1

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 advice stemmed largely from the most basic of scientific explanations: the “salt–blood pressure hypothesis.” This hypothesis held that eating higher levels of salt leads to higher levels of blood pressure--end of story. But that wasn’t the full story, of course. As with so many old medical theories, the real story was a bit more complex.

The hypothesis went like this: In the body, we measure blood pressure in two different ways. The top number of a typical blood pressure reading is your systolic blood pressure, the pressure in your arteries during contraction of your heart. The bottom number is your diastolic blood pressure, the pressure in your arteries when your heart is relaxed. When we eat salt, so the theory goes, we also get thirsty--so we drink more water. In the salt–high blood pressure hypothesis, that excess salt then causes the body to hold on to that increased water, in order to dilute the saltiness of the blood. Then, the resulting increased blood volume would automatically lead to higher blood pressure.

That’s the theory, anyway. Makes sense, right?

All of this did make sense, in theory, and for a while there was some circumstantial evidence supporting this claim. Data was gathered on salt intake and blood pressures in various populations, and correlations were seen in some cases. But even if those correlations were consistent, as we all know, correlation does not equal causation--just because one thing (salt) may sometimes lead to another thing (higher blood pressure), which happens to correlate with another thing (cardiovascular events), that does not necessarily prove that the first thing caused the third thing.

Sure enough, data that conflicted with the salt–blood pressure theory continued to be published right along with data that supported it. A heated debate raged in the scientific community about whether salt induced chronically elevated blood pressure (hypertension) versus a fleeting, inconsequential rise in blood pressure, with advocates and skeptics on both sides. In fact, compared to any other nutrient, even cholesterol or saturated fat, salt has caused the most controversy. And once we got on that salt–high blood pressure train, it was hard to get off. Governments and health agencies had taken a stance on salt, and to admit that they were wrong would cause them to lose face. They continued the same low-salt mantra, refusing to overturn their premature verdict on salt until they were presented with overwhelming evidence to the contrary. No one was willing to get off the train until there was definitive evidence that their presumptions were wrong--instead of asking, “Did we ever have any evidence to recommend sodium restriction in the first place?”

We believed so strongly in sodium restriction because we believed so strongly in blood pressure as a metric of health. Low-salt advocates posit that even a one-point reduction in blood pressure (if translated to millions of people) would actually equal a reduction in strokes and heart attacks. But evidence in the medical literature suggests that approximately 80 percent of people with normal blood pressure (less than 120/80 mmHg) are not sensitive to the blood-pressure-raising effects of salt at all. Among those with prehypertension (a precursor to high blood pressure), roughly 75 percent are not sensitive to salt. And even among those with full-blown hypertension, about 55 percent are totally immune to salt’s effects on blood pressure.2

That’s right: even among those with the highest blood pressure, about half are not at all affected by salt.

The stringent low-salt guidelines were based on a guess: we essentially gambled that the small benefits to blood pressure that we see in some patients would extend to large benefits for the whole population. And while taking that gamble, we glossed over the most important point: why salt may increase blood pressure in some people but not in others. Had we focused on that, we would’ve realized that fixing the underlying issue--which has nothing to do with eating too much salt--completely fixes one’s “salt sensitivity.” We also presumed that blood pressure, a fleeting measurement known to fluctuate depending on many health factors, was always impacted by salt. And because of that baseless certainty, we presumed that overconsumption of salt would logically result in dire health outcomes, such as strokes and heart attacks.

Our mistake came from taking such a small sample of people--unethically small!--and wildly extrapolating their benefits from low-salt eating without ever mentioning the risks. Instead, we focused on those extremely minuscule reductions in blood pressure, completely disregarding the numerous other health risks caused by low salt intake--including several side effects that actually magnify our risk of heart disease--such as increased heart rate; compromised kidney function and adrenal insufficiency; hypothyroidism; higher triglyceride, cholesterol, and insulin levels; and, ultimately, insulin resistance, obesity, and type 2 diabetes.

Perhaps most illustrative of this willful disregard for risk is the case of heart rate. Heart rate is proven to increase on a low-salt diet. This harmful effect occurs in nearly everyone who restricts his or her salt intake. Although this effect is documented more thoroughly in the medical literature, no food ad or dietary guideline says, “A low-salt diet can increase your risk of elevated heart rate.” And what has a bigger impact on your health: a one-point reduction in blood pressure or a four-beat-per-minute increase in heart rate? (In chapter 4, I’ll take a closer look at what these metrics mean and I’ll let you decide.)

If our bodies allowed us to isolate each of these risks, we might be able to say for certain that one or another is most important. But when you combine all of the known dangers of salt restriction, it’s easy to see that the harms far outweigh any possible benefits. In other words, we’ve focused on just one metric that might change with a low-salt diet--blood pressure--but completely disregarded all the other harmful effects in the process.

