IN this chapter the author will take the first consequence of the refining of carbohydrates, which is loss of fibre (pulp), and will trace the effects of this loss on the intestines. It has already been set out in Chapter II that the loss of fibre in the refining of sugar is greater than in the refining of flour, and therefore the effects of fibre-loss will -- as in all manifestations of the saccharine disease -- be more serious in the case of sugar consumption than in the case of white-flour consumption.
As regards the effects of this loss on the intestines, especially the colon, nearly everyone knows that the more fibre ('roughage') taken in the food, as in the form of fruits and vegetables, the more satisfactory becomes the action of the bowel. The loss of fibre occasioned by switching from these natural foods to sugar and white flour has the serious contrary result of intestinal, and more particularly colonic, stasis, as we shall now see.
First of all, what is the natural transit time of the intestinal contents? Following a letter to the British Medical Journal by the author and G. D. Campbell, [1] and through the kind co-operation of J. P. Bostock, radiologist to the Eshowe and Empangeni Hospitals in Zululand, Natal, and of W. E. G. Butler of the latter hospital, as arranged by Dr. Campbell, some pilot radiological studies were made on tribal Africans eating an unrefined diet, [2] and the figures obtained indicated (it is believed for the first time) that the natural transit time in the human intestines may be around 24-48 hours as against 48-96 hours or longer in Westernized countries. [3] In short, the unrefined diet halves the 'normal' transit times. Recently Burkitt, Walker, and Painter [4] have made comprehensive studies that indicate some, but not a serious, revision of these figures, the transit times with the unrefined diets still averaging less than half those with the refined diets.
I. Simple Constipation
As the result of the loss of fibre now under consideration, simple constipation is so common in these islands today that Medical Research Council observers [5, 6] have estimated that at least 15 per cent of the population are taking regular purgatives. Before discussing the easiest and cheapest way of correcting this state of affairs, it is desirable to pursue a further development of what has been set out above.
II. Diverticular Disease
This term covers two conditions, diverticula of the colon ('diverticulosis') and inflammation of these diverticula ('diverticulitis'). It may be added for the sake of clarity that until fairly recently the term 'diverticulitis' has very commonly been used for both conditions, it being assumed that the diverticulitis is a development and complication of a pre-existing diverticulosis. The author will argue here that both conditions stem from the refining of carbohydrates, though the mechanism in each is different.
a. Diverticulosis
It has long been considered that colonic diverticula may arise through excessive muscular contractions in the colon, which have the effect of raising the internal colonic pressures, thus forcing the lining mucous membrane to herniate through the muscular wall itself; and as a leader in The Lancet [7] Put it some years ago: 'It is tempting to relate these abnormal pulsion forces to the unwise sophistication of a Western diet, that eschews roughage, since there is some evidence that the condition is becoming more common. C. Wells [8] commented on the remarkable freedom from diverticulosis in Africans eating a high-residue diet; and A. J. Carlson and F. Hoelzel [9] found that while a low-residue diet encouraged the formation of diverticula in rats, the addition of roughage prevented their development.'
In short, a postulated sequence in the production of diverticulosis is a refined diet leading to a slower passage of the colonic contents, which slowing leads to increased absorption of water and hence to greater viscosity in these contents, with consequent excessive contractions in the colon in its efforts to move the viscous contents onwards.
A clear relationship of diverticulosis to a progressive refining of the diet might, in the author's opinion, have emerged much earlier had it not been that in all investigations the control subjects without the condition were on the same refined diet as the subjects with the condition, so that personal make-up, as described in Chapter I, entered the aetiological picture to a confusing extent. Let us examine two examples of this.
As long ago as 1925 Spriggs and Marxer, [10] in an investigation of 100 patients with diverticular disease, found that half the patients complained of constipation, and that of the remainder, who did not complain, many were also constipated; but they also found that 100 control patients without the disease were even more constipated. Likewise, Manousos, Truelove, and Lumsden [3] more recently showed that the intestinal transit times in subjects with this disease were accelerated rather than delayed, compared with control subjects without the disease.
However, it is crucial to the author's argument, as set out in the foregoing letter, [1] that these control subjects were taken from a population that was itself on a refined Westernized diet, in whom constipation has just been shown to be exceedingly common. Indeed, the control subjects showed retention of barium in the gut 3, 4, 5, or even more days in 90 per cent of the cases. Now it is easy to understand, as was, again, set out in the letter referred to, that the transit times in subjects with diverticular disease may be shorter than these times, because the condition is held here to be due, in certain people, to excessive muscular contractions in the colon designed to correct just this type of delay, but this is fundamentally different from the transit times in diverticular disease being shorter than the natural transit time set out above. On the contrary, they are certainly much longer than this time.
