WISHING OUR READERS A SUCCESSFUL NEW YEAR 2009

YOU CAN ESCAPE THIS HEART TRAP ARE YOUR DAILY MEALS CHOKING YOUR LIFELINE BLOCKING THE VITAL ARTERIES THAT FEED YOUR HEART?

NO SENSIBLE HOUSEWIFE pours grease from a frying pan into her kitchen sink day after day. She knows only too well that sooner or later, the fat will harden and stop up the drainpipe, causing mess, trouble and plumbers' bills.

Learn right now that the same thing can happen in the blood vessels that feed your heart. Scales of hard fat can plug these blood vessels, causing a coronary (heart) attack.

This, to our way of thinking, can be called . . . THE GREASE TRAP DISEASE!

When you eat foods containing a high percentage of any kind of fat, your blood becomes loaded with infinitesimally small fat droplets. Blood, as you know, is a watery medium; and in the blood, as elsewhere, water and fat don't mix.

Nature has devised certain special ways to get the fat droplets out of the blood, and some types of fat, called soft fat, travel in and out of the blood stream quite readily and easily. On the other hand, equally tiny drops of hard fat have to be bound with cholesterol to be transported out of the blood.

This hard fat causes the blood-cholesterol level to rise and some of the cholesterol tends to linger in the blood. Sooner or later, if you continue to have high blood-cholesterol levels, a particle of cholesterol and hard fat may cling to the inside of the blood vessel wall. In time, the speck of cholesterol and fat causes an irritation, which, in turn, makes changes in the affected area.

The waxy-like cholesterol and fat particles collect in the sore spot, and together the two form “scales.” From then on, the plaque, as doctors call it, tends to grow bigger and bigger.

Obviously, the space through which the blood once flowed freely gradually becomes narrower and narrower. Eventually, the blood flow may become entirely stopped up, much like the inside of a water pipe that has become clogged with rust or the calcareous material found in hard water.

In a human being, a piece of fat plaque may slough off and plug the artery involved. If this should happen in the blood vessels that nourish the heart, it is called a coronary thrombosis.

Although the coronary blood vessels can be stopped in several different ways as a result of being narrowed by plaques, each winds up with what we commonly call a coronary heart attack.

There is a world of scientific evidence to prove that you may entirely prevent, or markedly hold down, the formation of plaques by balancing your intake of hard and soft fats.

This means cutting down on the amount of hard fats you eat, and eating some soft fats to replace them. The “whys and wherefores” of this epoch-making discovery is the reason for this book.

Thank goodness, there is also every reason to believe that the same simple precautions can also help you to absorb and cleanse your blood vessels of those existing fat plaques which haven't already become calcified or sclerosed. In short, if you are now a prime candidate for a serious coronary attack, you can get yourself out of danger.

Let us assure you now, at the beginning that you won't have to become a diet crank to guard your heart and brain against fatty degenerative disease. You won't have to measure out grams of food or become a nutrition expert.

HEART SAVER EATING, as we call it, is not difficult to apply. Your meals will still please your palate, satisfy your appetite, and give you a full share of the joy of eating.

But we'll have to start with a few gloomy-sounding facts and figures to show you why it is so vitally important to use judgment in choosing the foods you eat. Bear with us while we take a quick look into the more-or-less recent developments in the new medical understanding of coronary and apoplectic attacks.

Comparatively few people know the difference between hard and soft fats—or for that matter the facts about the coronary story.  Much of the fat we eat is hidden in our foods. We get it in frankfurters and ice cream, our marbled steaks and tender meats.

We add it to our foods when we fry in butter, margarine, or the solid cooking fats. We load up on it when we butter our vegetables, or douse our potatoes with gravy. We take in a lot of hard fat in the cheese we eat, our hors d'oeuvres, and our television snacks.

Doctors and nutritionists figure that not more than 25 to 30 percent of the calories we eat (depending upon body weight) should come from fats of all kinds. Ideally according to our personal view, slightly more than one-half of the fat we eat should be of the soft kind, which means those derived from vegetable sources.

Unfortunately, most people, on the average, get from 39 to 50 percent of our calories from fat—and 85 percent of this amount is hard fat derived mainly from animal and commercial sources! Without doubt, this reckless and irrational pattern of eating has given us the highest death rate from coronary disease in the entire wide world.

People on diet not only keep their fat intake below the safe 25-percent calorie level; but what is more important, they get most of their fat from olive oil, a relatively soft fat, which is kind to the arteries and could wash plaques away. Their coronary death rate is one-fourth of a chance for severe heart attack.

Of course, this is thinking in a public health sense, where averages and statistics are the guiding lights.  As individual, you don’t have to think of the fats we eat in such specific amounts. But, we do have to acquaint ourselves with the fat-facts about foods.

We have to vary our meat eating in better fashion; eating beef and lamb less often, chicken and other fowl more frequently, and much more fish. We have to learn to switch to skim milk, or at least make it half skim and half whole milk.

We must cut away the fats from the meats we eat; butter our bread less abundantly. We should learn to drink black coffee. All frying should be done with soft-fat vegetable oils; never the white, hard, hydrogenated shortenings which have become so popular in the past twenty years.

In fact, the soft oils should be used for all cooking and baking purposes—especially in the preparation of sauces and gravies. It will mean a revolution in the kitchen for many housewives—but save millions of husbands' lives. The woman who brags, “I always cook with butter,” is helping to make her family more likely to fall prey to coronary attack.

As we shall discover later, there are a hundred-and-one ways to trim our hard-fat intake to a safe amount, or replace them with soft fats which will help to protect us from “The Grease Trap Disease”.

FATS HAVE THEIR ROLE

One of the several reasons why the housewife uses fat in the kitchen is the fact that fats have an extraordinary capacity for absorbing flavours. Anyone who has fried onions or fish in fats needs no laboratory demonstration of this fact. We put this principle to work when we rub a piece of lamb with garlic butter.

It's the main reason why we like a film of butter on carrots or peas. The fat, absorbing delicate flavours, intensifies them and spreads them out for the taste buds. Fat makes rough or hard-to-swallow foods more lubricous, in everyday language, smoother and more slippery.  All these aims are worthy enough to be continued—but only with soft fats.

A lot of people on the average consume at least three tablespoons of added hard fat per person per day. This includes the butter the housewife adds to spinach, the solid cooking fat used to make cakes, cookies and dressings, and the fats used to fry foods. The whole milk and cream added to recipes helps significantly to raise this total.

Consider a housewife who plans her menus and cooks her food in typical Western/Eastern fashion for a family of five. Statistically, she buys and uses three tablespoons of hard kitchen fat per person in her family, per day.

That's fifteen tablespoons for the family daily, 105 tablespoons a week. Since two tablespoons of fat weigh one ounce, the housewife is serving over fifty-two ounces, almost 3½ pounds, of cooking fat per week.

