Chapter 8
Coronary Disease

'Tu. ch'hai la bocca dolce ...
Tu che il zucchero porti in mezzo al core ...
(You, whose mouth is sweet ...
And who instil sugar into the depths of the heart ...)
-- Serenade, Mozart's 'Don Giovanni'

THIS condition has been left till late, because the inclusion of coronary disease amongst the manifestations of the saccharine disease will be seen to depend rather on general reasoning than on specific reasoning. For with each of the other conditions studied hitherto the mechanism of production of the condition shows up quite clearly, but with coronary disease this is not the case. Therefore, reasoning of a more general order will be submitted on this occasion -- which necessitates some consideration of the other conditions studied in this work.

It should be added that in these discussions it is accepted that differences in the pathology may reflect a rather different mechanism of production in the terminal thrombosis from that in the accompanying atherosclerosis, but as this is not a work on pathology such differences will not be pursued here, for that would interfere with the clarity of the general line of reasoning.

I. Coronary Disease, Human Evolution, and the Consumption of Fats

It will be advanced in this chapter that only an evolutionary approach to the tremendous and undiminished problem of the cause, prevention, and arrest of coronary disease is able to afford a solution sufficiently secure, and sufficiently quick, to be of any value to those alive at the moment. Prolonged investigations may help future generations, but not, it is submitted, our own. That the problem is a tremendous one is shown by the disease having now reached epidemic proportions, so that at present it accounts for a quarter of all deaths in the United Kingdom, [1] and in Scotland has become the commonest cause of death under the age of 35.

And that the problem remains undiminished is shown by the collective results of preventive dietary trials to date, which have centred on fat consumption, being essentially equivocal. [2, 3, 4] For example, the prolonged Framingham trial in the United States, that concerned itself mainly with fat consumption, has not achieved a convincing result, nor have similar trials in this country. A recently published trial in a mental hospital in Finland, [5] also interfering with fat consumption, does not, in the author's opinion, surmount the criticisms passed upon it [6, 7] over coincident differences in sugar consumption (which consumption, it may be observed, was far above the natural [i.e., evolutionary] level). Indeed he, himself, would regard these results as not only not invalidating the arguments presented in this chapter, but also as unlikely to be considered in a free society as an adequate inducement to forgo natural tastes and pleasures in the eating of fats. These criticisms have very recently been added to by M. Halperin and others (Lancet, 1973, 2, 438, 439).

That the problem remains undiminished is also shown, it is submitted, by the sombre fact that our own profession suffers from coronary disease just as much as does the rest of the population, and quite possibly more so, to judge by the last figures available from Somerset House. [8]

In the following pages it must be taken as very clear that it is not in any way the author's solution that is being put forward, but Nature's own solution (to use again the convenient term, Nature, for evolutionary adaptation). And in this connexion it is suggested that right at the start there is borne in mind the wonders of the heart as a machine -- a machine unparalleled, a machine whose action-cycle is repeated 100,000 times a day for 70 years, without a single refit or a single servicing. For a sense of wonderment is a valuable promoter of a sense of reverence, and without a sense of reverence for the body in general, and for the heart in particular, the following lines of reasoning can scarcely produce an impact on the mind of the reader.

From the above preliminary remarks it is beyond a doubt that the only chance of the heart preserving its structural integrity (that is, as a machine, continuing in serviceable repair) must lie in the meticulous maintenance of its natural environment -- the environment achieved by evolutionary trial and error over many millions of years. And since the environment of the heart consists essentially of the blood-stream, and since the constitution of the blood-stream is basically dependent on the type of food eaten, it is above all on the naturalness of the food that the structural integrity of the heart must ultimately depend. Herein, it is submitted, lies the key to the solution of the coronary problem, and in the following pages, which are an expansion of a much earlier work of the author's [9] on the same lines, it will be shown to what extent the evolutionary approach is being departed from, and even actively thwarted, today.

Evolution and Fat Consumption

The most glaring example of this departure from evolutionary principles is seen in the present-day interference with the fats in the diet, as already referred to. It is argued that because in coronary disease there tends to be an increase in some of the lipid, that is, fatty, components of the blood, such as cholesterol, and because this substance is also prominent in any atheromatous plaques that may be present, it is the fats in the diet that are in some way the cause of the trouble. Now, many consider that in coronary disease any pathological changes involving cholesterol are an associated, not a causative, event, similar to the deposition of cholesterol crystals in inflammations of the middle ear, but if cholesterol did play a causative role in coronary disease, would this be in conflict with the present conception, which will be seen shortly to involve the refined carbohydrates? The answer is no, for the following reason.

In the first place, cholesterol is not the only blood lipid that may be implicated in coronary disease. There are others, including the triglycerides, which are increasingly regarded as significant. [10] And though animal fats in the diet are well known to increase the blood lipids, sucrose in the diet is also becoming known to do this, especially as regards the triglycerides. A considerable and controversial literature, indeed, has accumulated on this latter point (involving sucrose and the triglycerides), I'll but the truth is that the relationship of any one component in the diet to the blood lipids is liable to be controversial. [12] One reason for this lies in the difficulty over the controls, as set out in a later paragraph in this chapter. What is least controversial [12] is that any over-consumption of food and consequent energy imbalance, often leading to obesity, and to pre-diabetes and diabetes, is especially prominent in increasing the blood lipids, particularly the triglycerides. And it is here that the present conception enters the picture.

For the present conception holds, as seen in Chapters II and VI, that the absolutely dominant cause of over-consumption of food, itself leading to obesity and diabetes, lies in the concentration produced in the carbohydrates by refining processes. If in due course this contention becomes accepted -- that in over-consumption Nature does not make a mistake, but is deceived in the sensations of hunger and satiety by the unnatural concentration present in products like sugar and white flour -- then the refined carbohydrates will emerge as not only the dominant cause of over-consumption but also of an increasing rise in the blood lipids. And this regardless of the capricious and controversial results of individual tests involving fat, sugar, etc. Whether, as stated above, the increase in blood lipids is causative in coronary disease, or merely associated with it, will be referred to again later.