To sum up: the difficulties in the past over relating diverticular disease to a refined diet appear to have been largely due to insufficient studies in persons on an unrefined diet. This latter aspect of the subject will shortly be extended to cover the historical and epidemiological features of the disease.
b. Diverticulitis
Although the inflammatory changes in diverticulitis are normally regarded as secondary to blocking of the exits of the diverticula, the author does not believe that this is fundamentally the case. The question of the bacterial population of the gut has also to be considered. It is to be noted that duodenal diverticula never progress to a diverticulitis, yet one could visualize that their exits also could at times become obstructed, in spite of the more fluid contents of the duodenum; is this freedom from infection connected with the sterile nature of the duodenal contents, due to the bactericidal powers of the gastric acid?
The subject will be pursued in Chapter IX, on Escherichia coli conditions, where, although stasis is freely conceded as sometimes a factor -- for example, in appendicitis -- a much bigger factor is held to be the swarming of bacteria in the gut on a food surplus (especially a sugar surplus) that, with the consumption of naturally dilute, unrefined carbohydrates, would never be present. The subject will also be raised later in this chapter when discussing the conditions (especially diabetes) associated with diverticulitis. All that need be said at this point is that the greater importance of sugar consumption than of white-flour consumption with regard to loss of fibre in the causation of diverticulosis, already noted at the beginning of this chapter, is greater still with regard to over-consumption in the causation of diverticulitis, owing to the specially serious effects of sugar on the bacterial population in the gut, as will be set out in Chapter IX.
In the past, in place of the view based on bacterial proliferation, just given, the view has been that coarse particles in the food led to blocking of the exits of the diverticula, and thus to the supervention of diverticulitis. That view has led for many years to a refined diet being prescribed for the condition -- the very diet that is held here to be responsible for it.
Epidemiology and History
Proceeding now to the epidemiological and historical aspects of diverticular disease, it may be stated that both show a clear light on the causation. Thus, it is quite easy to establish that Africans living tribally on an unrefined diet (such as unrefined maize) do not get the disease at all. Indeed, the surgical superintendent of the Charles Johnson Hospital in the Zululand Reserve of Natal, South Africa, Mr. Anthony Barker, to whom the author has been indebted in his works for so much valuable information, stated in a personal communication in 1965 that no case of diverticular disease had ever been seen in that hospital.
It is possible to compare this absence with the increasing frequency of the condition in Africans pursuing an urbanized existence, but, as in peptic ulcer, varicose veins, and other manifestations of the saccharine disease, the author has always preferred to try to establish comparisons with the Negroes in the United States, since these exhibit a much greater, and a much longer, deviation from the unrefined tribal diet than do their African cousins who have taken to the towns. In this quest he expresses his gratitude to D. D. Kozoll of the Cook County Hospital, Chicago, who in 1965 sent him the following personal communication: [14] 'We see every complication of diverticulitis with equal frequency in the Negroes and the whites. We would cite a reference to you by E. J. Kocour in 1937, in the American Journal of Surgery, 57, 433, in which he comments on the rarity of diverticulitis in the U.S. Negro. However, you will notice that the reference goes back nearly 30 years, and the picture has changed since then.'
Following the receipt of this key reference, the author tried to ascertain changes in the diet of American Negroes since those earlier days, and it transpired that in the past century they largely subsisted on 'hominy', which consisted of unrefined maize, just as their African cousins when living tribally largely do today. But during the past century, largely through replacement by refined cereals (and refined sugar), the consumption of maize in the United States -- in spite of the great increase in the population has shown a spectacular fall, as Table I reveals.
|
Table I -- Fall in Maize Consumption in the U.S.A.
|
| Year |
Maize Products Available to Retail Markets
(lb. per year per head)
|
| 1889 |
117.0
|
| 1899 |
103.3
|
| 1909 |
53.0
|
| 1924 |
32.4
|
| 1932 |
26.5
|
| 1942 |
19.8
|
| 1950 |
11.8
|
| 1961 |
7.2
|
| (From Antar, M. A., Ohlson, M. A., and Hodges, R. E. (1964), 'American Journal of Clinical Nutrition', 14, 169.) |
|
It could, of course, be argued that much of the high incidence of diverticular disease in U.S. Negroes, and of the other conditions to be described later in this work, is due to the fact that through intermarriage with the whites these Negroes are no longer of pure stock. That there exists impurity in the stock is very true, [11] but even so, if there were any racial factor at work, it would be bound to alter the incidence of the various conditions away from that in the whites, yet it will be shown that the two incidences are always remarkably similar. (This argument is repeated in Chapter IV, on varicose veins.)
