The World Until Yesterday: What Can We Learn from Traditional Societies? (73 page)

Let’s now pause for a quick crash course on blood pressure and hypertension, to help you understand what those numbers mean when your doctor inflates a rubber cuff about your arm, listens, deflates the cuff, and finally pronounces, “Your blood pressure is 120 over 80.” Blood pressure is expressed in units of millimeters of mercury: the height to which your blood pressure would force up a column of mercury in case, God forbid, your artery were suddenly connected to a vertical mercury column. Naturally, your blood pressure changes throughout each heart stroke cycle: it rises as
the heart squeezes, and it falls as the heart relaxes. Hence your physician measures a first number and then a second number (e.g., 120 and 80 millimeters of mercury), referring respectively to the peak pressure at each heartbeat (called systolic pressure) and to the minimum pressure between beats (termed diastolic pressure). Blood pressure varies somewhat with your position, activity, and anxiety level, so the measurement is usually made while you are resting flat on your back and supposedly calm. Under those conditions, 120 over 80 is an average reading for Americans. There is no magic cut-off between normal blood pressure and high blood pressure. Instead, the higher your blood pressure, the more likely you are to die of a heart attack, a stroke, kidney failure, or a ruptured aorta. Usually, a pressure reading higher than 140 over 90 is arbitrarily defined as constituting hypertension, but some people with lower readings will die of a stroke at age 50, while others with higher readings will die of a car accident in otherwise good health at age 90.

In the short run, your blood pressure increases with your anxiety level and with vigorous exercise. In the long run, though, it increases with other factors, especially with salt intake (for reasons discussed below) and (in us Westernized moderns but not in traditional peoples) with age. The relationship between salt intake and blood pressure was noted more than 2,000 years ago in the Chinese medical text
Huangdi neijing suwen
, which says, “Therefore if large amounts of salt are taken, the pulse will stiffen and harden.” In recent experiments on captive chimpanzees, our closest animal relatives, their blood pressure while consuming a Purina Monkey Chow diet providing 6 to 12 grams of salt per day (like most modern humans eating a Western diet) was a pleasingly healthy 120 over 50, but it increased with age (also like modern humans on a Western diet). After a year and seven months on a high-salt diet of up to about 25 grams per day, the chimps’ blood pressure rose to about 155 over 60, qualifying them to be called hypertensive by human standards, at least as judged by their systolic blood pressure.

For us humans it’s clear that salt intake does influence blood pressure, at least at the opposite extremes of very low and very high salt intake. The international INTERSALT project of the 1980s used a uniform methodology to measure salt intake and blood pressure in 52 populations around the world. The population that I already mentioned as having the world’s
lowest recorded salt intake, Brazil’s Yanomamo Indians, also had the world’s lowest average blood pressure, an astonishingly low 96 over 61. The two populations with the next two lowest salt intakes, Brazil’s Xingu Indians and Papua New Guinea Highlanders of the Asaro Valley, had the next two lowest blood pressures (100 over 62, and 108 over 63). These three populations, and several dozen other populations around the world with traditional lifestyles and low salt intakes, showed no increase in blood pressure with age, in contrast to the rise with age in Americans and all other Westernized populations.

At the opposite extreme, doctors regard Japan as the “land of apoplexy” because of the high frequency of fatal strokes (Japan’s leading cause of death, five times more frequent than in the United States), linked to high blood pressure and notoriously salty food. Within Japan these factors reach their extremes in northern Japan’s Akita Prefecture, famous for its tasty rice, which Akita farmers flavor with salt, wash down with salty miso soup, and alternate with salt pickles between meals. Of 300 Akita adults studied, not one consumed less than 5 grams of salt daily (three months of consumption for a Yanomamo Indian), the average Akita consumption was 27 grams, and the most salt-loving individual consumed an incredible 61 grams—enough to devour the contents of the usual 26-ounce supermarket salt container in a mere 12 days. That record-breaking Akita man consumed daily as much salt as an average Yanomamo Indian in three years and three months. The
average
blood pressure in Akita by age 50 was 151 over 93, making hypertension the norm. Not surprisingly, Akita’s frequency of death by stroke was more than double even the Japanese average, and in some Akita villages 99% of the population died before 70.

The evidence is thus striking that extreme variations in salt intake have big effects on blood pressure: very low salt intake results in very low blood pressure, and very high salt intake results in very high blood pressure. However, most of us will never follow a diet as extreme as that of a Yanomamo Indian or an Akita farmer. Instead, we would like to know whether more modest variations in salt intake, within the middle of the range of world salt intakes, have at least some modest effects on blood pressure. For several reasons, it really isn’t surprising that there is still some controversy about effects of variation within this middle range. The middle range encompasses only a narrow spread of salt intake: for instance, 48 of
the 52 populations in the INTERSALT study (all populations except the Yanomamo and the three other low-salt outliers) had mean salt intakes falling between 6 and 14 grams per day. Individual variation in salt intake and blood pressure within most populations is large and tends to obscure average differences between populations. Salt intake itself is notoriously difficult to measure consistently unless one confines people in a hospital metabolic ward for a week and measures salt levels in all of their foods consumed and urine produced. That’s completely impossible to do for Yanomamo Indians in the jungle, as well as for most of us city-dwellers wanting to lead normal lives outside metabolic wards. Instead, salt intake is commonly estimated from 24-hour urine collections, but those values are subject to huge variation from day to day, depending on whether one happens to eat a Big Mac or a can of chicken noodle soup on some particular day.