Now that we can recognize our folly, we’ve come to a moment in our nation’s public health when we need to ask ourselves: Have we subjected generations of people--especially those whose health was already compromised--to a “treatment” that may have escalated their health decline?

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

See where this is headed?

You start craving sugar and refined carbs like crazy, because your body believes carbohydrate is your only viable energy source. And, as the now-familiar story goes, the more refined carbs you eat, the more refined carbs you tend to crave. This overeating of processed carbs and high-sugar foods virtually ensures fat cell accumulation, weight gain, insulin resistance, and eventually type 2 diabetes.

What’s clear is that we have been focusing on the wrong white crystal all along. We demonized sodium before we had the evidence. And our health has been paying the price ever since. Had we left salt on the table, our health problems in general--and especially those pertaining to sugar--might be a little less dramatic.

It’s time to set the record straight. It’s time to drop the guilt, grab the shaker, and enjoy salt again!

Time for the Truth

I’ve always been very athletic, running cross-country and wrestling in high school, so I know a great deal about how nutrition (or lack thereof) impacts performance. All those afternoons of running, and then spending my days as a wrestler in the sauna to lose weight, made me appreciate how important salt is for athletes.

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.

Sure enough, her sodium levels were extremely low. Her doctor cut the dose of her diuretic in half and told her to eat more salt. After that, it wasn’t long before all of her symptoms went away. The following week, she came into the pharmacy to tell me that I was right and that I helped to dramatically improve the quality of her life--just about the best thing any person in a medical field can hear. I was extremely relieved and encouraged that the solution to her symptoms was so simple, so inexpensive, and so immediately effective.

That experience prompted me to take a deeper look into the low-salt guidelines. The deeper I looked, the more I could see that maybe the advice we had been giving people, to cut their salt intake, wasn’t correct after all. Around the same time, in 2013, I took a position as a cardiovascular research scientist at Saint Luke’s Mid America Heart Institute. After joining Saint Luke’s, I published nearly two hundred medical papers in the scientific literature, many relating to the impact of salt and sugar on health. Based on these academic publications, that same year I was offered a position as the associate editor of BMJ Open Heart, an official journal of the British Cardiovascular Society.

In total, I’ve spent nearly a decade examining the research on salt and working with clinicians to untangle the complexity of our salt intake and get to the heart of the issue. Should we do away with these outdated restrictions? Who really needs less salt--and who needs more? How much--and what kinds--are optimal? And perhaps most exciting, how might increasing our salt intake actually help us turn back the tide of obesity and stem the rising epidemic of type 2 diabetes that threatens to overwhelm our nation, and the entire world?

We can start by telling the truth:

Low salt is miserable.

Low salt is dangerous.

Our bodies evolved to need salt.

Low-salt guidelines are based on inherited “wisdom,” not scientific fact.

All the while, the real culprit has been sugar.

And finally: salt may be one solution to--rather than a cause of--our nation’s chronic disease crises.

Your body drives you to eat several grams of salt (around 8–10 grams, equal to 3,000–4,000 milligrams of sodium) every day to remain in homeostasis, an optimal state in which you put the least amount of stress on the body. But you could literally live the rest of your life--and probably a much longer one--if you never ingested another gram of added sugar.

Now, I understand that it will take a bit of time to unlearn years of indoctrination about the evils of salt--which is why I wrote this book. In these chapters, you’ll learn the entire story. (By the end, in chapters 7 and 8, you will find specific recommendations for how you can find and implement your ideal salt intake.) But that understanding begins with reeducation about the myriad ways our lives can be healthier, stronger, and longer when we welcome salt back into our lives.

If salt has always played such a fundamental role in human health, how did we ever begin to doubt it? Perhaps salt’s ubiquity was one of the factors in its downfall; perhaps we simply took it for granted. In order to understand how we could have gone so far off course, we first have to understand the critical role salt has always played in human health, from the moment life slithered out of the sea right up until the birth of modern medicine. By looking closely at salt’s crucial role in our past, we can start to restore its tarnished reputation and honor salt’s place in our future.

2 

We Are Salty Folk

We are essentially salty people.

We cry salt, we sweat salt, and the cells in our bodies are bathed in salty fluids. Without salt we would not be able to live.

Just a small dash of salt can take a bland dish and heighten all of its flavors, making it taste extraordinary. Salt knocks out bitterness and makes food taste sweeter, reducing the need for sugar. And just as much as we relish the satisfaction and savory heartiness that salt adds to our food, salt plays a fundamental role in dozens of critical functions in our bodies.

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.