studies that compare hypertension’s frequency in groups of people living under different conditions. It turns out that, besides salt intake, other significant risk factors include obesity, exercise, high intake of alcohol or saturated fats, and low calcium intake. The proof of this approach is that hypertensive patients who modify their lifestyles so as to minimize these putative risk factors often succeed in reducing their blood pressure. We’ve all heard the familiar mantra of our doctor: reduce salt intake and stress, reduce intake of cholesterol and saturated fats and alcohol, lose weight, cut out smoking, and exercise regularly.
So, how does the link between salt and blood pressure work? That is, by what physiological mechanisms does increased salt intake lead to a rise in blood pressure, in many but not all people? Much of the explanation involves an expansion of the body’s extracellular fluid volume. For normal people, if we increase our salt intake, the extra salt is excreted by our kidneys into our urine. But in individuals whose kidney salt excretion mechanisms are impaired, excretion can’t keep pace with increased salt intake. The resulting excess of retained salt in those people triggers a sensation of thirst and makes them drink water, which leads to an increase in blood volume. In response, the heart pumps more, and blood pressure rises, causing the kidney to filter and excrete more salt and water under that increased pressure. The result is a new steady state, in which salt and water excretion again equals intake, but more salt and water are stored in the body and blood pressure is raised.
But why does a rise in blood pressure with increased salt intake show itself in some people but not in most people? After all, most people manage to retain a “normal” blood pressure despite consuming over 6 grams of salt per day. (At least Western physicians consider their blood pressure normal, although a Yanomamo physician wouldn’t.) Hence high salt intake by itself doesn’t automatically lead to hypertension in everybody; it happens in only some individuals. What’s different about them?
Physicians apply a name to such individuals in whom blood pressure responds to a change in salt intake: they’re termed “salt-sensitive.” Relatively twice as many hypertensive individuals as normotensive individuals (people with normal blood pressure) turn out to be salt-sensitive. Nevertheless, most deaths due to elevated blood pressure are not among hypertensives, defined as people having greatly elevated blood pressure (140 over 90), but among normotensive individuals with only moderately elevated blood pressure—because normotensive people far outnumber hypertensives, and the greater individual risk of death in hypertensives isn’t by a sufficiently large factor to offset the larger factor by which normotensives outnumber hypertensives. As for the specific physiological difference between hypertensive and normotensive people, there is much evidence that the primary problem of hypertensive people lies somewhere in their kidneys. If one transplants a kidney from a normotensive rat to a hypertensive rat as an experiment, or from a normotensive human kidney donor to a seriously ill hypertensive human in order to help the hypertensive person, the recipient’s blood pressure falls. Conversely, if one transplants a kidney from a hypertensive rat to a normotensive rat, the latter’s blood pressure rises.
Other evidence pointing to a hypertensive person’s kidneys as the site of origin of the hypertension is that most of the many human genes known to affect blood pressure turn out to code for proteins involved in kidney sodium processing. (Remember that salt is sodium chloride.) Our kidneys actually excrete sodium in two stages: first, a filter called the glomerulus at the beginning of each kidney tubule filters blood plasma (containing salt) into the tubule; and second, most of that filtered sodium is then re-absorbed back into the blood by the rest of the tubule beyond the glomerulus; the filtered sodium that isn’t re-absorbed ends up excreted into the urine. Changes in either of those two steps can lead to high blood pressure: older people tend towards high blood pressure because they have lower glomerular filtration, and hypertensives tend to it because they have more tubular re-absorption of sodium. The result in either case—less sodium filtration, or more sodium re-absorption—is more sodium and water retention and higher blood pressure.