What a tremendous heart saving job she could do for herself and her family if she'd just think twice before adding hard fat to foods, and if she would switch to recipes and cooking techniques calling for soft fats only.

HOW TO KEEP THE ODDS IN YOUR FAVOR THIS NEW FOOD   KNOWLEDGE   CAN   MEAN   MORE YEARS, BETTER YEARS, FOR YOU.

FOR CENTURIES, doctors have well known that the blood vessels of the body harden, particularly in old age. In 1833, Dr. J. G. Lobstein, a noted French pathologist, coined the name arteriosclerosis for hardening of the arteries.

The word, like so many medical terms, was taken from the Greek; arteria—from which our word artery is derived, and skleros—meaning hard. Dr. Lobstein described a particular type, characterized by extensive chalk-like deposits of calcium, but the name was applied indiscriminately to all different kinds of “hardening” of the blood vessel walls.

In 1847, an American, Dr. J. Vogel, noted deposits of fat and cholesterol in the many sections of hard arteries he had examined under the microscope. Nine years later, the great pathologist, Rudolph Virchow, proved that such fatty deposits were the distinguishing feature of the by far most common type of arterial hardening. He used the term atherosis (Greek for mush-like) to describe the cheesy character of the artery changes.

In 1904, F. Marchand wrote a new classic description of the fatty type of arterial degeneration, and selected the name ATHERO¬SCLEROSIS to define it. (It is often described in medical literature by the initials AHD.)

It is important for you to thoroughly appreciate that atherosclerosis is different from the classical hardening of the arteries which may develop in old age. Atherosclerosis, the fatty type, which we described as “The Grease Trap Disease,” may be acquired very early in life.

It is not at all rare in teenagers, and has even been seen in babies a year-or-two-old. Post-mortem examinations of hundreds of young men, aged 20 to 30, have shown extensive fatty deposits in the coronary arteries.

It has been estimated that today, seven out of ten  men worldwide have developed much more than a token amount of atherosclerosis before the age of twenty-five. Their coronary arteries are already narrowed with developing plaques.

This is the inevitable result of the kind of eating we delight in eating too many rich and oily foods, and our present way of baby feeding. Very few mothers breast feed their babies today.

They substitute formulas which have as their base, hard cow's-milk. Certain Department of Agriculture bulletins (as will be noted later) even recommend feeding young children from six to eight glasses of whole per day.

We spend the biggest part of our food dollars for the hard-fat foods, and children, especially, are urged to eat them. Hydrogenated peanut butter, hamburgers, frankfurters, chocolate malts, and ice cream are all favourites with our young folks.

Each one of these foods is rich in hard fats; particularly frankfurters and hamburgers. Beef, bacon, and other meat drippings are carefully treasured in the home for use as cooking fat.

It is here that we lay the groundwork for the Hodiak-Garfield-Power type of tragedies. Sudden death at 35 or 40! This is indeed the “lost generation” as far as coronary disease is concerned.

In each decade after age thirty, the percentage of AHD deaths grows greater and greater. It doubles, triples, and quadruples as we grow older, until more than three-quarters of all deaths around the world past 75 years old are caused by coronary or apoplectic attacks.

Let us repeat. Atherosclerosis is the underlying blood vessel disease which brings on the vast majority (90 percent) of the millions coronary attacks hitting people worldwide every year. And these estimates are conservative!

Marchand's clear account of this fear-fully common type of arterial disease stirred up a great new interest in study and research which might lead science to better understand it. Almost at once, some workers wondered how and why drops of fat burrowed into the artery walls, and why the spot always contained a great deal of cholesterol.

Cholesterol is a fat-like, pearly substance which crystallizes into a needle-like form. It dissolves only in fat, and so in foods is associated with certain types of fat, particularly animal fats. The cholesterol found in the human body is manufactured by various body tissues from the fats found in foods.

Was there any link between diet and the fatty blood vessel changes?

Very early studies about cholesterol were conducted and more research done at the present Medical Research Centres. It was in 1908, A. Ignatowski, working on this problem at the Medical Academy in St. Petersburg, Russia, in a few weeks, produced fatty deposits in the arteries of rabbits by feeding them a diet consisting exclusively of meat, milk, or eggs.

Of course, it wasn't known at the time just which dietary factor produced the disease, but proteins were suspected. In 1910, Stukkeu, also working with rabbits in St. Petersburg, demonstrated quite convincingly that the damage was not caused by the proteins, but that foods containing both fat and cholesterol did work such harm.

He was positive that cholesterol in foods was the offending factor, and quite a few investigators enthusiastically agreed with him. This belief was gradually strengthened through the years until it was widely accepted. Eventually, it was shown that only the cholesterol that actually gets into the blood stream can cause AHD, and the dietetic road to coronary prevention was charted and cleared.

Yes thank goodness, to this wonderful scientist, now you can control the cholesterol levels of your blood, and act to prevent atherosclerosis. This knowledge is the greatest contribution that nutrition science has yet made to saving human life.

Meanwhile, to return to the earlier studies, there was no doubt that feeding rabbits an excess of milk, meat, and eggs could quickly cause atherosclerosis, and the big question that had to be decided was . . . could the same rule apply to human beings?

Most contemporary scientists felt it could not. Although they agreed that such foods might cause the blood vessel harm in a rabbit, they doubted that the same thing would hold for human beings, or other animals, for that matter. They argued that a rabbit lives mainly on vegetables, and doesn't normally eat fat- and cholesterol-containing foods.

Research on the subject lagged somewhat for the next thirty years. Then came a landmark! In 1942, Drs. Dauber and Katz produced experimental atherosclerosis in chickens; which eat both vegetable and animal foods.

Chickens were chosen because, of all animals, these fowls often develop an atherosis closely resembling the human type. In quick succession the disease was produced in dogs, ducks, geese, guinea pigs, hamsters, and monkeys, always, of course, with a diet rich in hard fats.

Scientists can't very well try such experiments on human beings because they would have to prove the study by sacrificing the subject and performing a post-mortem examination. However, the fact was one hundred-percent proven as far as some animals were concerned.

In the early 1950's, several investigators found that feeding animals an excess of certain fats which were entirely free of cholesterol could quickly cause the artery changes. Newspapers played up the new discoveries with headlines: “CHOLESTEROL FOUND NOT GUILTY! CHOLESTEROL NOT TO BLAME!” Of course, such articles couldn't tell the whole story because all the details weren't known.

But, to put it mildly, many people faith-fully following a low-cholesterol diet were upset and confused.

Was cholesterol really innocent?

Was their dieting to no avail?

These questions were answered by studying the behaviour of fat in the blood. When you eat any kind of fat, it is picked up by the blood stream immediately after digestion. When you eat a very fatty meal, your blood is literally suffused with infinitesimally small fat droplets called chylomicrons.