However, it is not with these biochemical trees that we are mainly concerned at the moment, but with the evolutionary wood. Those who incriminate animal fats in raising the blood lipids and causing coronary disease would have us stop eating the fats that we have been eating from immemorial time, such as the fat found in meat and in the butter and cream derived from milk, and eat instead a whole lot of new oils, mainly expressed from vegetable seeds, many of which oils are alien to us. The reason this substitution is recommended is because these oils contain greater amounts of polyunsaturated fatty acids, which when eaten increase the blood cholesterol little or not at all compared with their saturated analogues present in animal fats; and which are also considered to be more valuable to the body structurally. Indeed some, such as H. Malmros, [13] would have the above substitution carried out on a national scale, and in certain countries, like Australia, the very dairy industry has been threatened. Let us therefore look into this substitution more closely, from the evolutionary point of view, as suggested earlier by the author. [14, 15]

The keeping of flocks of sheep, herds of cattle, and other domestic animals, in order to provide a continuity of meat and milk, started with neolithic man many thousands of years before the Christian era, and even only 1500 years before that era Moses, in the Bible (Deuteronomy 32.14), was stating that Jehovah gave to his people to eat 'butter of kine, and milk of sheep, with fat of lambs'. It is true that the consumption of fat in some parts of the Old Testament is forbidden, but this is always in connexion with the making of burnt offerings, the fat being needed for the performance of this act. It was once explained to the author by a guide of the great temple at Karnak in Egypt that every particle of these burnt offerings was eaten by the priests. And no one reading the first ten verses of the seventh chapter of Leviticus can doubt that the guide was right. To these ancient fats we are therefore well adapted, quite apart from man, as a hunter, being well acquainted with the fat of animals in evolutionary times far more remote than the neolithic ones.

Contrast with these ancient fats the new oils, mainly expressed from vegetable seeds. Not only are many of these seeds not a natural food for man (e.g., cotton seed and sunflower seed -- and incidentally the sunflower does not even come from the Old World, as we do in the British Isles, but from the New), but also the oils expressed from many of them never existed in any quantity before the invention of the modern hydraulic press or the new solvent procedures, and consequently were scarcely eaten in this country before the introduction of margarine, circa 1916, during the First World War. Evolutionarily these oils make us not so much men as the equivalent of a flock of greenfinches, and the evolutionary incongruity is heightened by the fact that the coronary explosion amongst us, as will be seen later, came in since the introduction of just these oils at the period stated, though in margarine they are often saturated by a stream of hydrogen.

Evolution and Grass-fed Animals
At this stage we must digress to discuss an important point. Some have objected that the animal fats may be distorted by stall-feeding of the animals themselves. But even M. A. Crawford [16] has pointed out that the amount of polyunsaturated fatty acids in the fat of the domestic pig, which is perhaps the most stall-fed, as it were, of all the domestic animals, is some four times the amount in the fat of domestic cattle, largely fed on grass, and in the milk and butter obtained from cattle. However, let the battle be fought out where no stall-feeding is in question, as in the case of sheep. Not one of those who advise that animal fats be replaced by vegetable-seed and similar processed oils makes an exception over mutton fat, for this is a typical saturated fat. We are advised not to eat the mutton fat of grass-fed sheep, though we may love it. And this is the evolutionary crux -- the thwarting of a natural taste for a natural food.

Indeed, an elaboration of this point arises here, for Crawford, [17] having been at great pains to demonstrate that domestic animals, like cattle and sheep fed on grass, have much more fat between the muscle fibres ('marbling fat') than in the case of their wild counterparts, has suggested that eating the meat of these grass-fed animals may hold dangers for us, since it may be akin to taking into the body pathological material, or 'eating obesity', as he has called it. But it is contended here that evolutionary considerations show this argument to be in serious error.

For though it is true that large numbers of domestic cattle (and still larger numbers of sheep, as already said) are fattened up for market in this country on grass, it would not be possible to fatten up wild cattle in this way, any more than it would be possible to fatten up a wild rabbit on grass as compared with the various breeds of hutch rabbit. No, it has taken very long periods of selective breeding to evolve animals that will behave in this manner. The situation is even better seen in the case of domestic ducks, most of which cannot fly off the ground. This is true, from the Aylesbury duck in this country to the flocks of domestic ducks seen along the rivers of China, each flock attended by a small boy. Thousands of years of selective breeding have been needed to replace muscle by fat to this extent (and the same period of time has been available for some adaptation in man to such food ). We must, therefore, very sharply distinguish this evolved fat (using 'evolved' in its transitive sense) from any fat that is remotely pathological. Else we shall be banning our best eating apples because they are so far removed from crab-apples, and our best wheat because it is so far removed from the primitive ancestral grasses. And it should be added that it is the above 'marbling' with fat that is partly responsible for the taste in lean meat; [18] without it there is a tendency for lean meat to have a watery taste.

Why do our tastes seek to increase the fat in animals and birds in the above manner (for who would compare the pleasure in eating most wild ducks with that in eating an Aylesbury duck)? The answer must surely be that, just as the body seeks in every posture, and in every activity, to economize muscular action, in order to minimize work on the heart, so also it seeks, by increasing in meat the ratio of fat -- a food that is completely combusted -- to minimize work on the kidney, an organ that plays so big a part, via the blood-pressure, in the length of life in each one of us. We should do well not to dismiss this frequent preference for fat from our reflections, which is present in perhaps a minority of people -- but a very important minority.

