Salt’s Convoluted History and the Real Salt Science

Salt July Article

We all know the handful of basic tenants to follow in order to live a “healthy” lifestyle; exercise daily, sleep for at least eight hours a night, eat an abundance of vegetables, meditate, drink plenty of water—and avoid or reduce salt intake. While the bulk of these recommendations are undeniably beneficial for just about everyone, it’s time to question the blind adoption of the rule that dramatically cutting salt intake fosters health. Demonizing salt for decades has caused us to ignore the white crystal that’s truly to blame for poor health (it’s sugar), and at a great cost to our wellbeing. Not only is it time to overcome our salt-phobia, but to go beyond that and make the argument that consuming more, not less, salt is better for most of us. If that last sentence rattled any cages, read on for a scientifically founded objection that aims to shift current paradigms and add both health and flavor to our lives.

Salt: Public Enemy No. 1

Salt consumption is said to raise blood pressure, cause hypertension, and increase the risk of premature death. This is why the Department of Agriculture’s dietary guidelines still deem salt the most villainous culprit of America’s declining health, coming before fat, sugar, and alcohol. It’s why the director of the Centers for Disease Control and Prevention (CDC) has suggested that reducing salt consumption is as critical to long-term health as quitting cigarettes.

The current low-salt guidelines limit us to 2,300 milligrams of sodium (basically 1 teaspoon of salt) per day. It’s even lower 1,500 milligrams (2/3 teaspoon of salt)—if you are older, African American, or have high blood pressure. According to the 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

However, authors from a 2011 report published in the British Medical Journal declared, “It is surprising that many countries have uncritically adopted sodium reduction, which probably is the largest delusion in the history of preventive medicine.”2

Why Has Salt Been Wrongly Accused?

Since the late 1960s, a battle has raged among scientists over the extent to which elevated salt consumption has adverse health implications for the population and contributes to deaths from stroke and cardiovascular disease. Salt’s recent history is far too convoluted for this piece, but it reveals that the suppression of scientific uncertainty on salt’s role in health has served neither public policy nor the objectives of science. For a thorough review of the long-running dispute over salt, see The Salt Fix by Dr. James DiNicolantonio, or either of Gary Taubes’ award-winning synopses in The New York Times or the prestigious journal Science. Taubes’ controversial Science article (which won the National Association of Science Writers’ Science in Society Journalism Award) challenges the idea that there was incontrovertible evidence linking salt to morbidity and mortality. Taubes observed that “the controversy over the benefits, if any, of salt reduction now constitutes one of the longest running, most vitriolic and surreal disputes in all of medicine.”345

The original evidence that backed the current salt recommendations simply failed to demonstrate that salt was harmful. On the other hand, the evidence from the last few years actually suggests that eating as little salt as the USDA and the CDC recommend can be harmful and increase our likelihood of dying prematurely.6

Salt makes for an easy target because of the simplicity and “biological plausibility” of the Salt-Blood Pressure Hypothesis. The idea of salt’s deadliness sounds reasonable because it is theoretically convenient. The theory is that as one eats more salt, the body retains water to maintain a stable concentration of sodium in your circulation. This explains why eating salty foods tends to make us thirsty, which makes us drink more, and thus retain more water. This results in a temporary increase in blood pressure which persists until our kidneys eliminate both the salt and the water. It all makes sense, but it’s really only a hypothesis.

This leads to the necessary reminder of the mantra “correlation does not equal causation”—just because one thing (salt) may sometimes lead to another thing (high blood pressure), which happens to correlate with another thing (cardiovascular events), that does not necessarily prove that the first thing caused the third thing. And sure enough, the benefits of a low-salt diet have never been proven and instead hold more potential to magnify the risks of heart disease.

Recent research suggests that low salt intake leads to things like increased heart rate; compromised kidney and adrenal insufficiency; hypothyroidism; higher triglyceride, cholesterol, and insulin levels; and, ultimately, insulin resistance, obesity, and type-2 diabetes.7 This forces us to question whether the single (and miniscule) potential benefit of a reduction in blood pressure is worth disregarding the mountain of health risks caused by low salt intake. The latest research even shows that chronic salt depletion is likely a factor in what endocrinologists term “internal starvation.” When you start restricting salt intake, the body starts to panic. As a defense mechanism, the body increases insulin levels because insulin helps the kidneys retain more sodium. Unfortunately, high insulin levels also “lock” energy into your fat cells, leading to a more trouble with breaking down stored fat into fatty acids or stored protein into amino acids. When insulin levels are elevated, the only macronutrient that you can efficiently utilize for energy is carbohydrate.8

 

What’s Really To Blame? (Spoiler Alert—It’s Sugar)

We’ve all been told time and time again that salt raises blood pressure, which in turn increases risk of strokes and heart attacks. Looking at population data, however, it’s evident that high-salt diets don’t seem to cause strokes and heart attacks. If anything, the research shows that high-salt intakes lower the risk of cardiovascular disease and premature death.

For example, the average Korean eats over 4,000 milligrams of sodium per day. Yet Koreans somehow manage to have one of the world’s lowest rates of hypertension, coronary heart disease, and death due to cardiovascular disease.While deemed the “Korean Paradox,” you could swap out “Korean” for any one of thirteen other countries and see evidence of this “paradox.” The Mediterranean Diet has been deemed heart healthy but is very high in salt (consider sardines and anchovies, olives and capers, aged cheeses, soups, shellfish, and goat’s milk). The French eat just as much salt as Americans and have a low rate of death due to coronary heart disease.10 11 Norwegians eat more salt than Americans yet have a lower rate of death due to coronary heart disease. Even Switzerland and Canada have low rates of death due to stroke, despite  high-salt diets.12

Hiding in plain sight during the entirety of this controversy sat insulin resistance and diabetes, both consistently found to coincide with renal sodium retention and the development of hypertension. In other words, what causes diabetes can also cause hypertension, and that dietary substance that causes diabetes is… sugar.

