss/slideshow-salt-shockers; and
http://www.foxnews.com/leisure/2013/02/25/8-high-sodium-foods-that-are-ok-to-eat/.
INTRODUCTION:
DON’T FEAR THE SHAKER
1. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6425a3.htm.
CHAPTER
1: BUT DOESN’T SALT CAUSE HIGH BLOOD PRESSURE?
1. Bayer, R., D. M. Johns, and S. Galea. 2012. Salt and public health:
contested science and the challenge of evidence-based decision making. Health Aff (Millwood) 31(12): 2738–2746.
2. Overlack, A., et al. 1993. Divergent hemodynamic and hormonal
responses to varying salt intake in normotensive subjects. Hypertension
22(3): 331–338.
3. Taubes, G. 2007. Good Calories, Bad Calories.
New York: Knopf.
1. Denton, D. A. 1965. Evolutionary aspects of the emergence of aldosterone
secretion and salt appetite. Physiol Rev 45: 245–295.
2. http://see-the-sea.org/facts/facts-body.htm.
3. https://web.stanford.edu/group/Urchin/mineral.html.
4. http://water.usgs.gov/edu/whyoceansalty.html.
5. Denton, D. A., M. J. McKinley, and R. S. Weisinger. 1996. Hypothalamic
integration of body fluid regulation. Proc Natl Acad Sci U S
A 93(14): 7397–7404.
6. Denton.
Evolutionary aspects of the emergence of aldosterone secretion and salt
appetite. 245–295.
7. Denton, McKinley, and Weisinger. Hypothalamic integration of body
fluid regulation. 7397–7404.
8. Denton, McKinley, and Weisinger. Evolutionary aspects of the emergence
of aldosterone secretion and salt appetite. 245–295.
9. http://www.independent.co.uk/news/science/did-humans-come-from-the-seas-instead-of-the-trees-much-derided-theory-of-evolution-about-aquatic-8608288.html; https://answersingenesis.org/natural-selection/adaptation/did-humans-evolve-from-a-fish-out-of-water/; http://evolution.berkeley.edu/evolibrary/article/evograms_04; https://en.m.wikipedia.org/wiki/Evolution_of_tetrapods.
10. Denton. Evolutionary aspects of the emergence of aldosterone secretion
and salt appetite. 245–295.
11. Ibid.
12. https://answersingenesis.org/natural-selection/adaptation/did-humans-evolve-from-a-fish-out-of-water/; https://en.m.wikipedia.org/wiki/Evolution_of_tetrapods; https://en.wikipedia.org/wiki/Tetrapod.
13. Denton. Evolutionary aspects of the emergence of aldosterone secretion
and salt appetite. 245–295.
14. Ibid.
15. Ibid.
16. Denton, McKinley, and Weisinger. Hypothalamic integration of body
fluid regulation. 7397–7404.
17. http://www.scientificamerican.com/article/how-can-sea-mammals-drink/.
18. Luft, F. C., et al. 1979. Plasma and urinary norepinephrine values at
extremes of sodium intake in normal man. Hypertension
1(3): 261–266.
19. Russon, A. E., et al. 2014.
Orangutan fish eating, primate aquatic fauna eating, and their implications for
the origins of ancestral hominin fish eating. J Hum Evol
77: 50–63.
20. Denton, McKinley, and Weisinger. Hypothalamic integration of body
fluid regulation. 7397–7404.
21. Russon. Orangutan fish eating, primate aquatic fauna eating, and their
implications for the origins of ancestral hominin fish eating. 50–63.
22. Ibid.
23. Ibid.
24. Ibid.
25. Ibid.
26. Stewart, K. M. 2014. Environmental change and hominin exploitation of
C4-based resources in wetland/savanna mosaics. J Hum Evol
77: 1–16.
27. Brenna, J. T., and S. E. Carlson. 2014. Docosahexaenoic acid and human
brain development: evidence that a dietary supply is needed for optimal
development. J Hum Evol 77: 99–106.
28. Ibid.
29. http://www.dailymail.co.uk/sciencetech/article-2536015/Ancient-ancestors-ate-diet-tiger-nuts-worms-grasshoppers.html.
30. Agbaje, R. B., V. O. Oyetayo, and A. O. Ojokoh. 2015. Effect of
fermentation methods on the mineral, amino and fatty acids composition of Cyperus esculentus. Afr J Biochem Res
9(7): 89–94.