Turning now to the United Kingdom, as a country typical of Westernized civilization, it may be stated that though references to diverticula and diverticulitis occurred intermittently throughout the past century, and though these diverticula were related by some to the abnormal pressures in constipation, as set out above, they were always regarded as a rarity and were not described in textbooks of medicine. Like some other conditions constituting the saccharine disease, such as duodenal ulcer, which likewise was not described earlier in any textbook of medicine, diverticular disease emerged as an increasing clinical reality around the turn of the present century, i.e., around the year 1900, and has received growing attention ever since, in keeping with the rapidly rising incidence (so that a third of our population over the age of 60 now have diverticulosis [3]).
The epidemiology and history of diverticular disease, both in Westernized and primitive societies, have recently been succinctly presented by Mr. Painter and Mr. Burkitt, [12] but the author cannot agree that the rising incidence of the disease owed much to the introduction of the steel-roller flour mills around the year 1880. As explained in Chapter II, very little extra fibre was lost through this development, and a far more significant factor is considered here to have been the steeply rising consumption of sugar at this period. Indeed, the curve in Fig. 1 (Chapter II) shows that, in the 20 years straddling 1880, sugar consumption in the United Kingdom showed the remarkable rise from about 50 lb. to about 80 lb. per head per year, which in the author's opinion is of much the greater significance. For not only is more fibre lost in the refining of sugar, but also the effect of sugar on the bacterial population in the gut, as already set out, is of decisive importance. In any case, if the rising incidence of diverticular disease had been mainly due to the refining of the flour, it would have happened decades earlier, as by the year 1800 nearly everyone was eating white flour of 80 per cent extraction (see Chapter II).
Incubation Period
From epidemiological observations, including necropsy and clinical studies ranging from the past century to the present day, it would appear that the incubation period in diverticular disease is about 40 years. [12] That is, it needs some 40 years' exposure to a typical Westernized, refined diet before the fully developed disease presents itself Clearly, this fact has to be carefully borne in mind in all research on the causation of the disease, especially with regard to evidence from primitive communities moving on to a Westernized diet.
Relationship to the Saccharine Disease
It was many years ago that the author first came to relate diverticular disease (or diverticulitis, as the condition was then commonly called, as stated above) to the taking of refined carbohydrates; and indeed it was in 1945, when appointed to the R.N. Hospital, Chatham, that he started treating such cases on this basis, including not only the prescribing of a diet rich in fibre, but also the prescribing of unprocessed bran, where he drew on his experience with this material over the previous 15 years, shortly to be described. At Chatham he had the good fortune to work with Surgeon Commander E. T. S. Rudd, F.R.C.S. (now Surgeon Rear-Admiral E. T. S. Rudd, C.B., C.B.E., F.R.C.S., whose co-operation here I have much appreciated), who was on the surgical side of the hospital and had every sympathy with this approach.
Indeed his surgical colleague was himself a sufferer from diverticular disease and achieved salvation over this disease from the taking of the bran.
In his original paper in 1956 [13] the author therefore included diverticular disease in his conception and likewise in 1966, in the first edition of the joint work, [14] where he set down 'that the whole probable sequence of diverticulitis is in harmony with the view that the condition is a manifestation of the saccharine disease. For the removal of fibre in the refining of carbohydrates is not only responsible for the stasis that leads to diverticulosis, but also, via over-consumption, for the abnormal numbers of B. coli present in the gut, the attack of which bacteria on the wall, in the diverticular areas of stagnation, constitute the final diverticulitis.'
At this stage the author would again like to pay a tribute to Mr. N. S. Painter to whose support since 1967 he has been greatly indebted. [15] Mr. Painter's experimental investigations in diverticular disease have been given in the second edition of the joint work, [16] and will now be outlined here.
