The World Until Yesterday: What Can We Learn From Traditional Societies?

by Jared Diamond

  Many environmental or lifestyle factors contributing to the risk of hypertension have been identified by 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 a
nd 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.

  A different picture for the breakdown of the sources of consumed salt emerges in East and South Asia and most of the developing world, where most ingested salt doesn’t come from processed or restaurant foods but from salt added in the consumer’s own house. For instance, in China 72% of ingested salt is added during cooking or at the table, and another 8% is in salty soy sauce. In Japan the main sources of ingested salt are soy sauce (20%), salty miso soup (10%), salted vegetables and fruits (10%), fresh and salted fish (10%), and salt added in restaurants, in fast-food outlets, and at home (10%). That’s why salt intake in many Asian countries exceeds 12 grams per day. In developing countries, salt in sauces, seasonings, and pickled foods contributes along with salt added during cooking.

  The high national health costs that hypertension, stroke, and other salt-related diseases inflict in the form of medical and hospital expenses and lost work lives have now motivated some governments to mount long-lasting national campaigns to help their citizens decrease their salt intake. But the governments quickly realized that they couldn’t achieve that goal without enlisting the cooperation of the food industry to reduce the amounts of salt added by the industry to processed foods. The reductions have been gradual ones of just 10% or 20% less salt added to foods every year or two—a reduction too small for the public to notice. The UK, Japan, Finland, and Portugal have operated such campaigns for between two and four decades, resulting in the decreases in salt intake and consequent reductions in national medical costs and improvements in national health statistics that I already mentioned.

  Are we citizens of industrial nations thus helpless pawns in the hands of food manufacturers, and is there little that we can do to lower our salt intake and blood pressure except to pray for an effective government anti-salt campaign? Actually, there is a big step that you can take besides avoiding use of salt-shakers: you can eat a healthy diet high in fresh foods and low in processed foods—specifically, a diet high in vegetables, fruits, fiber, complex carbohydrates, low-dairy products including cheeses, whole grains, poultry, fish (yes, you can eat fatty fish), vegetable oils, and nuts, but low in red meat, sweets, sugar-containing beverages, butter, cream, cholesterol, and saturated fats. In controlled experiments on volunteers, such a diet, termed a DASH diet—Dietary Approaches to Stop Hypertension—markedly lowers blood pressure.

  Perhaps you’re already thinking: “There’s no way that I’ll subject myself to a tasteless low-fat diet and destroy my pleasure in food, just in order to live 10 more years! I’d rather enjoy 70 years filled with great food and wine than 80 years of tasteless low-salt crackers and water.” In fact, the DASH diet is modeled on the so-called Mediterranean diet, with a luscious fat content of 38%, getting its name from the fact that that’s what Italians, Spaniards, Greeks, and many French people actually eat traditionally. (That fat of the DASH and Mediterranean diets is high in so-called mono-unsaturated fat, the type of fat that is good for us.) Those people aren’t eating crackers and water: they’re enjoying the greatest cuisines of Western civilization. Italians, who spend hours every day consuming their glorious pastas, breads, cheeses, olive oils, and other triumphs of Italian kitchens and farms, are still on the average among the slimmest people in the Western world. At the same time, we Americans, whose diet is anything but Mediterranean, have on the average the biggest waistlines in the Western world. One-third of adult Americans are obese, and another one-third of us are “merely” overweight, but we don’t even have the consolation of knowing that it’s the price we pay for the pleasures of Italian cuisine. You, too, can enjoy great food and be healthy.

  Diabetes

  Western diets that are high in sugar and in sugar-yielding carbohydrates are to diabetes as salt is to hypertension. When my twin sons were still too young to have learned healthy eating habits, taking them to a supermarket meant for my wife and me traversing a gauntlet of sweet dangers. Among breakfast foods, my kids were tempted by the choice between Apple Cinnamon Cheerios and Fruit Loops, respectively 85% and 89% carbohydrate according to their manufacturers, with about half of that carbohydrate in the form of sugar. Boxes picturing the famous turtles with Ninja powers seduced children to ask for Teenage Mutant Ninja Turtles Cheese Pasta Dinner, 81% carbohydrate. Snack choices included Fruit Bears (92% carbohydrate, no protein) and Teddy Graham’s Bearwich chocolate cookies with vanilla cream (71% carbohydrate); both listed corn syrup, as well as sugar, among their ingredients.