31. Payne, C. L., et al. 2016. Are edible insects more or less ‘healthy’
than commonly consumed meats? A comparison using two nutrient profiling models
developed to combat over- and undernutrition. Eur J Clin
Nutr 70(3): 285–291.
32. Xiao, K., et al. 2010. Effects of dietary sodium on performance,
flight and compensation strategies in the cotton bollworm, Helicoverpa
armigera (Hübner) (Lepidoptera: Noctuidae). Front
Zool 7(11): 1–8.
33. Ibid.
34. Payne. Are edible insects more or less ‘healthy’ than commonly
consumed meats? A comparison using two nutrient profiling models developed to
combat over- and undernutrition. 285–291.
35. Meneely, G. R., and H. D. Battarbee. 1976. High sodium-low potassium
environment and hypertension. Am J Cardiol 38(6):
768–785; Neal, B. 2014. Dietary salt is a public health hazard that requires
vigorous attack. Can J Cardiol 30(5): 502–506.
36. Eaton, S. B., and M. Konner. 1985. Paleolithic nutrition. A
consideration of its nature and current implications. N Engl
J Med 312(5): 283–289.
37. Denton, D. 1997. Can hypertension be prevented? J
Hum Hypertens 11(9): 563–569.
38. Gleibermann, L. 1973. Blood pressure and dietary salt in human
populations. Ecol Food Nutr 2(2): 143–156.
39. O’Keefe, J. H., Jr., and L.
Cordain 2004. Cardiovascular disease resulting from a diet and lifestyle at
odds with our Paleolithic genome: how to become a 21st-century hunter-gatherer.
Mayo Clin Proc 79(1): 101–108.
40. Denton. Evolutionary aspects of the emergence of aldosterone secretion
and salt appetite. 245–295.
41. Denton, McKinley, and Weisinger. Hypothalamic integration of body
fluid regulation. 7397–7404.
42. Folkow, B. 2003. [Salt and blood pressure—centenarian bone of
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43. Ibid.
44. Milligan, L. P., and B. W. McBride. 1985. Energy costs of ion pumping
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45. Folkow. [Salt and blood pressure—centenarian bone of contention].
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46. Overlack, A., et al. 1993. Divergent hemodynamic and hormonal
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22(3): 331–338.
47. Ritz, E. 1996. The history of salt—aspects of interest to the
nephrologist. Nephrol Dial Transplant 11(6): 969–975.
48. Moinier, B. M., and T. B. Drueke. 2008. Aphrodite, sex and salt—from
butterfly to man. Nephrol Dial Transplant 23(7):
2154–2161.
49. Ibid.
50. Ibid.
51. Ibid.
52. Denton, McKinley, and Weisinger. Hypothalamic integration of body
fluid regulation. 7397–7404.
53. Ritz. The history of salt—aspects of interest to the nephrologist.
969–975.
54. https://en.wikipedia.org/wiki/Mud-puddling.
55. Moinier and Drueke. Aphrodite, sex and salt—from butterfly to man.
2154–2161.
56. Ibid.
57. Wassertheil-Smoller, S., et al. 1991. Effect of antihypertensives on
sexual function and quality of life: the TAIM Study. Ann
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58. Jaaskelainen, J., A. Tiitinen, and R. Voutilainen. 2001. Sexual
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CHAPTER
3: THE WAR AGAINST SALT—AND HOW WE DEMONIZED THE WRONG WHITE CRYSTAL
1. Meneely, G. R., and H. D. Battarbee. 1976. High sodium-low potassium
environment and hypertension. Am J Cardiol 38(6):
768–785; Dahl, L. K. 2005. Possible role of salt intake in the development of
essential hypertension. 1960. Int J Epidemiol 34(5):
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2. Ha, S. K. 2014. Dietary salt intake and
hypertension. Electrolyte Blood Press 12(1): 7–18.
3. Kurlansky, M. 2003. Salt: A World History.
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4. Ibid.
5. Ibid.
6. Ibid.
7. Mente, A., M. J. O’Donnell, and S. Yusuf. 2014. The population risks
of dietary salt excess are exaggerated. Can J Cardiol
30(5): 507–512.
8. Ritz, E. 1996. The history of salt—aspects of interest to the
nephrologist. Nephrol Dial Transplant 11(6): 969–975.
9. Johnson, R. J. 2012. The Fat Switch.
Mercola.com.