The fatter you eat, the more “greasy” your blood will be. In fact, if you eat a very, very fatty meal, your blood plasma actually becomes murky or cloudy. It is no easy problem to get this fat out of the blood and into the various parts of the body where it belongs. Immensely complicated chemical transactions of various kinds take place. There is one very important fact that you need remember.

Much of the fat in your blood is changed into special molecules called lipoproteins, which means a combination of fat, protein, and cholesterol. The cholesterol is needed to dissolve the fat and make it transportable in the blood, which is water medium.

Your liver is the factory which manufactures lipoproteins, and it automatically supplies all the cholesterol needed. It is here that we find the crux of the atherosis question.

When certain of the components in hard fats are made into lipoproteins, large amounts of cholesterol are needed. Later, when these particular lipoproteins are broken down so that the fat they carry can be freed for use, the cholesterol is left in the blood.

A good deal of it may be cleared out, but some of it sticks around to give the eater a high blood-cholesterol level, which in turn can lead to the formation of plaques—and eventually, coronary disease.

Of course, we have oversimplified a very involved chemical process—but these very pertinent facts remain:

1.            Certain components of hard fats are transformed into a special kind of lipoprotein by your liver.

2.            A part of the cholesterol which is used for this purpose may be left in your blood stream when the lipoprotein is broken down for body use.

Therefore, when you eat hard fats, cholesterol appears in your blood. The more hard fats you eat, the higher your blood-cholesterol level goes.

It even gets down to such points as—the harder the fat, the more cholesterol needed. So, you can act to control your cholesterol levels according to the amount and type of hard fats you eat.

The blood chemistry of soft fats is quite different. There is no need to go into the fine details, but the important thing is that the soft fats don't raise your blood cholesterol. In fact, soft fats contain certain factors which tend to lower the blood-cholesterol levels, and are sometimes used for this purpose in medical practice.

To summarize: It is only the cholesterol which gets into your blood that can cause plaques or fatty blood vessel deposits. The cholesterol you get in foods does not enter your blood stream. It is screened out by the process of digestion.

The cholesterol made in other parts of your body serves good and useful purposes. Some of it is turned into life-giving hormones; some makes compounds necessary to life. Only the cholesterol which gets into your blood stream, because of hard fats, does coronary damage.

It is up to you to keep your blood cholesterol down to a reasonable level, and it is the purpose of this article to tell you how to do it. While it is true that, from a coronary view, you don't need to concern yourself about the cholesterol you get in foods; you will wish to know that a given food contains cholesterol, for it serves as a guide to tell you that there is also hard fat present. The two go together. The presence of cholesterol is an indicator that warns you there is hard fat in a specific food!

The further we travel along life's road, the more we can benefit by heart saver eating and living. Whether you are young or old, this is the greatest health service you can render yourself. Don't wantonly plug your coronary arteries with hard fat.

We call atherosclerosis the “long word for a short life.” When you set out to eat less hard fats, you are taking steps to prevent it in all its forms. Whenever you are tempted to overindulge—think of “The Grease Trap Disease!” Don't dig your grave with your teeth!

PAYING RESPECT TO A PROPHET WITH HONOR

Sir William Osier (1849-1919) was, without doubt, the most beloved and respected physician of modern times. Handsome, cultured, and by many considered the all time wisest of clinicians, his basic grasp of the coronary problem has only begun to be recognized and appreciated today.

In 1896, Dr. Osier emphasized, as had others before him, that coronary was a man's disease. Only one woman was numbered among the 40 coronary patients he reported upon at that time.

Later, as his experience broadened, he wrote what we realize only too well today: “The greatest incidence of the disease (coronary) occurs among men who eat, drink, and smoke to excess . . . Perhaps this is the nemesis through which nature exacts retributive justice for the transgression of her laws.”

Dr. William Dock, writing in the Journal of the American Medical Association (5-9-59) recalls that as early as 1907, Dr. Osier counselled his students: “In the treatment of many cases of coronary disease Diet is the central point.”

Dr. Osier's reference to “breaking Nature's laws” most certainly applies to the laws of right eating. Your blood stream is geared to take care of a certain quantity of hard fat. When you consistently burden this fluid with an overload of cholesterol and hard fat—deposits will form.

Just as an excess of silt and mud can build a sand bar on a river bed, so your blood vessels can be occluded by cholesterol and fat. The process can begin in the first year of life, and you may have to pay the penalty before you reach forty.

A TEST THAT MAY SAVE YOUR LIFE NOW YOU CAN READILY LEARN WHETHER YOUR DIET IS HEADING YOU FOR TROUBLE

CHOLESTEROL has interested doctors since 1785, when it was found to be the main constituent of gall stones. We have already traced the history of its association with coronary disease since Vogel discovered this waxy-like material was a principle ingredient of blood vessel plaques.

Today, as you must have gathered by now, up-to-date doctors use the cholesterol test to determine your probable susceptibility to a coronary attack.

Blood-cholesterol readings are expressed in milligrams, and range from a low of 40 to a high of 1000 or more. A high cholesterol reading may lead your doctor to believe that your coronary arteries are narrowed by deposits of hard fat.

At present, cholesterol tests are the surest way of enabling your doctor to help you prevent or control the mistakes which may lead to a coronary attack. He can check how efficiently your heart saver eating is helping you, and whether you need a stricter diet. He can also decide whether or not you need more exercise, or more relief from tension.

The average man should take a cholesterol test at least once every six months. Don't let your doctor keep you in the dark about the results. You have a right, and a duty to yourself to know what they are.

Tens of thousands of cholesterol tests, performed on people between the ages of 40 and 60, show that average cholesterol levels will range from 200 to 300. People in all other countries of the world (except Finland) have much lower averages. By the same token, their death rates from coronary disease are much lower than ours.

Coronary disease is comparatively rare among rural Guatemalans. Their cholesterol levels average less than 175. The Eskimos are particularly exempt from coronary disease. Sever-al series of tests indicate that their blood-cholesterol levels average around 140, due presumably to the fact that they eat many fish-fats, which are highly unsaturated.

Don't be misled by the notion that the terms average and normal, as used in this country, means that everything is all right. You often hear it said that it is normal for people to have cholesterol readings over 200. That is normal only in the sense that it's average in certain country, where we expect more than 2500 individuals per day to suffer a coronary attack.

 It is not normal in the sense of what is right and safe in terms of coronary prevention. Don't feel safe with a 250 cholesterol level because “everybody else” around you has high readings. “Everybody else” includes your fellow human who are being stricken by coronary attacks at the rate of a million a year.

Personally, I would not feel safe from a possible coronary attack if the cholesterol readings averaged 200, or over. It is firmly (and this is entirely a personal opinion), that it is safest and best for an individual to keep his blood-cholesterol reading at 175 to 190. Work to this end, no matter what your age may be, with diet and exercise, plus avoiding mental and emotional stress.

