The Heart Of The Matter
CIVILIZED living is an intelligent search for durable satisfaction, a nice compromise between the pleasures of the moment and those of the future. So it is with eating; a balance should be struck between first impulse and appreciation of the consequences of such indulgence. The child learns to save room for pudding; the civilized adult knows that the continuance of pleasure, in eating as in other things, demands a measure of denial. But how, actually, is this nice balance struck?
The appetite is normally a good guide as to how much to eat but it can be deceived by rich foods. The most concentrated source of calories, the fats, are easily concealed by skilful cookery so that palate and stomach do not detect the excessive concentration of food values until obesity threatens. However, the accumulation of body fat is soon seen and felt so there is at least a delayed basis for restraint and correction in regard to simple over-eating. The sensible person who is getting fat recognizes that some dietary adjustment is necessary, and the most obvious solution is to eat portions smaller than prompted by his appetite. A further step in wisdom, we think, would be to change the character of the diet so that the appetite would be able to exercise more effective automatic control. This means the selection of a bulkier diet with fewer calories per bite.
During most of human evolution down to recent times only very few people had an opportunity, except on special occasions, to eat too much and too richly, so it is natural that we have little instinct to curb an appetite for luxurious eating. If we are confronted with an abundance of fat foods and no persuasion otherwise, we may maintain a high fat diet pattern and still, with an effort, control obesity. And this seems to be where more and more prosperous people find themselves today.
Prosperity has produced a new situation where an almost endless supply of all kinds of foods encourages us to eat more and more of the foods formerly limited by scarcity and expense. Moreover, as the need for physical work and therefore that for food calories has decreased, the diet tends to be adjusted by cutting down on the simple staples; why eat bread when there is plenty of cake and you cannot eat both?
But all this may not be pure gain. The pleasure of eating demands hunger, and the delights of rich foods pall in everyday use. Most important, there is reason to believe that the road to a good diet in the long run is not pursued by an increase in the use of softer, sweeter, and fatter foods. Suspicion is strong that luxurious high fat diets may promote coronary heart disease and that much of the current "plague" of this disease, the leading threat to the health of adults in the more well-to-do classes in many countries, has its origin in our modern dietary habits. Many medical scientists would say that suspicion is too mild a term in view of the evidence.
This evidence does not prove that fats in the diet are the sole cause of coronary heart disease; it is probable that several factors contribute to the eventual appearance of the disease. But the case for dietary fats being a very important factor is impressive and the inferences are obvious.
We do not propose to lead a campaign to persuade everyone to change his diet. The first part of this book is a review of what we know about the diet and heart disease. If your logic and personal bias and the best advice you can get elsewhere leads you to agree with our conclusions, the next step is practical application; the dietary suggestions in this book are for this purpose. They are designed for eating pleasure in a dietary pattern capable of endless variation within a framework of basically sound nutrition and moderation in fats. These menus and recipes are not guaranteed to save you from coronary heart disease. But they should keep your blood cholesterol at a more favourable level than an uncontrolled diet and, we trust, will afford new interest in the kitchen and enduring pleasure at the table.
The Evidence In Outline
Coronary heart disease is basically a disorder of the coronary arteries. Fifty years have passed since experiments first proved that common human foods can produce serious disease in the arteries of rabbits. Many years and much careful research showed that a fatty substance in the blood, cholesterol, is responsible for the effects on the arteries in such animal experiments and that these arterial changes experimentally produced are almost identical with those seen in patients dying of coronary heart disease. Recently, coronary heart disease itself has been produced in animals by diets containing much cholesterol and fat. In the meantime, there were doubts about the relevance to man of these animal experiments because man, unlike the rabbits and chickens studied in the laboratory, can eat a great deal of cholesterol with no change in the cholesterol in the blood. It was not realized that in man the amount of cholesterol in the blood is affected by ordinary food fats much more than by pure cholesterol in the diet.