Despite those causes of uncertainty, many natural experiments as well as manipulative experiments indicate to me that variations of salt intake within the normal range do affect blood pressure. Regional variation, migration, and individual variation provide natural experiments. Salt intake is higher for coastal people than for interior people in Newfoundland and in the Solomon Islands, and it’s higher for rural Nigerians living near a salt lake than for nearby rural Nigerians not living near a salt lake; in each case the higher-salt population has higher average blood pressure. When rural Kenyans or Chinese move to cities, their salt intake often rises, and so does their blood pressure. Salt intake in Japan nearly doubles from south to north to reach its maximum in the already-mentioned Akita Prefecture in the north, and that salt trend is paralleled by a trend in hypertension and in deaths from stroke. Among individual Japanese in a single city (Takayama), hypertension and stroke deaths increase with salt intake.

As for manipulative experiments, Americans on a (mildly) low-salt diet for 30 days, New Guineans on a (mildly) high-salt diet for 10 days, and Chinese on a (mildly) low-salt or high-salt diet for 7 days all experienced a rise or fall in blood pressure paralleling the experimental rise or fall in salt intake. Epidemiologists in a suburb of the Dutch city of The Hague, with the cooperation of the mothers of 476 newborn infants, randomly assigned the infants (most of them breast-fed) for six months to either of two diets of food supplements differing by a factor of 2.6 in salt content.
The blood pressure of the slightly high-salt babies increased progressively above the blood pressure of the slightly low-salt babies over the course of the six months, when the experimental intervention ended and the babies proceeded to eat whatever they wanted for the next 15 years. Interestingly, the effects of those six months of salt intake in infancy proved to be permanent: as teen-agers, the former slightly high-salt babies still had blood pressures above those of the slightly low-salt babies (perhaps because they had become permanently conditioned to choose salty food). Finally, in at least four countries notorious for high average levels of salt consumption and resulting stroke deaths—China, Finland, Japan, and Portugal—government public health campaigns that lasted years or decades achieved local or national reductions in blood pressure and in stroke mortality. For instance, a 20-year campaign in Finland to reduce salt intake succeeded in lowering average blood pressure, and thereby cut 75% or 80% off of deaths from stroke and coronary heart disease and added 5 or 6 years to Finnish life expectancies.

For us to be able to deal with the problem of high blood pressure, we have to understand what else besides high salt intake can cause it, and why high salt intake can cause it in some individuals but not in others. Why is it that some of us have much higher blood pressure than do others of us? In 5% of hypertensive patients there proves to be a clearly identifiable single cause, such as hormonal imbalance or use of oral contraceptives. In 95% of patients, though, there is no such obvious cause. The clinical euphemism for our ignorance in such cases is “essential hypertension.”

We can assess the role of genetic factors in essential hypertension by comparing how closely blood pressure agrees between closer or more distant relatives. Among people living in the same household, identical twins, who share all of their genes, have quite similar blood pressure; the similarity is lower but still significant for fraternal twins, ordinary siblings, or a parent and biological child, who share about half of their genes. The similarity is still lower for adopted siblings or a parent and adopted child, who have no direct genetic connection but share the same household
environment. (For those of you familiar with statistics and correlation coefficients, the correlation coefficient for blood pressure is 0.63 between identical twins, 0.25 between fraternal twins or parent and biological child, and 0.05 between adopted siblings or parent and adopted child. A coefficient of 1.00 between identical twins would mean that blood pressure is almost completely determined by genes, and that nothing you do [after being conceived] has any effect on your blood pressure.) Evidently, our genes do have a big effect on our blood pressure, but environmental factors also play a role, because identical twins have very similar but not identical blood pressures.

To place these results in perspective, let’s contrast hypertension with a simple genetic disease like Tay-Sachs disease. Tay-Sachs disease is due to a defect in a single gene; every Tay-Sachs patient has a defect in that same gene. Everybody in whom that gene is defective is certain to die of Tay-Sachs disease, regardless of the victim’s lifestyle or environment. In contrast, hypertension usually involves many different genes, each of which individually has a small effect on blood pressure. Hence different hypertensive patients are likely to owe their condition to different gene combinations. Furthermore, whether someone genetically predisposed to hypertension actually develops symptoms depends a lot on lifestyle. Thus, hypertension is not one of those uncommon, homogeneous, and intellectually elegant diseases that geneticists prefer to study. Instead, like diabetes and ulcers, hypertension is a shared set of symptoms produced by heterogeneous causes, all involving an interaction between environmental agents and a susceptible genetic background.

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.