At what age should a person have his first cholesterol test?

In the Specialist opinion, so far as males are concerned, the younger the better. Ordinarily, newborn infants have cholesterol levels approximately half the readings of an adult aged twenty; but large variations are found, depending upon the amount and kind of fat in the infant's formula.

By the time the average infant reaches two months, the cholesterol readings are not much different from that of a grownup’s. This is to be expected, because so few mothers nurse their babies, or guard their own cholesterol levels.

One day, prenatal feeding will include cholesterol precautions, because the embryo, nestled in the womb, is fed from the mother’s blood. Also, our babies' formulas will no longer be super-charged with hard cow's milk. We will fight the threat of coronary disease where it first begins—in the womb, in the cradle, and in the critical time during which the infant develops.

In the last few years, more than several instances of advanced coronary disease have been discovered upon post-mortem examination of infant’s one- or two-years-old. Cholesterol levels running well over 250 have regularly been found in teenagers—which are not surprising, considering the amount of hot dogs, ice cream, and hamburgers they eat, and the quantity of whole milk they drink.

It is logical to presume that if cholesterol tests were made routine for children and young male adults, and readings of 200 weren't considered safe, we could forestall a considerable number, and perhaps most, of our early coronary deaths.

All this, of course, would be predicated upon more sensible feeding, from birth up. If young men who have high blood-cholesterol levels would adopt a better choice of foods, exercise more, and avoid continued mental tension, we could win a major battle right now.

To emphasize the important point: You are not living a true heart saver way of life unless you keep your cholesterol readings below 200. Take advantage of the vital in-formation a cholesterol test gives you, until better checks and counterchecks come along.

FIND THE TROUBLEMAKER IN YOUR MEAL HERE ARE THE KITCHEN HEROES AND VILLAINS THAT CAN MEAN LIFE OR DEATH IN THE DRAMA OF HEART DISEASE.

EACH FOOD HAS its own particular kind of fat, which is always just as individual as the food itself, not only in taste and appearance, but in chemical composition. Each of these fat types plays a role in the unfolding of our great tragic drama: atherosclerosis.

The bulk of any fat is composed of three different kinds of fatty acids. It is these that you must know about, because one of the three is the big troublemaker that causes the blood-cholesterol level to rise.

Chemists class the fatty acids in the following three different groups:

a.            Saturated fatty acids, which we will call SATTS, or “hard”

b.            Mono-unsaturated   fatty   acids, which we will call MONOS.

c.             Poly-unsaturated fatty acids, which we will call POLYS, or “soft”

Fix those simple and convenient names in your mind—SATTS and MONOS and POLYS. Bacon fat differs chemically from the fat in peanuts by its ratio of the three different fatty acid classes, as shown by the following percentages:

Bacon;

Satts - 44       

Monos - 45 

Polys - 11

Peanuts              

Satts - 20

Monos - 52   

Polys - 28

Bacon fat is called a “hard” fat because the percentage of SATTS (44) is greater than the POLYS (11). Peanut fat is called a “soft” fat because the percentage of POLYS (28) is greater than the SATTS (20).

This is the way that chemists classify food fats into “hard” and “soft” fat types:

Whenever the percentage of SATTS in a fat is appreciably greater than the POLYS, the fat is called a “hard” fat. By the same token, a “soft” fat is one in which the POLYS predominate. The MONOS are considered neutral.

Your doctor views the fatty acids in a clinical sense because he knows that:

A /Saturated   fatty   acids   (SATTS) make the blood cholesterol rise.

B /Mono-unsaturated    fatty   acids (MONOS) neither raise nor lower the blood-cholesterol level.

C /Poly-unsaturated fatty acids (POLYS) tend to lower the blood-cholesterol level.

For heart saver eating, of course, we rate food fats by the same measure; and try to balance our fat intake so that the POLYS predominate in the diet, keeping our blood cholesterol at a safe level.

In the year 1952 there were only sure of two things:

1)      That the cholesterol in foods was not, in it-self, the cause of atherosclerosis;

2)      That the animal fats were in some way implicated. We didn't know the SATT-MONO-POLY story then. So, we could only make one recommendation for heart saver eating; viz., radically reduce the total fat intake.

This did help to lower blood-cholesterol levels, but the diet called for considerable will power, and it wasn't very pleasant to follow. How different with the heart saver diet of today! It can be much more varied, far tastier, and so much easier to carry out. Also, today you can take advantage of the most welcome fact that the soft-fat POLYS definitely help to lower the blood-cholesterol levels.

Please! Please! Be sure to acquaint your-self with the fatty-acid composition table included in this chapter. Get a good working knowledge of the SATTS and POLYS. It is good to know that pork is safer to eat than beef, while chicken is the safest meat of all.

You can feel happy about the fact that you are dodging a lot of SATTS when you cut away the fat from a piece of beef; or if instead of beef, you eat veal, which has so much less total fat.

Please understand that the term “hard fat” refers only to the chemical composition and to the relative percentage of SATTS and POLYS present. Melting a “hard fat” makes it soft physically, but it does not change the chemical composition. A melted “hard fat” is still “hard!”

Study the SATT and POLY line-up of all the oils listed. Actually buy and try several of the high-POLY type. See which best suits your taste. Then, learn to use it in cooking and recipe making. The more POLYS you can get into a recipe, the better it will be for your cholesterol levels. This will also enable you to have a greater quantity of hard-fat foods in your daily menus, and make your heart-saver eating more enjoyable.

Note particularly that milk fats are very rich in SATTS, and low in POLYS, Naturally, this includes the fat in ice cream, butter, and cheese made from whole milk, for these are all milk fats, one as hard as the other, and not at all good for your blood-cholesterol levels.

Get up to date on the margarine story, too. People who still maintain that margarine is safer than butter are one hundred percent mistaken, and behind the times. Margarine, which is an artificially hardened fat, is significantly harder than butter, and not quite so safe to eat.

A few years ago, when most authorities believed that cholesterol in foods was the coronary culprit, many people were advised to switch from butter to margarine because margarine contains no cholesterol whatever. However, as you now know, it is the SATTS that you have to look out for—and there are less SATTS in butter.

The fat in oleomargarine contains more SATTS (and thus is harder than the fat in butter) because it has been artificially saturated by the commercial process of hydrogenation. The same story holds for any and all of the white, solid shortenings, sold under various trade names. They are all made of fats which were once soft, but through this same process of hydrogenation, have been saturated and made hard. Peanut butter, when hydrogenated (and almost all better quality ones are) also falls into the same category.

When soft oil is made solid by hydrogenation, a big percentage of the POLYS present are turned into SATTS. Some of the MONos are also converted to SATTS in the same manner. And so, what was once a cholesterol-lowering fat becomes cholesterogenic: a word which means “sends the cholesterol up.”