But Crawford [16] attacks not only the quantity of fat, but also the quality, in grass-fed animals. He points out that the fat in domestic cattle is more saturated -- i.e. has a higher ratio of saturated fatty acids -- than occurs in the fat in wild African cattle feeding on a more varied diet. Yet his list of wild animals includes the Uganda kob, of the plains, with the identical fatty acid ratios present in our own cattle and in the milk and butter obtained from them. Is it to be supposed that we should come to harm, especially coronary harm, if we often ate the African kob?

Furthermore, nearly all the fat we eat is combusted for heat, only a small part being retained for structural replacement. Why should not the body combust the fat that is less valuable and retain for replacement the fat that is more valuable, just as it does so miraculously with other foods? How quickly do scurvy and other deficiency diseases disappear directly the missing substances appear in the diet!

It may well be, in fact, that sometimes the body may prefer a high ratio of saturated, combustible fat. It will be recalled that only some 67 years ago Metchnikoff, [19] Director of the Pasteur Institute, in his Prolongation of Life directed the attention of all Europe to the longevity of certain Bulgarian peasants living on milk and milk products -- which abound in saturated fats. The influence of this work is still with us today, as seen in the common taking of yoghurt, and stands as a perpetual challenge to those who would have us depart from eating natural foods, naturally desired.

Far from indicating, therefore, that the substitution of unsaturated vegetable and other oils for saturated animal fats has any value in the prevention and arrest of coronary disease, the evolutionary approach points to the exact opposite -- and in addition points to the following danger. For, as touched on above, it was not until the invention of the modern hydraulic press, or the new solvent procedures, that cotton-seed oil and some other processed oils ever appeared in any quantity on the surface of this planet. With the exception of olive oil, few of them, as already stated, were eaten at all before the First World War. The question, therefore, arises as to whether the consumption in large amounts of substances that are essentially alien to the human body carries any risk with it -- especially the risk of cancer, which always tends to be related to substances foreign to the natural environment. This risk would certainly not be lessened by the passing of a saturating stream of hydrogen through some of these processed oils, in the interests of achieving a greater solidity for table use, as in margarine.

It may therefore be no coincidence that in a recent dietary trial in the United States, [20] involving just the substitution in fats now under consideration, there appeared an undue occurrence of cancer cases. Years of observation, or careful animal experiments (of which the results to date are not wholly reassuring [21] ), may or may not throw further light on this event, but what is important is the principle involved. It is submitted that no one who has any reverence for the human body, as set out at the beginning of this chapter, will ever choose to substitute these new processed oils for animal fats of ancient lineage. What economic forces dictate, alas!, is another matter.

Before concluding this part of the present chapter the author would add that he, himself, no longer attaches much importance to the condition of essential (familial) hypercholesteraemia in the search for the causation of acquired coronary disease. He considers the element of hereditary defect in this complaint is too great for it to be of very much value in this respect, involving as it does the metabolism of cholesterol itself, which need be no more related to the deposition of cholesterol in the atherosclerosis of higher age groups than congenital flat foot is related to acquired flat foot. Furthermore, some of the types of essential hypercholesteraemia distinguished by D. S. Frederickson [22] appear to be verging on the acquired type (and it is worth remembering that no known hereditary defect, as seen in Chapter I, occurs more often than five times per 1000 live births), with carbohydrate consumption often strongly implicated. But this rare and complicated disorder cannot be discussed at length in a wide-ranging work of the present type.

Finally, in the previous evolutionary study already mentioned, the author advanced that if fat consumption played any part in the causation of coronary disease, it did so via the agency of arbitrary food mixtures, as set out in Chapter X, Section IX. These include fried foods, where people may have to eat fat they do not want in order to eat meat, fish, or eggs they do want; or such foods as chocolate or ice-cream, where unwanted fat may be eaten for the sake of the accompanying sugar. (The vast increase in ice-cream consumption is shown in the accompanying table.) A causative fat consumption of this type, which, as was explained, is not seen in Nature, would never be in conflict with human evolution, and the value of avoiding these mixtures as much as possible in any system of natural nutrition is referred to in the diet card at the end of this volume. (But the application is not especially to coronary disease; it is also applicable to such conditions as peptic ulcer and the dyspepsias.)

Thus ice-cream, previously alluded to, shows the following increased consumption in the British Isles during the period stated, in thousands of gallons:

1920 1930 1938 1951
870 7890 35,607 39,612
Board of Trade (1951) 'Report on the Census of Production for 1951. Ice-cream'. London: H.M.S.O.

Not only is the study of this unnatural type of fat consumption neglected at present, but in the author's opinion the study of other, allied aspects of fat consumption is also neglected. These aspects concern the markedly different personal inclinations that exist over fat consumption, so that some people, like Jack Sprat, desire very little fat, whilst others, like Mrs. Sprat, desire a great deal of it. These striking personal differences are of evolutionary origin, as set out by the author in his earlier work. For in man a higher proportion of calorific needs is derived from fat in cold climates than it is in hot climates. Even in Europe some 40 per cent of the calories are derived from fat in northern parts, as against some 20 per cent in southern parts, like the south of Spain and the south of Italy. [23] Thus in Great Britain, where the population is of mixed descent, due to past invasions from the north and south of Europe, and in the United States, where the white population is also of heterogeneous descent, both Jack Sprats and their opposites abound. Consequently in some people a low fat consumption, when evolutionarily considered (that is, in terms of natural tastes), may be too high, whilst in other people a high fat consumption may, similarly, be too low. Such departures from the natural level may be due to financial or other factors, including mass feeding in schools and institutions.

Clearly any attempt to relate fat consumption to coronary disease would have to take into consideration not only the above evolutionary differences, but preferably also any marked departure from these differences, due to the external factors mentioned. Yet there is little or no evidence of such consideration and we find bold comparisons being made between, for example, fat consumption in the Danes and in the African Bantu. [23] More particularly, those who contest the relationship of refined carbohydrates to coronary disease, and especially those who contest certain clinical studies relating personal sugar consumption to the disease, forget that clinical studies [24, 25] have never demonstrated any relationship whatever between personal fat consumption and the disease.