These investigations [17, 18] were made by using open-ended polythene tubes, which measure the intra-colonic pressure accurately (previous work with intra-colonic balloons is suspect, as it has been shown that 'such balloons measure the pressure in the balloon and not the pressure in the lumen of the bowel'). These tubes were passed into the sigmoid colon through a sigmoidoscope, which was then withdrawn and the intra-sigmoid pressures were recorded, both in healthy subjects and in patients with diverticulosis. This pressure-recording was combined with simultaneous cine-radiography, which showed that when pressures were produced in the sigmoid colon, the colon was contracting so as to become demarcated into segments. This segmentation was due to the contraction of inter-haustral muscle rings, which probably occur at fixed sites in the colonic wall. By stimulating the colonic musculature with morphine and other drugs it can be shown that this segmental type of contraction can under certain circumstances generate pressures as high as 90 mm. Hg, and it is easy to see that in these circumstances diverticula of the mucous lining can be forced through the muscular wall.
These studies clearly form an important step in understanding the production of diverticula in the colon, but the present author does not, if he may say so, consider that a narrowed state of the colon, which has been greatly emphasized in connexion with the effects of segmentation, would favour the development of diverticula, for he believes that the necessarily thicker colonic wall in the narrowed state would more than counterbalance the effect of the narrowing. He believes, on the contrary, that it is distension of the colon by the unnatural accumulations in stasis, and the resulting thinner state of the colonic wall, that favours the production of diverticula. With a natural diet the greater bulk in the food eaten likewise produces some colonic distension, but now any thinning of the wall is more than compensated by the much faster transit time and big fall in viscosity. Later, of course, when the damage is done, the wall thickens from infection.
In connexion with a narrowed state of the colon in rats on a refined (low-residue) diet, Carlson and HoelzeI [9] in their phrase, 'more or less', do not rule out intermittent accumulations occurring in the colons of such rats, which the author would regard as inevitable for the reason given below. Certainly he is convinced that with a refined diet the colon in man is often in a more, not less, distended state than is natural. For to the drier contents of yesterday (and very likely of some days before that) must be added the moister contents of today, and this accumulation constitutes an addition, not a subtraction! Indeed, what does the term 'loaded colon' mean if it does not mean just this? That is why the author, himself, has always believed that the increase in viscosity of the colonic contents, so typical of stasis, is the decisive factor in the production of diverticulosis.
Clinical Associations
The subject of the clinical association between the conditions constituting the saccharine disease has already been alluded to in Chapter II, but here attention will be drawn to those associations involving diverticular disease, which are deeply revealing.
Some of the associations noted in the past have recently been contested [19] but in a recent paper Parks, [20] reviewing 521 cases of diverticular disease, found the following associated conditions: appendicitis 14 per cent, cholecystitis and/or gallstones 13.8 per cent, abdominal hernia 12.5 per cent, duodenal ulcer 10.9 per cent, and dysentery 1 per cent. All these conditions could be included in the saccharine complex, if the abdominal hernias were related to straining at stool, due to stasis, and if the dysentery signified an irritable colon, shortly to be described. Recently, Mr. Conrad Latto [21] has demonstrated a most significant association with varicose veins, which had a doubled incidence in diverticular disease patients.
It will be noted that in the past no attempt has been made to differentiate associations with diverticulosis from those with diverticulitis. Yet if the author's conception is correct, a condition like abdominal hernia should be particularly associated with diverticulosis, since in this the related straining at stool likewise arises from stasis due to loss of dietary fibre; and E. coli conditions, like appendicitis and cholecystitis, should be particularly associated with diverticulitis, since in this work these latter are related to over-consumption, especially of sugar. It is, therefore, in the author's opinion, of deep significance that in another series of 740 cases of diverticular disease, [22] brought forward to demonstrate a strong association with diabetes, the association of diabetes with the diverticulitis cases (22.8 per cent) was over double that with the diverticulosis cases (10.5 per cent). For later in this work it will, it is hoped, be shown that diabetes arises from the same over-consumption, especially of sugar, that has already been blamed here for the supervention of diverticulitis.
III. Irritable Colon and Cancer of the Colon
As stated above in connexion with diverticulitis, there will be set out in Chapter IX the effect of over-consumption, arising from the refining of carbohydrates, on the bacterial population in the intestines -- especially in the colon. In that chapter attention will be drawn to the evil-smelling nature of the stools of Westernized man, in marked and sustained contrast with those of any wild creature (but not in contrast with those of the domesticated dog or pig, often living quite substantially on our own refined carbohydrates). In that chapter the subject of intestinal toxaemia will be built up in outline from this simple basis. However, it is desirable to devote here a few words to the local effects of the toxic products discussed in that chapter.
