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.
Causes of hypertension
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?