With these points very much in mind we now proceed to the second part of this chapter, where the historical and epidemiological aspects of fat consumption will be discussed with the refined carbohydrates.

II Coronary Disease, Human Evolution, and the Consumption of Refined Carbohydrates

In the second part of this chapter there will be brought forward evidence relating coronary disease to the consumption of refined carbohydrates, and for including it in the saccharine disease. This evidence will be presented under evolutionary, historical, and epidemiological aspects.

Evolutionary Aspect

In contrast with the evolutionary incompatibility in relating coronary disease to the consumption of animal fats, as set out above, the relating of the disease to the consumption of refined carbohydrates presents no incompatibility whatever. For in the latter case the disease is being related, not to ancient and natural products, to which we are now well adapted, but to new and unnatural products, to which we can hardly be adapted at all. This aspect will be further elaborated in some of the following paragraphs.

Historical Aspect

The new event of the refining of carbohydrates, as exemplified in the production of white flour and commercial sugar, has already been described in Chapter II, together with the relevant dates of the period concerned, and to that chapter, in order to avoid repetition, the reader is now referred. For the reasons carefully given in that chapter there has been little increase in fat consumption during a similar period of time. Indeed, two of the four references that were cited, M. A. Antar, M. A. Ohlson and R. E. Hodges, as also B. Friend, showed not only that total fat consumption in the United States increased by only 12 per cent over a recent 70-year period, but also that such increase took place chiefly in the consumption of just those processed vegetable and other oils that were seen in Part I often to be recommended in the prevention of coronary disease today.

In contrast with this small increase in fat consumption, the increase in sugar consumption, over the period shown in the chart in Chapter II, has been no less than sevenfold, and although the consumption of white flour, which was pointed out as already widespread at the beginning of the period (circa 1800), has fallen somewhat during the later part of the period, this affords no consolation, for, as was also pointed out, such fall has been due to the greater, and more dangerous, consumption of the still more refined carbohydrate, ordinary sugar.

Meanwhile, as regards coronary disease itself, and more particularly coronary thrombosis, the main explosion in the incidence has by common consent occurred since 1900, and especially since 1920. [1] A. Keys has recently argued that this is too long after the main rise in sugar consumption for the disease to be related to this consumption. But in his paper Keys makes no reference to the all-important incubation period. Indeed, in by-passing this aspect of the problem, his argument appears to become meaningless. For the incubation period in diabetes has already been shown to average some 20 years, and since over 50 per cent of maturity-onset diabetics die of coronary disease, and since, also, the latter disease is seldom seen under the age of 30, we must regard 30 years as the minimum incubation period in most cases of the disease -- and it may be very much longer. This 30-year minimum incubation period, which points to the fuse as it were, of the beginning of the coronary explosion being lit around the year 1890, when sugar consumption was rapidly approaching the 100-lb. mark, is just as vital in seeking the cause of coronary disease as, for example, the 40-year incubation period is in seeking the cause of diverticular disease. No comparable fuse is to be seen in fat consumption. Indeed, a review of dietary changes in Britain [26] points to the consumption of dairy produce and fats having increased mainly in the 1930s -- 'some time after, and certainly not before the start of the coronary epidemic'. [1]

Epidemiological Aspect

1. The Clinical Association of Coronary Disease with Diabetes and with Obesity

In coronary disease far and away the most important epidemiological fact (to record it under this heading) is considered here to be the association of the disease with diabetes, which is well accepted. (Though diabetes itself is strongly associated with obesity, the association of coronary disease with obesity is somewhat more complicated, so we shall mainly confine ourselves here to the association with diabetes.) If, now, the causation of diabetes (and, for that matter, of obesity) lies essentially in the consumption of refined carbohydrates, as contended in Chapters VII and VI, then the argument for coronary disease having the same basic causation becomes strong indeed. Meanwhile, such crucial association cannot be explained in terms of fat consumption. This is seen in Chapter VII as regards diabetes; and as regards obesity, a high-fat diet has actually been used as a reducing diet. [27]

The key value of the clinical association of coronary disease with diabetes, in the elucidation of the cause of coronary disease itself, is shown in the following examples. Thus, when again remembering the 100,000 beats of the heart each day, one is ever amazed that, amongst other things, the endothelial lining of the coronary artery is able, in the midst of such gross physical turmoil, to maintain its integrity -- especially as the least impairment of that integrity, the least injury (e.g. of a 'crinkling' nature, as it were) to that endothelial lining, would initiate a deposition of clot, and from that a possible thrombosis of the artery. Now since the C vitamin is well known to be one of the food substances most intimately concerned in the nutrition of the endothelial lining of arteries (and hence the widespread escape of blood from the small vessels in scurvy, where this vitamin is lacking), it would seem a plausible hypothesis that coronary thrombosis should reflect the known and frequent deficiency of this vitamin in the food of Westernized peoples today, through its effect on the nutrition of the endothelium, especially at the points of greatest strain. G. F. Taylor [28] has shown how real is the present lack of vitamin C, especially in older people, but such lack cannot be the basic cause of coronary thrombosis, for it cannot explain the association of the disease with diabetes. That a lack of vitamin C could be an aggravating factor in coronary disease, yes, but the basic cause, no. And exactly the same argument will be seen later to apply to smoking; a powerful aggravating factor, yes, but the basic cause, no.

At this point it is desirable to reflect on the distinction between the basic cause of a condition and multiple aggravating factors. For unless such distinction is carefully preserved, the very unhelpful phrase 'of multifactorial origin' is liable to be used, especially in connexion with coronary disease. Not only does such a phrase, in the author's opinion, usually not reflect clear thinking, but it also has the serious objection of interfering with the attack on the causative factors in order of their importance. The distinction is well seen in the case of tuberculosis. [29] This disease, also, was once thought to be of multifactorial origin, because of the accompaniments of under-nutrition, overcrowding, heredity, and other factors. But directly the tubercle bacillus was discovered, this diffuse aetiology was replaced by a single basic cause and multiple aggravating factors -- and a big step forwards in prevention became possible. For the removal of aggravating factors merely dents the incidence, whereas the removal of the basic cause reduces the incidence to zero. And in this lies the true importance of the distinction.