Such complications delayed acceptance of the theory that the diet is a major influence on the development of coronary heart disease in man. For example, physicians long failed to realize that the first heart attack is usually only a late result of underlying disease in the coronary arteries. In a given patient it may be difficult to see any relation between his clinical condition and his current blood cholesterol level or his recent dietary history. This is particularly true when comparison is made only with other members of a population who are generally characterized by a national diet of fatty foods and high blood cholesterol levels. It is now known that, for the most part, the "clinically healthy" persons taken as "controls" in such comparisons are as often as not, themselves also afflicted with disease in the arteries in the silent, pre-clinical form. The picture is very different when comparison is made between our coronary patients and persons of the same age in other populations not so prone to the disease. The blood cholesterol of our coronary patients, with their high fat diets, the usual diets of populations for which coronary heart disease is such a plague, stand out like sore thumbs in the world picture.
Much, too, was made of the fact that a few individuals, sometimes grouped in families, have very high blood cholesterol levels even though their diets are no different from the average. Such persons were found to be especially susceptible to coronary heart disease, but the point was emphasized that they did not get into trouble simply because of the diets they ate. Fair enough; diet is not the only factor, at least in these rare cases.
But lately, controlled experiments on man, including tests of some of these unfortunate men with naturally high blood cholesterol levels, have conclusively shown that the amount and the kind of fat in the diet have a powerful effect on the blood cholesterol. We can change the diet and predict with fair accuracy what the average response will be in the blood.
These dietary experiments have their counterpart on the grand scale in nature. Many comparisons between populations habitually subsisting on diets differing in fat content show associated consistent differences in blood cholesterol levels and the frequency of coronary heart disease. In some instances it has been possible to study populations who change their diets; in each case changes in the blood cholesterol and in the frequency of coronary heart disease tended to follow changes in the fat in the diet.
A Summary of Facts Suggesting Prevention by Dietary Means The facts leading to the belief that a large measure of prevention of coronary heart disease can be achieved by dietary regulation may be summarized as follows: The frequency of coronary heart disease varies greatly between populations that eat different amounts and kinds of fats. Coronary heart disease is a minor problem among populations whose diets contain relatively little of the common meat and dairy fats that bulk so large in the current diet of the prosperous Western world. Such populations are not all in "under-developed" countries and they may have good health in other respects, too.
These differences between populations are not dependent on climate or race. There is a great difference in the frequency of the disease between rich and poor Italians in Naples and Neapolitans living in Boston, between rich and poor Spaniards in Madrid, between economic classes of people in Guatemala. Japanese in Southern California are like other Californians in the frequency of the disease but are more often affected than their semi-Americanized relatives in Hawaii who, in turn, have far more coronary heart disease than men in Japan.
These differences between populations are not explained by personal habits such as the habitual use of tobacco or alcohol. Many of the populations who suffer relatively little coronary heart disease contain plenty of men who are heavy smokers or drinkers or both. If tobacco or alcohol have any effect, this does not seem to be primary.
Coronary heart disease is much more common in populations in whom the average blood contains large amounts of cholesterol than among those whose blood cholesterol levels are relatively low. Investigations embracing more than a score of populations around the world suggest that the frequency of early, severe coronary disease in a population is closely proportional to the average serum cholesterol concentration in the population.
The serum cholesterol level in man rapidly responds to changes in dietary fat, falling when meat and dairy fats are reduced, rising when they are replaced in the diet, even when calories, proteins, and vitamins are kept constant. Some vegetable oils have no such effect and may even reduce the serum cholesterol.
Animals fed diets that raise the cholesterol level in the blood serum develop disease in the coronary arteries, and the extent of the disease tends to parallel the serum cholesterol level. Return to a more favourable diet restores the cholesterol level to normal and the artery disease tends to regress.
Though only a minority of coronary patients are obese, it is certain that fat people are unusually prone to heart disease. In some populations the fatter people eat the fattest diets and tend to have higher blood cholesterol values. But merely being thin is small protection, and differences in the frequency of obesity do not explain the differences between populations in the frequency of coronary heart disease. These differences in disease appear to parallel the character of the diet.
After a fatty meal the red cells in the blood may tend to stick together, and some tests show that the blood clots more readily than before. This causes us to think when we realize that blood clots ("thrombi") are often the final cause of a heart attack.
Populations whose diets are changed in regard to fat content have been reported subsequently to show important differences in the frequency of coronary heart disease. Examples are European countries during and after World War II, immigrants into Israel, Japanese moving from Japan to Hawaii to California. No exceptions have been reported.