Physicians commonly refer to the postulated high tubular sodium re-absorption of hypertensive people as a “defect”: for example, physicians say, “Kidneys of hypertensives have a genetic defect in excreting sodium.” As an evolutionary biologist, though, I hear warning bells going off inside me whenever a seemingly harmful trait that occurs frequently in a long-established and large human population is dismissed as a “defect.” Given enough generations, genes that greatly impede survival are very unlikely to spread, unless their net effect is somehow to increase survival and reproductive success. Human medicine has furnished the best example of seemingly defective genes being propelled to high frequency by counter-balancing benefits. For example, sickle-cell hemoglobin is a mutant gene that tends to cause anemia, which is undoubtedly harmful. But the gene also offers some protection against malaria, and so the gene’s net effect in malarious areas of Africa and the Mediterranean is beneficial. Thus, to understand why untreated hypertensives are prone to die today as a result of their kidneys’ retaining salt, we need to ask under what conditions people might have benefited from kidneys good at retaining salt.
The answer is simple. Under the conditions of low salt availability experienced by most humans throughout most of human history until the recent rise of salt-shakers, those of us with efficient salt-retaining kidneys were better able to survive our inevitable episodes of salt loss from sweating or from an attack of diarrhea. Those kidneys became a detriment only when salt became routinely available, leading to excessive salt retention and hypertension with its fatal consequences. That’s why blood pressure and the prevalence of hypertension have shot up recently in so many populations around the world, now that they have made the transition from traditional lifestyles with limited salt availability to being patrons of supermarkets. Note the evolutionary irony: those of us whose ancestors best coped with salt-deficiency problems on Africa’s savannahs tens of thousands of years ago are now the ones at highest risk of dying from salt-excess problems today on the streets of Los Angeles.
Dietary sources of salt
If by now you’re convinced that it would be healthy for you to decrease your salt intake, how can you go about it? I used to think that I had already done it, and that my own salt habits were virtuous, because I never, ever, sprinkle salt on my food. While I’ve never measured my salt intake or output, I naively assumed it to be low. Alas, I now realize that, if I did measure it, I would find it to be far above Yanomamo levels, and not so far below the levels of Americans who use salt-shakers.
The reason for this sad realization has to do with the sources from which we actually ingest our dietary salt. In North America and Europe only about 12% of our salt intake is added in the home and with our knowledge, either by whoever is cooking or by the individual consumer at the table. It’s only that 12% that I virtuously eliminated. The next 12% is salt naturally present in the food when it’s fresh. Unfortunately, the remaining 75% of our salt intake is “hidden”: it comes already added by others to food that we buy, either processed food or else restaurant food to which the manufacturer or the restaurant cook respectively added the salt. As a result, Americans and Europeans (including me) have no idea how high is their daily salt intake unless they subject themselves to 24-hour urine collections. Abstaining from the use of salt-shakers doesn’t suffice to lower drastically your salt intake: you also have to be informed about selecting the foods that you buy, and the restaurants in which you eat.
Processed foods contain quantities of salt impressively greater than the quantities in the corresponding unprocessed foods. For instance, compared to fresh unsalted steamed salmon, tinned salmon contains 5 times more salt per pound, and store-bought smoked salmon contains 12 times more. That quintessential fast-food meal of one take-away cheeseburger and fried potatoes contains about 3 grams of salt (one-third of a day’s total average salt intake for an American), 13 times the salt content of an otherwise similar home-made unsalted steak and fried potatoes. Some other processed foods with especially high salt content are canned corned beef, processed cheese, and roast peanuts. Surprisingly to me, the biggest source of dietary salt in the U.S. and UK is cereal products— bread, other baked goods, and breakfast cereals—which we usually don’t think of as being salty.
Why do manufacturers of processed foods add so much salt? One reason is that it’s a nearly costless way to make cheap unpalatable foods edible. Another reason is that increasing the salt content of meat increases the weight of water bound in meat, so the final product weight can cheaply be increased 20% by bound water. In effect, the manufacturer provides less meat itself and still gets the same price for a “pound” of meat, which actually now consists of only 83% original meat plus 17% bound water. Yet another reason is that salt is a major determinant of thirst: the more salt you consume, the more fluid you drink, but much of what Americans or Europeans drink is soft drinks and bottled waters, some of them sold by the same companies selling you the salty snacks and processed foods that made you thirsty. Finally, the public has become addicted to salt and now prefers salted to unsalted foods.