With further reference, now, to the clinical association between coronary disease and diabetes, since it is considered here that both conditions arise from a common cause (the consumption of refined carbohydrates), and not that one of these conditions arises from the other, it follows that either condition may be the first to arise, depending on the personal make-up in the person concerned, though usually it is the diabetes that appears the first. In this connexion the author wishes to refer to the illuminating studies of Professor H. Keen and others, [30, 31, 32] who have shown that people with high blood-sugar curves (the forerunner of overt diabetes) have a much higher incidence of coronary disease than those without this sign. These studies, which are of several years' duration and still continuing, are in close accord with others in Tecumseh, U.S.A., in Paris, and in Australia. Unfortunately space precludes their pursuit here, but they are lucidly set out in the references given and their importance to the present argument is clear. The subject has been well summarized by F. H. Epstein. [33]

From this work it is also clear that a persuasively simple mechanism might be concerned in the production of coronary thrombosis, which is more direct than one centred on the blood lipids, previously mentioned, though it must be repeated that the latter is by no means incompatible with the present conception, as will be enlarged on shortly.

For an unnaturally high blood-sugar, constantly impinging on the endothelial lining of the arteries, over many years, might cause degenerative changes in this endothelium, and, by diffusion, in the arterial wall, too, especially at the sites of greatest strain (of which the commencing aorta and the coronary arteries are the supreme examples). This degeneration could then initiate the thrombosis which so often brings the sequence to a close. Such a sequence, indeed, involving the conversion of glucose into non-diffusible sorbitol in the arterial wall, is under present investigation. [34]

The high blood-sugar in such a mechanism would stem primarily from a concentrated (refined) diet, any pancreatic exhaustion from the same cause then raising the blood-sugar still higher. Whether such pancreatic exhaustion, raising the blood-sugar still higher, proceeded to overt diabetes before, or after, the endothelial degeneration reached the critical stage of producing' a (coronary) thrombosis would depend on the personal make-up in the individual concerned, but usually the diabetes appears the earlier, as already said.

In connexion with the above mechanism a recent paper by S. Wapnick [35] and others becomes of great importance, for these workers, who studied 50 poor Africans, 35 African medical students, and 12 Europeans, with increasing Westernization of the diet accompanying the higher economic status in each of the three groups, showed how closely the consumption of sugar and white flour affected the fasting and active blood-sugar levels. Thus the natural blood-sugar levels are probably as different from the 'normal' levels in people on a Westernized diet as the natural transit times of the intestinal contents have been shown to be different from the 'normal' transit times in people on this diet, too (Chapter III). And just as the difference in transit times gives the vital clue to the causation of diverticular disease, so it is contended here may the difference in blood-sugar levels give the vital clue to the causation of coronary disease.

Though it would probably take years to prove, or disprove, that the above mechanism does lie at the centre of the many collateral changes that take place in coronary thrombosis, at least the suggested sequence gives an immediate guide to natural prevention, as set out at the end of this work.

Meanwhile, it must be repeated that the fall in the glucose tolerance and the rise in the blood-sugar, which are both so characteristic of pre-diabetes and diabetes itself, are accompanied by striking increases in some of the blood lipids, especially the triglycerides. Hence if it is preferred to relate coronary disease to changes in the blood lipids, rather than to changes in the blood-sugar, it is still not difficult to involve the refined carbohydrates in the former changes. Of one thing the author is very confident; the key to causation of coronary thrombosis lies in the causation of diabetes (and also of obesity ).

2. Racial Studies

In the search for the causation of coronary disease, important racial evidence has been advanced from South Africa. In the first place there has been the almost complete freedom from coronary disease in Africans living tribally on unrefined carbohydrates, which is generally recognized. Typical of these Africans are the members of the Zulu tribe described in certain chapters of this work, especially in Chapter VII, where the rarity of diabetes in them has also been stressed. This freedom from coronary disease is, however, gradually being lost in urban Africans, on a more Western diet, with much refined carbohydrate. However, this change is far better seen in their cousins, the Negroes in the United States, where, in comparable occupations, the incidence of the disease, like the incidence of diabetes, is not greatly different from that in the whites, [36] just as their consumption of refined carbohydrates is not either. I am privileged to quote the following personal communication from G. E. Burch of Tulane University, New Orleans, to Mr. Denis Burkitt, F.R.S., 13 July, 1971: 'Concerning the incidence of coronary disease among the Negroes, it is true that the incidence was extremely low among Negroes, and practically non-existent among the Negro females, many years ago. At the present time, however, the incidence is essentially the same as in the whites... There is no doubt that the incidence has increased considerably in the past ten years.'

Turning now, in the second place, to the Natal Indians, their case is even more instructive. This is partly because their exceptionally high incidence of diabetes, described in Chapter VII, is matched by an exceptionally high incidence of coronary disease also; and partly because, as set out in the earlier chapter, their high consumption of sugar and other refined carbohydrates contrasts with a fat consumption where the animal fats are far less in evidence than the processed vegetable oils. Consequently, as regards coronary disease, the fat consumption in these Indians may well be as illuminating as their sugar consumption. Meanwhile it is generally recognized that in India itself, where sugar consumption has already been shown to be extremely low, coronary disease is relatively inconspicuous, except amongst the upper strata of society, where the food structure often resembles that in Westernized countries.