Most of the soybean and cottonseed oils produced in this country are made into margarine and solid cooking fats. Natural soy-bean and cottonseed oils bring your cholesterol down. When hydrogenated, these same oils send it up! Note the difference in SATT percentages brought about by hydrogenation:

Satts -  Monos -  Polys

Soybean oil, before hydrogenation – 13 = 28 = 58

Soybean oil, after hydrogenation, and made into margarine – 52 = 2 = 27

Cottonseed oil, as you buy it – 27 = 22 = 51

Cottonseed oil, hydrogenated and made into solid shortening – 60 = 10 = 21

In each case, genuine soft oil is trans-formed by commercial processing into a very hard fat which, in its new form, is cholesterol-raising. This is perhaps one of the great nutritional tragedies of our time.

Hydrogenation has distinct commercial advantages. A cheap, soft oil can be factory-hardened and made to look and act like butter, which is far more expensive to produce. The factory prospers, and the housewife saves money. Hydrogenated shortenings are not only easier to work with, but stay fresh for a longer time than soft fat which, in its original state, tends to grow rancid.

A big percentage of our modern recipes call for the use of a hydrogenated fat because the recipes are more foolproof. It is easier for a housewife to obtain better results because the physical characteristics of a hydrogenated fat are apt to be more stable, particularly at the melting point.

When you can make a better cook of the average housewife, and save her money at the same time, you gain a tremendous competitive advantage.

The makers of hydrogenated fats are very heavy advertisers in women's and household magazines. The writers for these same publications also tend to push the use of hydrogenated fats. This may not necessary be for the express purpose of helping the advertisers, but simply because, in truth, the hydrogenated fats actually are simpler and more convenient for the housewife to use.

At any rate, for these and various other reasons, the use of hydrogenated fats in this country has grown by tremendous leaps and bounds some estimates place our average daily consumption at three ounces (90 grams) per person. We are literally loading ourselves with SATTS in our daily eating. Is it, therefore, any wonder that our coronary death rates are so high?

You can, in fact, trace a chart which indicates that in the United States the rise of coronary death rates has climbed in almost direct proportion to the use of hydrogenated fats.

Of course, this might not be a fair way to put it, because we consume more milk and dairy products, too. However, there is one thing we must again emphasize. If you, the homemaker, would henceforth use the soft, unsaturated oils as much as possible, in your cooking, baking, and recipe making, you would win a major battle in the fight to keep your blood-cholesterol level low!

HYDROGENATION

Hydrogenation is the process of artificially hardening soft oil by heating it to 200 degrees in the presence of a catalyst such as nickel. Hydrogen is then passed over it. The hydrogen molecules combine with certain free atoms in the unsaturated acids present, completely saturating, or hardening them.

For example, the abundant unsaturated fatty acids in cotton-seed oil can be made to pick up hydrogen. The oil becomes hardened or solidified, resembling lard.

This type of cooking fat made from different oils has become most popular in American kitchens, because, among other things, it doesn't spoil easily or pick up doors. It is often more satisfactory to use.

FATTY ACID COMPOSITION TABLE

Carefully check the percentage of SATTS, MONOS, and POLYS in the following list of foods. The higher the percentage of SATTS in a fat, the more cholesterogenic (cholesterol-raising) it will be. You'll see at once why the fat in beef is so apt to raise the cholesterol level, and why chicken is the best of the heart saver meats. You'll see why cheese, ounce for ounce, is far more cholesterogenic than eggs.

Keep this Table as a reference in planning your heart saver eating, and remember, please, that all figures given are only averages. The fatty acid composition of any class of food varies slightly according to circumstance—how the animal was fed, where the cereal or vegetable was grown. Thus, a corn-fed hog may yield a lower percentage of SATTS, and a higher percentage of POLYS than a hog fed on city slops. We need only to concern ourselves with averages to safely balance our diet

Satts     Monos      Polys

Animal Fats                                      

Beef - 53 = 41 = 6

Lamb – 42 = 53 = 5

Lard – 39 = 48 = 13

Mutton – 52 = 42 = 6

Pork – 44 = 45 = 11

Suet – 56 = 40 = 4

Veal – 41 = 56 = 3

Satts     Monos      Polys

Variety Meat Fats                                            

Beef Heart – 44 = 44 = 12

Beef Liver – 40 = 20 = 40

Lamb Liver – 49 = 26 = 25

Pork Liver – 35 = 21 = 44

Satts     Monos      Polys

Poultry Fats                                       

Chicken – 25 = 51 = 24

Duck – 29 = 49 - 22

Goose – 26 = 51 = 23

Pigeon (squab) – 24 = 52 = 24

Rabbit – 39 = 45 = 16

Turkey – 27 = 50 = 23

Satts     Monos      Polys

Fish Fats                                             

Fresh Water – 24 = 00 = 76

Salt Water – 21 = 00 = 79

Shell Fish - Practically Fat     Free

Satts     Monos      Polys

Dairy Product Fats                                          

Butter – 59 = 38 = 3

Cheese – 58 = 39 = 3

Cream – 59 = 38 = 3

Eggs (hens) – 37 = 52 = 11

Ice Cream – 59 = 38 = 3

Milk (cow's) – 60 = 36 = 4

Satts    Monos    Polys

Vegetable Fats                                

Chocolate – 54 = 43 = 3

Cocoa – 51 = 46 = 3

Coconut – 94 = 5 = 1

Satts     Monos      Polys

Grain and Cereal Fats

Corn – 15 = 35 = 50

Oats – 11 = 58 = 31

Rice – 18 = 47 = 35

Rye – 22 = 60 = 18

Wheat – 15 = 26 = 59

Satts     Monos      Polys

Salad and Cooking Oils

Corn – 15 = 28 = 57

Cottonseed – 27 = 22 = 51

Linseed – 10 = 54 = 36

Olive – 10 = 75 = 15

Peanut – 20 = 52 = 28

Safflower – 11 = 10 = 79

Sesame – 12 = 42 = 46

Soybean – 13 = 29 = 58

Sunflower – 9 = 16 = 75

Satts     Monos      Polys

Nut Fats                                              

Almonds – 7 = 75 = 18

Brazil – 16 = 56 = 28

Peanut – 20 = 52 = 28

Pecans – 5 = 77 = 18

Walnuts – 5 = 32 = 63

Satts     Monos      Polys

Miscellaneous Fats

Satts     Monos      Polys

Home fats – 45 = 49 = 6

Margarine – 63 = 31= 6

Shortenings – 25 = 66 = 9

In principle then, certain oils are made soft by the presence of the POLYS, which have the happy faculty of washing cholesterol out of the blood.

The higher the percentage of POLYS, the more effective the particular soft fat will be in acting to reduce the blood-cholesterol levels.

There is also good reason to believe that a high-POLY diet can go even further; and help to clear already existing deposits of fat and cholesterol from the blood vessel walls.