High sugar consumption leads to high insulin production by the pancreas. High insulin levels have been shown to stimulate the reabsorption of sodium by the kidneys13 14 (in other words, rather than excreting salt in urine, those with diabetes would hold on to salt in their bodies). Additionally, insulin interferes with the Na/K/ATPase activity—the pump that regulates the amount of sodium in our cells.15 Thus, this sodium pump can also become insulin resistant. This research is compounded by animal studies that found that giving rats metformin (a common diabetes drug that decreases insulin resistance) prevented salt-induced hypertension.16

Data also shows that sugar increases both blood pressure and heart rate. Way back in 1964, researchers were able to show over and over again that 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.17 18 But somehow, the blame continued to sit on salt’s shoulders.

We Need Salt

Salt is necessary for health because it plays a key role in maintaining the optimal amount of blood in our bodies; it’s even required by the heart to pump blood throughout the body. Salt is essential for digestion, cell-to-cell communication, bone formation and bone strength, and to prevent dehydration. Sodium is critical for reproduction, the proper functioning of cells and muscles, and the optimal transmission of nerve impulses to and from organs such as the heart and the brain. Our bodies rely on elements called electrolytes—sodium, potassium, magnesium, and calcium—in bodily fluids to help carry out electrical impulses that control many of our bodies’ functions. Without an adequate sodium intake, our blood volume decreases, which could lead to the shutting down of certain organs like the brain and kidneys.

Salt is necessary for life. Without it, we could not survive. Our brain and body automatically regulate how much sodium we eat, reabsorb, and excrete. The ability of our body to conserve salt and water is thought to be controlled by our hypothalamus as part of the system that drives us to crave salt and feel thirsty. The water and sodium levels in our body are constantly balancing each other out, a process called osmoregulation. Whenever there is an increase in sodium concentration in circulation, the kidneys simply reabsorb less sodium, the excess is excreted in our urine, and the body maintains a normal serum sodium level. This mechanism helps to prevent cellular damage from fluid shifting in and out of cells. If blood sodium levels drop too low, water from the blood will go into our tissue cells in order to raise the level of sodium in circulation back to normal, but this fluid shift can lead to cellular swelling. If the sodium level in the blood goes up, water is 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 salt balance are so tightly regulated.19

The Salty Solution

Believe it or not, the easiest way to guide salt consumption is to listen to your salt cravings. Consume as much salt as you crave to fulfill your body’s needs and please your taste buds without going overboard. Your internal salt thermostat controls your taste buds in order to raise or lower overall salt intake. If you crave everything salty and notice a heavy hand with the saltshaker, your body is likely telling you that it needs extra salt for optimal health—this is in contrast to sugar, which can hijack your body and brain and cause your intake of sugar to steadily increase to dangerous levels, all driven by cravings and dependence. For most people, the body constantly tells us 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 3,000-5,000 milligrams of sodium consumed. As sodium accounts for 40 percent of salt, that would equate to 7.5-15 grams of salt per day.

Salt makes food delicious and satisfying. Hopefully the recommendation to consume salt liberally inspire a “happy dance,” but it’s also important to note that salt consumption should accompany a diet comprised of real, unprocessed foods rather than processed foods that also just happen to be high in salt. Think of our favorites like olives, sardines, anchovies, cured meats, aged cheeses, and soups. Liberate the salted nuts, pickles, sauerkraut, seafood, beets, seaweed, and artichokes. And adding salt to healthy but generally less palatable foods (such as Brussels sprouts, cabbage, and turnips) allows us to eat more of what we know is good for us.

 

Fuel Your Exercise with Salt

The more you exercise, the more salt your body will need because you lose salt through sweating. Eating more salt will help your body to appropriately retain more water, leaving you more hydrated to have more energy to exercise in the first place. Just one teaspoon of salt improves stamina due to an increase in circulation. Even if you’re not an avid exerciser yet, eating enough salt is a great way to increase your energy levels and help you want to exercise, one of the best things you can do for improving internal starvation (the increase in insulin when your sodium levels are too low). Incorporating salt or electrolyte tabs, or even adding a teaspoon of salt to your water bottle with some lemon juice, can also leave you feeling invigorated.

 


References

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10 Survey on Members States’ Implementation of the EU Salt Reduction Framework. https://ec.europa.eu/health//sites/health/files/nutrition_physical_activity/docs/salt_report1_en.pdf
 
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12 Elliot P and Brown I. Sodium Intakes Around the World. WHO Library Catalog. 2006. https://www.who.int/dietphysicalactivity/Elliot-brown-2007.pdf
 
13 Bagrov YY, et al. Endogenous sodium pump inhibitors, diabetes mellitus and preeclampsia. Pathophysiology. 2007; 14(3-4): 147-151.
 
14 DiNicolantonio JJ, O’Keef JH, and Lucan SC. Added fructose: a principal driver of type 2 diabetes mellitus and its consequences. Mayo Clin Proc. 2015; 90(3):372-381.
 
15 Pazarloglou M, et al. Evaluation of insulin resistance and sodium sensitivity in normotensive offspring of hypertensive individuals. Am J Kidney Dis. 2007; 49(4): 540-546.
 
16 Muntzel MS, Hamidou SI, and Barrett S. Metformin attenuates salt-induced hypertension in spontaneously hypertensive rats. Hypertension. 1999; 33(5): 1135-1140.
 
17 Yudkin J. Dietary fat and dietary sugar in relation to Ischaemic Heart Disease and Diabetes. Lancet. 1964; 2:4-5.
 
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