But what is of particular importance to the present work is that S. L. Malhotra [37] has shown that the incidence of the disease is seven times commoner in the south of India than it is in the north. For in the south the diet is largely refined rice, with only 31 per cent of the calories supplied by fat (and largely seed oils at that), whereas in the north the diet is largely unrefined wheat and maize, with no less than 23 per cent of the calories supplied by fat (and largely animal fats at that). Indeed, the polyunsaturated fats constitute 45 per cent of the fats in the south but only 2 per cent of the fats in the north (Indian Council of Medical Research). [38] Yet, as stated, coronary disease is much commoner in the south.

At this point it must be interjected that Malhotra has performed these geographical studies in India on railway workers, so as to eliminate socio-economic and certain other factors as much as possible, since the north of India is often economically better off than the south. This makes it easier to compare staple dietetic differences between the two parts.

It is true that sugar consumption is lower, not higher, in the south, but, as has been stressed in the case of diabetes (Chapter VII), it is the consumption of all types of refined carbohydrates that is important, not only that of sugar, and in this respect the south of India, with its predominant diet of white rice, easily leads the north. It is worth noting, too, that as regards the conception of the saccharine disease, the same southern part of India, where coronary disease is relatively common, is just the part where peptic ulcer is also common (see Chapter X).

While Malhotra in his paper states that the seven times greater incidence of coronary disease in the south of India, in spite of the nine times greater consumption of fat in the north, does not support the view that coronary disease is related to fat consumption, including the saturation present in the fat, he appears to the author to miss the point when he says that the epidemiological picture does not support the view that the disease is related to sugar consumption, either. It is submitted that if Malhotra had regarded the consumption of all refined carbohydrates, he would have perceived a very accurate correlation indeed, and need not then have sought out a complicated aetiology based on local cooking patterns, which would seem to have little application in other parts of the globe. But his references to dietary fibre strongly support the present conception, as this has already been shown to decide the crucial question of over-consumption.

However, lack of fibre cannot be the direct cause of coronary disease, since that would make the clinical associations all wrong, set out in Chapter II. That is to say, it would cause the disease to be most associated with conditions directly due to loss of fibre, such as constipation, haemorrhoids, varicose veins, and diverticulosis, instead of, as it is, with conditions due to over-consumption, such as diabetes, obesity, and gall-stones. This is set out in Chapter II, and has a vital bearing on prevention and treatment, as also set out there. For if the cause lay directly in loss of fibre, the treatment would consist in the giving of bran, instead of, as it should, mainly in the replacement of sugar consumption.

At this stage a further reference must be made to the Yemeni or 'Black Jews', referred to in Chapter VII, in whom A. M. Cohen [39] and others have shown that coronary disease, no less than diabetes, has dramatically increased during 25 years' residence in Israel, where by far the biggest change in the diet has been in sugar consumption, with relatively little change in fat consumption.

Finally, other primitive peoples than the tribal Africans described above could be referred to, such as the Polynesians. [40] None, whose food structure still continues at the evolutionary level, have been found to suffer from coronary disease, but only the Eskimoes and the Masai tribe in South Africa can be given space here. Both these peoples pursue a highly carnivorous existence, with an abundant consumption of meat and fat, which latter in the Masai includes large quantities of milk. [41] If the freedom from coronary disease in these two peoples is advanced as fatal to the fat-consumption cause, it is countered by the holders of that view with two arguments that are gravely weakened by their total dissimilarity -- that the fats eaten by the Eskimoes are unsaturated compared with our own animal fats, and that the Masai, in their metabolism, have learnt to accommodate the saturated fats eaten by them, by suppressing their own cholesterol synthesis. [41]

Expressed in evolutionary terms, however, it cannot be concealed that those advancing these arguments allow the Eskimoes and Masai to eat the fats they are evolved to, but do not allow us to eat the fats that we are evolved to, such as the fat of lambs fed on grass, which, as was realized even by the priests of thousands of years ago, is when roasted so delicious.

3. The Importance of Considering All Forms of Refined-carbohydrate Consumption

This importance has been stressed in Chapter VII, in connexion with diabetes (Chapter VII), and in the earlier paragraphs of the present chapter, but the time has now come to look into this matter more closely.

Let us suppose that some investigator was engaged in a project, which at first sight would seem a sitting target, to relate obesity to the consumption of sugar. Surprisingly, someone opposing such a relationship would have no trouble at all in turning the tables on the investigator, for he would be able to assemble a collection of the fattest men in any town, who did not have a sweet tooth between them and in consequence consumed very little sugar at all. These people would represent the formidable army of beer-drinkers in this country -- people who, in their tastes, prefer the bitter to the sweet. [42] And the reason the beer often causes extreme obesity lies not in its content of alcohol (which substance, of itself, when taken to excess, causes wasting), but in its content of malt sugar. Indeed, through the presence of this malt sugar (which is not a sweet sugar), beer becomes a perfect example of a refined carbohydrate. This case, like the case of diabetes in Trinidad (Chapter VII), shows the importance of relating any manifestation of the saccharine disease to the consumption of all forms of refined carbohydrates and not only to one form. For all of them end up substantially as glucose in the blood, as noted in Chapter II.

This crucial point, in the author's opinion, partly explains why J. Yudkin's findings of a high sugar consumption in coronary sufferers has not been confirmed by other investigators and in particular by a Medical Research Council working party. [43]

The same point can be used against the paper by A. Keys, [11] previously referred to, who found that certain countries having a higher sugar consumption had a lower incidence of coronary disease, for no refined carbohydrates, e.g. malted liquors, other than sugar were ever taken into account. Furthermore, Keys did not distinguish, in countries like Cuba, between natural sugar consumption, as in chewing sugar-cane, and unnatural sugar consumption, as in eating the refined sugar of Westernized countries today. The vital difference between these two types of consumption has been set out in Chapter II. And, lastly, the ignoring by Keys of the equally vital incubation period in coronary disease has already been referred to. His countries having a high sugar consumption, but a low incidence of the disease now, may well be heading for a very high incidence indeed -- just as Great Britain was doing around the year 1890.