One thing, however, is certain. We know enough about the blood-cholesterol story to pinpoint the basic principles of heart saver eating.

a.            It is entirely possible to live safely on a diet which includes hard fats (SATTS), providing that soft fats (POLYS) are eaten in slightly greater proportions.

b.            This principle seems to work in a mathematical ratio, so when you eat more POLYS than SATTS, your diet can be called anti-cholesterogenic.

Whenever you eat foods containing hard fats, eat some soft fats in the same meal by way of salad dressings, gravies, or sauces. For every ounce of hard fat that you eat, try to offset it with one ounce of the more highly unsaturated fats. (See Table)

Do not, under any circumstances, eat too much fat—even the softest kind! There is always the calorie count to concern you, and the several body disorders that can result from an over-indulgence in fat of any kind—gall bladder trouble and skin afflictions, to mention only two. Your diet should always be balanced for health.

It has been calculated that for real well being, the calories derived from all fats should not exceed 25 percent of all the calories you consume.

Sometimes, in actual clinical practice, doctors find that they are unable to appreciably reduce the cholesterol levels of certain patients by juggling the POLYS and SATTS. They can only achieve satisfactory results by reducing the total intake of fats.

This happens because certain people are so geared that it is difficult for their body metabolism to clear the blood of an excess of any kind of fat. In such cases, the doctor has to keep the patient on a very strict diet— low in both hard and soft fats.

Because the fatty acids (both hard and soft) of animal and vegetable fats alike occur mainly in “triglyceride” form; a diet restricting all kinds of fat is called a “low triglyceride” diet.

Forget the term “triglyceride” for a moment. By any name, there is a definite coronary and apoplectic threat when too much fat of any kind gets into the blood. (Recall that the blood becomes “milky” with fat droplets when you eat a fat-laden meal.)

Not all the fat in the blood is made into lipoproteins. The free fat which circulates in chylomicron form is hard to get rid of, sometimes lingering in the blood for many hours after a meal. This hazard increases as people grow older—and the ability of the blood to clear itself of fat is always delayed in individuals with atherosclerosis.

The presence of a lot of fat in the blood causes it to become sticky and slow moving. The blood cells develop a tendency to clump and, as shown by tests, clot more readily. Both apoplexy and coronary attacks are often precipitated by small clots completely stopping up arteries already narrowed by fatty deposits.

So, as you can see, there are several very good reasons for balancing the diet as far as total fat intake (triglycerides) is concerned.

Some of the “crash” and formula reducing diets are vicious in this respect. They literally swamp the blood with fats. Many of the old-time therapeutic diets, high in fats, had the same dangerous defect. Ulcer diets are an example—rich in cream and whole milk.

It is not unusual to find cholesterol levels of well over 300 among patients living on a typical, old-fashioned ulcer diet. Several of the standard diabetes diets depended mostly upon fat for calories—and the patients died of coronary disease.

The diets which offended in this respect are rapidly being revised, but this newer knowledge may be a long time getting into print. Meanwhile, be guided by these maxims: Have your cholesterol levels checked frequently when you are on any rich diet! Never follow any fat-rich diet for an extended length of time!

Last, but not least: The coronary rule, like all others, has its exceptions. At least one individual in this country has been eating a diet very rich in hard fats for many years, and hasn't yet had a coronary attack. Valdimar Steffanson, the famed explorer, has made a career out of his unique ability to thrive on proteins and fats.

Those who still won't admit that a high-fat diet can cause coronary disease are making great capital of the Steffanson feat. He does eat a lot of meat and fat, and he has lived to a ripe old age. We've heard tell that, for several years now, his cholesterol readings have been well above the 400 level.

Lucky man! For apparently he is endowed with a built-in immunity to cholesterol disease. But, let's not take this one man's good fortune as a guide to our way of living.

Steffanson gets by with his high-cholesterol living—the overwhelming majority of Americans won't. There are the ten million coronary cripples now living in the United States to prove that Steffanson is only one great exception.

At least one million people will have a coronary attack globally in the year ahead, and they too will prove the same point. Undoubtedly, some men will still continue to hope that they have the Steffanson talent. On the day they suffer a coronary attack, they will discover—too late—that they are cast in the same mould as the rest of us.

The Steffanson saga proves only that there are exceptions to every rule. To gamble that you, too, are so physiologically geared, is betting your life at fantastic odds. The chances against your winning are at least ten million-to-one.

If any of you are going to fret about your chances of developing a coronary heart attack, here are some comforting facts which will count on the credit side of your coronary ledger. Being lean and lanky or at least long boned helps! Short, stocky, square-built individuals seem to be definitely more prone to develop coronary disease.

Tall or normally built individuals have better chances of escaping coronary disease or, at worst; they are more likely to develop it at a much later age.

There has been a lot of study done in this field but of course more facts and determinations are needed. It comes under the heading of Anthropometry: the science of measuring the human skeleton and various body parts, and relating them to health and disease. Researchers are gathering these and various other biological facts and correlating them with blood chemistry studies to the point that today a doctor can expertly single out the prime candidate for coronary disease.

He can say with authority to some patients, “You are a marked (coronary prone) man!”

There can be little doubt that hereditary factors, too, weigh heavily for or against your coronary fate. If you are from a family where coronary disease has often taken a toll, it definitely counts against you.

If this has happened on both sides of your family line, the doctor calls another coronary “strike.” A “bad” heredity means that you must be doubly careful of your satt and poly intake, and just that much more conscientious about getting adequate exercise, avoiding tension, and generally leading a prudent heart saver life.

Now, let's go on to clinch the evidence that an excess of hard fat in the diet can cause coronary disease.

STARTLING PROOF YOU CANT IGNORE RID YOURSELF   OF   ANY DOUBT, AND   TAKE   HEART FROM THIS POSITIVE EVIDENCE.

I N THE SPRING of 1958,a team of Harvard medical scientists furnished the final, incontrovertible proof that a surplus of cholesterol in the blood stream can, and does, cause coronary disease.

The scientists took little bits of blood vessel wall tissue, and kept them alive in a culture medium (which, in a real sense, means an artificial blood). They then began to add tiny drops of cholesterol to the feeding mixture—which, let us remind you again, corresponds to blood.

In four or five days, fat deposits formed in the blood vessel cells. By check-testing, they soon found that the size of the fat deposit in the blood vessel wall was directly proportional to the amount of cholesterol added. If the blood vessel cells were allowed to remain in the cholesterol-fed medium, the fat deposits soon increased to such size that the blood vessel cells finally withered and died.

Mind you, the doctors actually watched cholesterol produce blood vessel disease, but the experiments went much further. They found that satt-rich stearic acid, which occurs in certain animal fats, aided and abetted the formation of fatty deposits and caused them to increase rapidly and markedly in size.