10. Johnson, R. J., et al. 2007. Potential role of sugar (fructose) in the
epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney
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11. http://www.heart.org/idc/groups/heart-public/@wcm/@sop/@smd/documents/downloadable/ucm_462020.pdf.
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13. DiNicolantonio, J. J., and S. C. Lucan. 2014. The wrong white
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14. Kurlansky. Salt:
A World History.
15. Johnson. The Fat
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16. Graudal, N. 2005. Commentary: possible role of salt intake in the
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17. Ibid; https://books.google.com/books?id=SFUcAQAAMAAJ&pg=PA652&dq=ambard+lowenstein+salt+1907&hl=en&sa=X&ved=0ahUKEwig-p-9vKvPAhWCcD4KHUjKD0QQ6AEIHDAA#v=onepage&q=lowenstein&f=false; https://books.google.com/books?id=pTTQAAAAMAAJ&pg=PA417&lpg=PA417&dq=lowenstein+salt+1907&source=bl&ots=6hE8bSq3YD&sig=WIq6enQs0TnJaDi1_ZN72y7N2Ew&hl=en&sa=X&ved=0ahUKEwi2xsTt4arPAhXJzIMKHWHOAb0Q6AEIIDAB#v=onepage&q=lowenstein%20salt%201907&f=false.
18. Chapman, C. B., and T. B. Gibbons. 1950. The diet and hypertension: a
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19. Ibid; Pines, K. L., and G. A. Perera. 1949. Sodium chloride
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20. Chasis, H., et al. 1950. Salt and protein
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21. Chapman and Gibbons. The diet and hypertension: a review. 29–69.
22. Klemmer, P., C. E. Grim, and F. C. Luft. 2014. Who and what drove
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23. https://en.wikipedia.org/wiki/Rice_diet.
24. Kempner, W. 1948. Treatment of hypertensive vascular disease with Rice
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25. Klemmer, Grim, and Luft. Who and what drove Walter Kempner? The Rice
Diet revisited. 684–688.
26. Kempner. Treatment of hypertensive vascular disease with Rice Diet.
545–577.
27. Ibid.
28. Batuman, V. 2011. Salt and hypertension: why is there still a debate? Kidney Int Suppl 3(4): 316–320.
29. Ratliff, N. B. 2000. Of rice, grain, and zeal: lessons from Drs.
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30. https://news.google.com/newspapers?nid=1955&dat=19971021&id=mEkwAAAAIBAJ&sjid=nKYFAAAAIBAJ&pg=3810,3940249&hl=en.
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32. Ibid.
33. McCallum, L., et al. 2013. Serum chloride is an independent predictor
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34. Kempner. Treatment of hypertensive vascular disease with Rice Diet.
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35. http://www.turner-white.com/memberfile.php?PubCode=hp_mar07_hypertensive.pdf.
36. Kempner. Treatment of hypertensive vascular disease with Rice Diet.
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37. Chasis. Salt and protein restriction: effects on blood pressure and
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38. Rice Diet in hypertension. Lancet. 1950.
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39. Chasis. Salt and protein restriction: effects on blood pressure and
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40. Laragh and Pecker. Dietary sodium and essential hypertension: some
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pressure. 458–463; Watkin, D. M., et al. 1950. Effects of diet in essential
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41. Laragh and Pecker. Dietary sodium and essential hypertension: some
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42. Ibid; Reisin, E., et al. 1978. Effect of weight loss without salt
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43. Corcoran, Taylor, and Page.
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44. Loofbourow, Galbraith, and Palmer. Effect of the Rice Diet on the
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47. Schroeder. Low sodium chloride diets in hypertension: effects on blood
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48. Joe, B. 2015. Dr Lewis Kitchener Dahl, the Dahl
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49. Dahl. Possible role of salt intake in the development of essential
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140. Ibid.
141. https://en.wikipedia.org/wiki/Refrigeration.
142. http://www.cdc.gov/nchs/data/databriefs/db88.pdf.
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9. Elliot and Brown. Sodium intakes around the world.
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14. http://ec.europa.eu/health/nutrition_physical_activity/docs/salt_report1_en.pdf; http://ec.europa.eu/eurostat/statistics-explained/index.php/Causes_of_death_statistics; Elliot and Brown. Sodium intakes around the world.
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17. Ibid.
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CHAPTER 5: WE ARE STARVING INSIDE
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7. Taubes. Good
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10. Prada. Low salt intake modulates insulin signaling, JNK activity and IRS-1ser307
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23. Heaney. Making sense of the science of sodium. 63–66; Wald and Leshem.