4. The Nature of the Controls used in Some of these Investigations Today

A further point must now be raised in connexion with many investigations today relating coronary disease to the consumption of refined sugar, or denying such relationship. This concerns the nature of the controls.

Consider once more the case of hallux valgus discussed in Chapter I. In this condition the basic cause was held to be the new environmental factor of wearing shoes (new, because the majority of mankind still go barefoot even today). But, as was shown, the factor of personal make-up also comes into the picture, because the make-up of certain feet, which are entirely free from any hereditary defect, may render these feet unduly vulnerable to the new factor now under consideration. Consequently, if an investigation of hallux valgus were made in those who wear shoes and those who do not, the basic cause would be starkly revealed; but if, instead, an investigation were made in subjects all of whom wear shoes, to see if the condition were related to narrowness in the shoe, such cause might not by any means be easily revealed. Some subjects with a high degree of vulnerability might have hallux valgus with shoes showing little narrowness, [44] and vice versa. Very large numbers of subjects might have to be investigated to establish the cause in this way.

And so it is with coronary disease and sugar consumption. It is far easier to establish the truth by investigations contrasting those who get much coronary disease and consume much sugar with those who get no coronary disease and consume no sugar either (as has, for practical purposes, been the case until recently with the tribal Africans described in this work) than by investigations of coronary disease and sugar consumption in those who all belong to a high-sugar-consuming community.

Directly following the publication of the author's letters in The Lancet [45, 46] on these lines there appeared, by a remarkable coincidence, a paper in the British Medical Journal describing an actual investigation on hallux valgus, in St. Helena, by I. B. Shine, [47] which corroborated in practice every detail of the above argument.

The same argument has been very well summarized by D. Jennings: [48] 'If everyone smoked 30-60 cigarettes a day, I doubt if even Doctor Richard Doll would have had the patience to compile the enormous statistics needed to show that 50-60 cigarettes a day were more damaging than 30-40.'

5. Smoking and Coronary Disease

Whilst fully persuaded of the importance of smoking in the aetiology of coronary disease, possibly through its constricting the terminal arterioles, the author is convinced that smoking constitutes an aggravating factor and not a basic cause. The main reasons for his conviction lie in the fact that though there is still a very considerable incidence of the disease in non-smokers, there is no incidence at all in primitive societies (such as the tribal Africans dealt with in this work). In short, the tubercle-bacillus argument used above is considered to apply very much here, too. Furthermore, smoking cannot explain the crucial association of coronary disease with diabetes. There are also historical considerations, as summarized by L. Michaels. [49]

In connexion with smoking, a further comment is indicated on the report of the M.R.C. Working Party mentioned earlier. This study referred only to the consumption of sugar and not to the consumption of all refined carbohydrates, and the controls were all from a high-sugar-consuming population, on the lines set out above. The report is not, therefore, considered to constitute a threat to the present conception. [50] The report associated coronary disease with the smoking of cigarettes, induced by the taking of hot sweet drinks, rather than with the consumption of sugar, but the present author has suggested [42] that if the consumption of other refined carbohydrates -- especially beer -- had been added to the consumption of sugar, exactly the opposite conclusion would have emerged. The report itself shows how marked is the association between smoking and alcohol consumption.

6. Exercise and 'Stress'

It is not possible to conclude this chapter without some consideration of exercise and of 'stress', since a deficiency of the former, or an excess of the latter, is so frequently blamed for coronary disease today. As already set out in Chapter VI and Chapter X, the blaming of either of these factors is not remotely compatible with human evolution, especially as neither factor is ever considered in association with natural desires in these matters. For with regard to exercise, evolved sensations tend always to keep physical exertion in any pastime to the agreeable minimum, in order to reduce wear and tear of the body in general and of the heart in particular; and with regard to stress, the very mainspring of evolution has always consisted of the struggle for existence, where the killing of one organism by another represents stress in its starkest form. If we are adapted to anything in this world, we are certainly adapted to stress. To advise someone, who wants to rest, to take exercise is as unnatural as to advise someone, who wants to throw himself into the fight and get on in the world, to moderate his effort. Furthermore, this latter advice, applied to a whole country, would inevitably lead to national decline.

This is not to say that worry -- another and serious example of stress -- is desirable. It is very undesirable, but it is implicit in the struggle for existence, representing part of the mental effort in that struggle, and though it may cause loss of appetite and weight, it will not -- in the properly nourished body -- cause organic disease.

Since this book is based on natural, that is to say, evolutionary, principles, the author does not propose to pursue these two suggested causes of coronary disease any further. Neither of them can explain the crucial association of the disease with diabetes. And to allude to epidemiological details, such as the longevity attributed to hermits, who take little exercise, and to the longevity certainly occurring in many zoo animals, who take even less, would savour to him of setting out to prove an evolutionary axiom. Suffice it to say that, in the author's opinion, trying to be clever at Nature's expense, so well seen in combating the above two suggested causes of coronary disease, is the exact reason why, in spite of all the expenditure of money, time, and energy, so little has been achieved in the prevention of the disease to date. In particular, the countering of excess consumption, arising from the eating of refined carbohydrates, by the taking of unwanted exercise is considered a perfect example of two wrongs not making a right, even though the extra exercise is well known to reduce the consequences of such over-consumption.


The author would like to end this chapter with a quotation from the earlier joint work, with which A. Keys [11] ended his own paper, alluded to above:

'But the propaganda keeps on reverberating and is reflected in such statements as the following: "We ourselves are confident that if the refined carbohydrates were avoided by reducing the diet to the practical evolutionary level we have set out, the incidence of coronary disease would in due course be reduced to almost nil".' [51] But Keys refrained from giving the vital end of this sentence, which ran: 'as indeed it actually is in those communities, like the tribal Zulus in Natal, where carbohydrates until recently have been at this evolutionary level'.