Then the researchers did an even more astonishing thing. They added linolenic acid, a rich, primary source of polys, to the culture medium, and cholesterol as before; but the fat deposits didn't form! Thus, they proved experimentally, with live human tissue, that the linolenic-acid polys could offset and counteract the effects of cholesterol, and keep it from forming deposits in the blood vessel walls.

The team continued the experiment. Was the action of the linolenic-acid polys more than protective and preventive? Would the polys actually decrease the size of the deposits which had been laid down in blood vessel cells? This is what they found.

Once a deposit of fat had been formed, the more linolenic acid added to the culture medium, the more the size of the deposit decreased. This can also be interpreted in another sense; viz., the more polys in a fat, the better it will work in preventing “The Grease Trap Disease,” and diminishing the size of fat deposits already formed.

However, don't take this to mean that you can simply swallow linolenic acid, or any other rich source of polys, and magically cure yourself of coronary disease.

Your fat intake still has to be “balanced.” Remember that an excess of any kind of fat droplets in the blood stream can also cause trouble; and remember, too, that the blood becomes sticky and sludgy, and clots more readily, when you eat too much of any kind of fat. So, keep your total fat intake down.

Remember this, also: These experiments were done only with initial fat deposits, newly formed in the blood vessel cells. There had been no chance for the deposit to become “set,” or for secondary changes to occur.

Usually certain length of time after humans develop a plaque, scar tissue forms in the blood vessel wall at the site of the spot. Later, the spot may be encrusted with calcium as a further protection.

In short, several changes eventually take place in the blood vessel walls which probably wouldn't be affected by linolenic acid, or abundant polys from any source. Obviously, however, fat plaques which haven't yet been “fixed” with calcium and fibre can at least be partially absorbed and cleaned out—when polys predominate in your diet.

Linolenic acid is an integral part of many fats, but much more abundant in some cereal and vegetable oils, than in others—especially corn, cottonseed, and soy bean oils. Several nut oils are made soft, and rich in polys, by the presence of linolenic acid; and by the same token all hard fats, whether they occur in meat, milk, or cheese, are very low in their content of linolenic acid.

So much for the nutritional, chemical, and physical reasons why a diet high in the satts found in hard fats can cause coronary disease. Call them scientific reasons, if you wish. But, in actual practice, what happens to men, to women, or to nations of people the world over on a low-fat poly-rich diet?

One of the most striking features of population studies is the consistent ratio between frequency of atherosclerosis and the percentage and amount of hard fat eaten.

The inhabitants of Costa Rica scarcely ever show signs of atherosclerosis on post-mortem examination. They live on a diet which is very low in fat, practically all of it soft fish-fat, a rich source of polys.

The inhabitants of Okinawa are also extraordinarily free of this type of degenerative disease. Their diet, too, is low in fat; and again mostly soft fish-fats, loaded with polys.

The ailment is extremely rare among the Chinese, who live mainly on rice and eat very little fat, mostly soft sesame oil, abundantly endowed with polys. Ditto for Ceylon. The Japanese eat far less hard fats than we do; consuming mainly soft fish-fats. Their coronary death rate for men, aged 55 to 59, is one-fifth of ours.

The Bantus of South Africa eat one-tenth the amount of hard fat that we do, and their coronary death rate is one-tenth of ours. Population studies in Hawaii and Iraq also confirm the satt-hard-fat, poly-soft-fat, low-fat story.

Perhaps the most telling studies have been those which show a startling difference in coronary death rates among people of the same nation, who are eating larger amounts of hard animal-fat than are their friends and neighbours. Prosperity and income has much to do with this.

Rich Spaniards, living in Madrid, have high coronary death rates; poor Spaniards, also living in Madrid, seldom die of the disease.  And so do we find corresponding differences in the rich and poor of Guatemala. The Japanese who live in Hawaii and Southern California have higher coronary death rates than those who live in Japan.

The Italians who live in the United States have much higher coronary death rates than those in Naples or Rome.

When people have more money, they buy more meat, milk, and eggs. When emigrants leave their native lands to live in the United States, their coronary death rate climbs in a few years to equal that of average Americans. There can be only one reason—they eat as we do.

We are not the only nation in the world to serve as a horrible example. There are one or two smaller groups that qualify. The Kirghiz plainsmen of Asia, for example, live mainly on meat and milk, rich in the hard fats, and they are notably subject to death very early in life from apoplexy, coronary disease, and other forms of AHD.

The most convincing evidence that modern principles of heart saver eating are sound and right may be found in a wealth of data gathered by the World Health Organization and the Food and Agricultural Organization of the United Nations. Studies made in twenty nations of dietary habits and coronary death rates of men aged 55 to 59 show facts and figures that should lead even the sceptic to try for a balanced poly-satt intake.

The data shows hard-fat consuming nations lead the coronary death parades—the United States, Canada, Finland, and Australia. Portugal vies with Japan and Ceylon for honours as a coronary-free country—with a dietary ratio of hard to soft fat high on the safe side. The Portuguese eat upto30 percent more polys than satts, thanks to a love of olive oil and fish.

In Norway, too, fish swing the balance. Statistically, the Norwegians eat a bigger proportion of polys than satts. Their coronary rate is one-third of ours.

Frenchmen do an amazing job of escaping fatal coronary attacks. Their death rate is roughly one-sixth of ours—eating only two-thirds the fat we do. The difference, it appears, is in the fact that with their meals they prefer wine to whole milk!

West Germans, with a coronary death rate approximately one-fourth of ours, have a fat-intake balance superior to ours—the polys almost offsetting the satts. They differ from us by preferring beer to milk as a meal beverage.

We realize that an unthinking few may charge us with making a case for the use of alcohol. Such is not our purpose or intent. We want only to help save you—and your loved ones—from the terror of coronary disease. We must wage war against an excessive intake of hard fats—regardless of the food or its component nutritional virtues.

Milk would be an ideal beverage were it less laden with the satt-rich fats ordered by state and federal laws—which could be and should be amended. We will take a major public health step against coronary disease when we lower the legal butter fat content of whole milk as sold and delivered.

Never in public-health history has there been such worldwide statistical proof of a medical fact; namely, that there is a direct relation between the amount of hard-fat satts eaten and the rate of coronary disease.

Such a mountain of evidence exists that no thinking individual can disregard it. There can be —and should be—such an endeavour as heart saver eating!

You will find “authorities” who loudly proclaim that the fat facts haven't been proven. At best, they are sadly and hopelessly mistaken, or badly misinformed. At the worst, you may find that they have an axe to grind; and you can usually ask your-self—which side is their bread “buttered” on?

The business of producing and selling hard fats runs into several billions of dollars a year. It is not in the nature of profitable business to give up without a fight!

ATHEROSCLEROSIS IN ARTIFICIAL ARTERIES

Surgeons have developed an amazing technique whereby atherosclerotic patches in certain arteries can be removed and replaced with plastic materials.