  All of these foods contained little or no fiber. Compared with the diet to which our evolutionary history adapted us, they differed in their much higher content of sugar and other carbohydrates (71% to 95% instead of about 15% to 55%) and much lower protein and fiber content. I mention these particular brands, not because they are unusual, but precisely because their content was typical of what was available. Around the year 1700 sugar intake was only about 4 pounds per year per person in England and the U.S. (then still a colony), but it is over 150 pounds per year per person today. One-quarter of the modern U.S. population eats over 200 pounds of sugar per year. A study of U.S. eighth-graders showed that 40% of their diet consisted of sugar and sugar-yielding carbohydrates. With foods like the ones I just mentioned lurking in supermarkets to tempt kids and their parents, it’s no wonder that consequences of diabetes, the commonest disease of carbohydrate metabolism, will be the cause of death for many readers of this book. It’s also no wonder that we readers suffer from tooth decay and cavities, which are very rare in the !Kung. While living in the 1970s in Scotland, where consumption of pastries and sweets was prodigious, I was told that some Scottish people had already as teen-agers lost most of their teeth due to tooth decay.

  The ultimate cause of the many types of damage that diabetes wreaks on our bodies is high blood concentrations of the sugar glucose. They cause the spilling-over of glucose into the urine: a manifestation from which stems the disease’s full name, diabetes mellitus, meaning “running-through of honey.” Diabetes isn’t infectious or rapidly fatal, so it doesn’t command press headlines, as does AIDS. Nevertheless, the world epidemic of diabetes today far eclipses the AIDS epidemic in its toll of death and suffering. Diabetes disables its victims slowly and reduces their quality of life. Because all cells in our body become exposed to sugar from the bloodstream, diabetes can affect almost any organ system. Among its secondary consequences, it is the leading cause of adult blindness in the U.S.; the second leading cause of non-traumatic foot amputations; the cause of one-third of our cases of kidney failure; a major risk factor for stroke, heart attacks, peripheral vascular disease, and nerve degeneration; and the cause of over $100 billion of American health costs annually (15% of our costs due to all diseases combined). To quote Wilfr
id Oakley, “Man may be the captain of his fate, but he is also the victim of his blood sugar.”

  As of the year 2010, the number of diabetics in the world was estimated at around 300 million. This value may be an underestimate, because there were likely to be other undiagnosed cases, especially in medically undersurveyed countries of the developing world. The growth rate in the number of diabetics is about 2.2% per year, or nearly twice the growth rate of the world’s adult population: i.e., the percentage of the population that is diabetic is increasing. If nothing else changes in the world except that the world’s population continues to grow, to age, and to move to cities (associated with a more sedentary lifestyle and hence increased prevalence of diabetes), then the number of cases predicted for the year 2030 is around 500 million, which would make diabetes one of the world’s commonest diseases and biggest public health problems. But the prognosis is even worse than that, because other risk factors for diabetes (especially affluence and rural obesity) are also increasing, so that the number of cases in 2030 will probably be even higher. The current explosion in diabetes’ prevalence is occurring especially in the Third World, where the epidemic is still in its early stages in India and China, the world’s two most populous countries. Formerly considered a disease mainly of rich Europeans and North Americans, diabetes passed two milestones by the year 2010: more than half of the world’s diabetics are now Asians, and the two countries with the largest number of diabetics are now India and China.

  Types of diabetes

  What normally happens when we consume some glucose (or other glucose-containing carbohydrates)? As the sugar is absorbed from our intestine, its concentration in our blood rises, signaling the pancreas to release the hormone insulin. That hormone in turn signals the liver to decrease glucose production, and signals muscle and fat cells to take up the glucose (thereby halting the rise in blood glucose concentration) and to store it as glycogen or as fat, to be used for energy between meals. Other nutrients, such as amino acids, also trigger the release of insulin, and insulin has effects on food components other than sugar (such as preventing the breakdown of fat).