The present author composed that sentence and he repeats it here. Nor is it always necessary to study such primitive peoples as these. Even amongst advanced countries, anyone who is aware of the difference between the food seen in France, often still consisting of natural materials, and the food seen in Britain -- for example, in a great city like Glasgow -- often consisting of tinned or refined materials, quite apart from a much smaller sugar consumption in France and much beer drinking replaced by wine drinking, will have little difficulty in understanding the striking difference in coronary mortality in the two countries, with France having about the lowest, and Britain (especially Scotland) about the highest, in Europe. [52]

To sum up, the author believes that solely by close attention to evolutionary principles can we hope to escape the coronary danger menacing each one of us today. This naturalness, and the simplicity in reasoning referred to in the Preface, have been the two objectives that he has tried specifically to pursue in the present chapter.


1. Meade, T. W., and Chakrabarti, R. (1972), Lancet, 2, 913.

2. Medical Research Council (1965), Ibid., 2, 501.

3. Medical Research Council Report (1968), Ibid., 2, 693.

4. Leader (1968), Ibid., 2, 901.

5. Miettinen, M., and others (1972a), Ibid., 2, 835.

6. -- (1972b), Ibid., 2, 1418

7. Yudkin, J., and Rivers, J. (1972), Ibid., 2, 1026.

8. Population Censuses and Surveys. Data for 1961. London: H.M.S.O.

9. Cleave, T. L. (1957), Fat Consumption and Coronary Disease. Bristol: Wright.

10. Carlson, L. A., and Bottiger, L. B. (1972), Lancet, 1, 865.

11. Keys, A. (1971) Atherosclerosis, 14, 193.

12. Kannel, W. B. (1971), Nutrition Today, 6, No. 3, 2.

13. Malmros, H. (1969), Lancet, 2, 479.

14. Cleave, T. L. (1969), Ibid., 2, 600.

15. -- (1969), Ibid., 2, 961.

16. Crawford, M. A. (1968), Ibid., 1, 1329.

17. -- (1969), Ibid., 2, 1419.

18. Commonwealth Bureau of Animal Nutrition, Aberdeen (1970), personal communications from D. L. Duncan, Director.

19. Metchnikoff, E. (1907), Prolongation of Life. London: Heinemann.

20. Pearce, M. L., and Dayton, S. (1970), Lancet, 1, 464.

21. Carroll, K. K., and Khor, H. T. (1971), Lipids, 6, No. 6, 415.

22. Frederickson, D. S., and Levy, R. I. (1972), 'Familial Hyperlipoproteinaemia', in The Metabolic Basis of Inherited Disease, 3rd ed. (edited by Stanbury, J. B., Wyngaarden, J. B., and Frederickson, D. S.), 545. New York: McGraw-Hill.

23. Keys, A. (1955), in National Research Council, Washington, Symposium on Atherosclerosis, 187 and 238.

24. Paul, O., Lepper, M. H., Phelan, W. H., Dupertuis, G. W., MacMillan, A., McKean, H., and Park, H. (1963), Circulation, 28, 20.

25. Kannel, W. B., and Gordon, T. (1970), The Framingham Study, Section 24. National Institute of Health, U.S. Dept. of Health, Education and Welfare.

26. Greaves, J. P., and Hollingsworth, D. F. (1966), World Rev. Nutr. Diet., 6, 34.

27. Kerwick, A., and Pawan, G. L. S. (1956), Lancet, 2, 155,

28. Taylor, G. F. (1972), J. Inst. Public Health Hygiene, 3, 244.

29. Fowler, P. B. S. (1968), Brit. Med. J., 4, 57.

30. Boyns, D. R., Crossley, J. N., Abrams, M. E., Jarrett, R. J., and Keen, H. (1969), Ibid., 1, 595.

31. Abrams, M. E., Jarrett, R. J., Keen, H., Boyns, D. R., and Crossley, J. N. (1969), Ibid., 1, 599

32. Keen, H. (1971), Acta Diabetologica Latina, vol. VIII, Supplement 1.

33. Epstein, F. H. (1967), Circulation, 36, 609.

34. Morrison, A. D., Clements, R. S., and Winegrad, A. I. (1970) Atherosclerosis (ed. by Jones, R. J.). New York: Springer-Verlag.

35. Wapnick, S., Wicks, A. C. B., Kanegoni, E., and Jones, J. J. (1972), Lancet, 2, 300.

36. Cassel, J. C. (1971), Arch. Intern. Med., 128, 887.

37. Malhotra, S. L. M. (1967), Brit. Heart J., 29, 337.

38. Indian Council of Medical Research (1963), Spec. Rep. Ser., No. 42, 141.

39. Cohen, A. M., Bavly S., and Poznanski, R. (1961), Lancet, 2, 1399.

40. Hunter, J. D. (1962), Federation Proceedings (1962), 21, Suppl. No. 11, 36.

41. Bliss, K., and others, quoted in Shafer, A. G. (1972), Brit. Med. J., 4, 32.

42. Cleave, T. L. (1971), Lancet, 1, 43

43. Bennet, A. E., Doll, R., and Howell, R. W. (1970), Ibid., 1, 1012.

44. Haines, R. W., and McDougall, A. (1954), Ibid., 2, 1308.

45. Cleave, T. L. (1965), Ibid., 1, 1069.

46. -- (1965), Ibid., 1, 1331.

47. Shine, I. B. (1965), Brit. Med. J., 1, 1648.

48. Jennings, D. (1968), Lancet, 2, 1249.

49. Michaels L. (1966), Brit. Heart J., 28, 258.

50. Heaton, K. W. (1971), Lancet, 1, 185.

51. Cleave, T. L., Campbell, G. D., and Painter, N. S. (1969), Diabetes, Coronary Thrombosis and the Saccharine Disease, 2nd ed. Bristol: Wright.

52. (1968) United Nations Statistical Yearbook, and World Health Statistics Annual.

Next chapter

Table of Contents

Back to the Small Farms Library Index