It was hoped that such artificial blood vessels might help to solve the coronary problem. However, detailed research showed that high-fat, high-cholesterol diets caused patches to form in the plastic blood vessels, just as they did in the real thing.

DIFFERENCES IN FINLAND

Three tremendously important, recent diet studies made in coronary-plagued Finland help to explain why Finlanders living in the eastern part of the country have higher cholesterol levels and a correspondingly higher coronary death rate than those who live in the western part of the country.

Western Finns ate slightly less of the hard fats and proportionately more of the soft fats than those who lived in the east. West Finns ate more foods containing Vitamin E, more foods containing Vitamin C. They were much less subject to the type of goitre caused by an iodine lack.

A HEART LESSON FROM ISRAEL

When Lord Balfour and England paved the way for what is now Israel, the immigrants came mainly from the countries of Europe, the Middle East, and the United States. A scant few thousand came from the ancient land of Yemen, and were gradually absorbed.

By this, we mean they abandoned their old ways of living. They were led away from the simple life they had been living, no different in essence from that of the Biblical Jews.

In Yemen, their diet consisted largely of bread and vegetables of various kinds. They ate meat rarely, scarcely ever drank milk. Only one of their dishes called for butter. They had never heard of margarine or hydrogenated fats.

After a few years in Israel, they began to eat as their compatriots did. It had been a well-known medical legend that coronary disease was practically unknown in Yemen.  This was later substantiated by intensive local research, while concurrent studies indicated that the Jewish people living in Europe were particularly susceptible to the ravages of coronary attack.

Some four or five years ago, events took place in Yemen which led to a tremendous exodus of Jews. Yemenites flocked to Israel by the thousands—men and women of simple habits, not yet initiated into modern eating, and pace of living. Here was an unparalleled opportunity for doctors to study people who had lived on about one-tenth as much hard fat as we customarily eat.

A large-scale investigation was undertaken, with controlled scientific techniques. Two classes of Yemenites were compared. A group which had lived in Israel less than five years was checked against an equal number which had been there for more than twenty.

The first group, not yet weaned away from their old way of eating, had very low blood-cholesterol levels. The readings in the second group were relatively high.

The coronary death rate of Yemenites who had lived in Israel more than twenty years proved to be six times that of the five-year group. Every bit of medical evidence went to show that the tremendous difference in the coronary picture was definitely linked to foods.

The only difference in the status of the two groups was the length of time they had lived in Israel. Their heredity was exactly the same. Their body builds were equal and, while they dwelt in Israel, they lived under the same stresses and strains.

Their work, their joys, their sorrows, by and large, was practically the same. The only demonstrable difference which could be found in their existence was in the food they ate.

The Yemenites who had lived in Israel longer ate less bread and vegetables; more meats and richer dishes. Statistically, they ate from five to ten times more total fat than they did before they came to Israel.

They learned to enjoy “civilized” menus and foods such as whole milk for everyday use, corned beef, and sour cream. They changed their diet to the American-European pattern, and their coronary death rate dutifully followed suit.

ONE MEAL ALONE CAN BE A KILLER THEY USED TO CALL IT “ACUTE INDIGESTION" BUT “HEART ATTACK” IS THE RIGHT TERM FOR IT. AND ONE SIMPLE MISTAKE IN EATING CAN BRING IT ON.

THIS IS THE SAGA of angina pectoris, an excruciating heart pain which spells heart attack, and which can be caused by a single fatty meal.

Angina pectoris is not a disease in itself —only the name given to the pain which results when the blood supply is shut off to some part of the heart. Thus, a true angina pain signifies that one of the coronary arteries is not supplying the heart with enough blood.

This, of course, is a coronary attack —in the true sense of the word! Remember this truth, without fail, for many men and women have experienced a mild angina attack, and written it off as unimportant.

Angina pectoris is always of consequence, because at present it is the most positive evidence that the coronary arteries have narrowed to a dangerous degree.

Remember, too, that while it has been clearly described in textbooks of pathology for the past hundred years, coronary disease still can't be positively diagnosed until an actual attack has occurred.

In 1912, Dr. Herrick, of Chicago, wrote a masterful description of the symptoms which characterized a coronary attack. Thereafter, an attack itself was occasionally recognized, but not nearly as often as it should have been.

The fact that a coronary artery is filling up with fat cannot as yet be detected by any physical sign. It can only be suspected when the blood-cholesterol levels are consistently high.

This again highlights the fact that a true angina attack is the most positive proof that the coronary arteries are narrowed.

In the early 1920's, the electrocardiograph apparatus was brought to this country. From that time on, a doctor could tell for sure if a patient had suffered a coronary attack. Also, thereafter, it was clearly recognized that angina pectoris is always a sign of coronary disease.

At any rate, in 1930, coronary disease was given a separate category in the official causes of death. Since 1940, it has been agreed that all deaths listed as angina pectoris must rightfully be ascribed to coronary disease—another mystery solved by knowledge.

It is equally certain that probably 100 percent of the deaths once ascribed to “acute indigestion” were the result of a coronary attack. Mary Tudor, Queen of England, died suddenly while hearing Mass— after a rich, heavy dinner. Ivan the Terrible, who sat quietly playing checkers after a heavy meal—suddenly uttered a stifled cry and fell back, dead.

The doctor called it “acute indigestion.” We now know that the great religious leader died as the result of a coronary attack.

Even as late as the final days of William Jennings Bryan, who died at the conclusion of the Scopes trial, July 21, 1925 (after gorging himself on sandwiches), many newspapers carried the headlines, “BRYANT DIES OF ACUTE INDIGESTION.”

Now, here again is something you should never forget for one moment!

It has been positively shown by several dramatic experiments, that one fatty meal can cause a coronary attack!

The first of these “proofs” was published four years ago. Page 1008 of the July 23, 1955 issue of The Journal of the American Medical Association, featured an article by Drs. Peter T. Kuo and Claude R. Joyner, Jr., of Philadelphia, under the title:

ANGINA PECTORIS INDUCED BY FAT INDIGESTION IN PATIENTS WITH CORONARY ARTERY DISEASE

The text which followed described a carefully controlled scientific experiment in which the investigators actually produced angina pectoris in six human beings, solely by feeding them one meal rich in fats.

The doctors presented undeniable proof that an increase in the amount of blood-fat can clog up the coronary arteries and produce a coronary attack in a person who already has “The Grease Trap Disease.”

The Kuo-Joyner subjects had a doctor at their side. You with plaques, or a history of angina or a diagnosed coronary attack, are not likely to be so lucky. You may unsuspectingly eat a meal rich in hard fats, wend your way to the theatre, or lounge contentedly in front of your television set.

Then— with lightning suddenness—you may feel the vise-like constriction in your chest. The high level of fat in your blood has closed your n