Salt conditions a flavor preference or aversion after exercise depending on
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24. Heaney. Making sense of the science of sodium. 63–66.
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27. Ibid.
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37. DiNicolantonio, J. J., J. H. O’Keefe, and S. C.
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43. DiNicolantonio and Lucan. Sugar season: it’s everywhere and addictive.
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58. Ibid.
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84. Liamis, Liberopoulos, Barkas, and Elisaf. Diabetes mellitus and
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88. Liamis, Liberopoulos, Barkas, and Elisaf. Diabetes mellitus and
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89. AlZahrani, Sinnert, and Gernsheimer. Acute kidney injury, sodium
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90. Liamis, Liberopoulos, Barkas, and Elisaf. Diabetes mellitus and
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91. AlZahrani, Sinnert, and Gernsheimer. Acute kidney injury, sodium
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98. Agarwal, M., et al. 1999. Hyponatremic-hypertensive syndrome with
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99. AlZahrani, Sinnert, and Gernsheimer. Acute kidney injury, sodium
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100. Walker, W. G., et al. 1965. Metabolic observations
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102. Ibid.
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104. Faull, Holmes, and Baylis. Water
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107. Schroeder, H. A., et al. 1949. Low sodium chloride diets in
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108. Grollman, A. R., et al. 1945. Sodium restriction in the diet for
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109. Pines and Perera. Sodium chloride restriction in hypertensive vascular
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110. Pines and Perera. Sodium chloride restriction in hypertensive vascular
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111. Ibid.
112. Kovesdy. Significance of hypo- and hypernatremia in chronic kidney
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115. Kovesdy. Significance of hypo- and hypernatremia in chronic kidney
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116. Ibid.
117. Ibid.
118. Wannamethee. Mild hyponatremia, hypernatremia and incident
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119. Kovesdy. Hyponatremia, hypernatremia, and mortality in patients with
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123. Nakayama. Dietary fructose causes tubulointerstitial injury in the
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136. Ibid.
137. Simpson, F. O., et al. 1984. Iodide excretion in a salt-restriction
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138. Ibid.
139. Jantsch, J., et al. 2015. Cutaneous Na+ storage strengthens the
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145. Ibid.
146. McCarty, M. F., and J. J. DiNicolantonio. 2014. Bioavailable dietary
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147. Good, P. 2011. Do salt cravings in children with autistic disorders
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148. Ibid; http://rehydrate.org/resources/jianas.htm.
149. AlZahrani, Sinnert, and Gernsheimer. Acute kidney injury, sodium
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150. Ibid; Luft. Clinical salt deficits. 559–563.
151. Urso, C., and G. Caimi. 2012. [Hyponatremic syndrome]. Clin Ter 163(1): e29–e39. [Article in Italian.]
152. Agarwal. Hyponatremic-hypertensive syndrome with renal ischemia: an
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Nicotine-stimulated release of neurophysin and vasopressin in humans. J Clin Endocrinol Metab 41(06): 1113–1117.
CHAPTER
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9. http://en.wikipedia.org/wiki/RealSalt; http://www.realsalt.com/wp-content/uploads/2013/03/realsalt_analysis.pdf; http://www.realsalt.com; http://www.realsalt.com/sea-salt/comparing-real-salt-to-himalayan-celtic/.
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15. Ibid.
16. http://www.realsalt.com/sea-salt/know-your-salts/; http://drsircus.com/medicine/salt/real-salt-celtic-salt-and-himalayan-salt
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19. http://www.sfsalt.com/black-hawaiian-sea-salt.
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27. http://articles.mercola.com/sites/articles/archive/2010/08/25/why-has-this-lifesustaining-essential-nutrient-been-vilified-by-doctors.aspx; http://articles.mercola.com/sites/articles/archive/2011/09/20/salt-myth.aspx.
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3. Ibid.
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5. Ibid.
6. Ibid.
7. Ibid.
8. Ibid.
9. Grollman, A. R., et al. 1945. Sodium restriction in the diet for
hypertension. JAMA 129(8): 533–537.
10. Dahl, L. K., and R. A. Love. 1954. Evidence for relationship between
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To my colleagues Jose Carlos Souto, Sean Lucan, Dmitri Vasin, and David Unwin, who contributed by humanizing my research through personal
anecdotes. Thank you.
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