a. Irritable Colon (formerly often known as Simple Colitis)
The author is confident that the non-specific diarrhoea, of considerable chronicity and unattended by any constipation, that not infrequently characterizes this condition, is due to the impact of these irritating putrefactive products on the wall of the gut. He is also confident, as the result of practical experience, that the successful treatment of this diarrhoea does not lie, as has recently been suggested by Harvey, Pomare, and Heaton, [23] in the giving of unprocessed bran, though a wholemeal loaf is always correct, but in the careful replacement of table sugar in all forms by raw and dried fruits and certain fresh vegetables, as set out in the diet card at the end of this work. Unless the offensive odour of these motions is attacked in this manner no real relief will in his experience be obtained. [24] He regards the direct action of unprocessed bran on the gut as invariably aperient.
b. Cancer of the Colon
In 1959, in the Journal of the New Health Society (Vol. XXXIV, No. 4, page 7) founded by the late Sir Arbuthnot Lane and now unfortunately in abeyance, the author wrote the following, to which he equally subscribes today: 'The first of these local consequences is an intermittent putrefactive diarrhoea, and the chronic simple colitis to which, in the writer's firm opinion, this may gravitate. But a graver local consequence is probably cancer of the colon. It is noteworthy that the frequency of cancer increases steadily in each successive part of the colon, cancer of the rectum being one of the commonest in the body. It is significant that the irritant action of any toxins on the intestinal wall must increase steadily in each of these successive parts, both on account of the actual greater production of toxins, and also on account of the progressive slowing that normally occurs, in the colonic contents as they pass onwards.' He repeated this in 1960. [25] But an amendment is needed in that stasis, and the incidence of cancer, are both high in the case of the caecum.
It is clear that any unnatural stasis must aggravate the above sequence, but as regards the actual irritants involved, the author believes that, although these have been blamed on the degradation of bile-salts, the labour of generations might be needed to establish which toxic products are mainly responsible for tumour formation -- and yet that this labour would not achieve any greater practical prevention than is achieved by the foregoing reasoning plus the use of the nose, which will be alluded to in the later chapter. As one instance of the enormous difficulties that would be involved, the author has only to point to the problem of establishing in natural stools, let alone Westernized ones, the faecal microflora themselves, in which it has been stated by one authority, and quoted by several others, [26] that 'whenever a man gets the idea that he is going to work out the bacteriology of the intestinal tract of any mammal, the time has come to have him quietly removed to some suitable institution'.
What has been written above on cancer of the bowel is based on simplicity in reasoning and the presence of the unnatural feature just mentioned in the stools of Westernized man. The epidemiology has been set out convincingly by Walker [27] and by Burkitt [28] and shows how closely the condition follows the consumption of refined carbohydrates.
IV. The Natural Treatment of Intestinal Stasis
At first sight the natural treatment of intestinal stasis, that plays so big a part in the production of the condition just described, would appear to lie in taking all bread as wholemeal bread, and in taking all sugar as raw and dried fruit and as certain sweet vegetables such as beetroot, carrots, etc. This indeed is theoretically the most correct, and certainly the most pleasant, way of restoring to the diet the fibre that has been taken from it. But in practice serious obstacles at once present themselves. Quite apart from any trouble in getting hold of a true wholemeal bread, i.e. a brown bread that still contains all the natural bran (and some brown bread contains no bran at all), there is the question of expense. For to effect the above substitutions, at least as regards fruit, often requires more money than many people can afford to spend.
Faced with this problem many years ago, when advising his naval patients and at times their families, the author began to experiment with himself in the taking of natural, unprocessed bran (that is, raw bran), as sold for a negligible sum at any corn chandler, at any seed shop, or even at any pet shop; or at a 'health store'. He proceeded cautiously, but was soon widely prescribing this natural substance, and in 1941 wrote his first letter to the British Medical Journal, [29] describing 10 years' experience with it and disposing of certain possible objections to its use. He was at that date the senior medical officer of the battleship King George V, and owing to the wartime scarcity of fruit and vegetables, especially at sea, found such bran invaluable for correcting constipation in the ship's company. The ship's canteen bought the bran by the hundredweight sack and sold it at the present equivalent of 1p per pound -- which amount often lasted a man for several weeks. The bran was very popular with the sailors, as it enabled them to do without purgatives, and on one occasion, when the supply failed, many fell in at 'Captain's Request-Men' to ask if it could be restored to them.
Not only has the author used unprocessed bran in thousands of naval personnel at sea, but he has also used it for nearly 20 years during specialist duties as a physician in naval hospitals, where he always declined to use aperients, but relied instead on an enema if any serious arrest was already present and then solely on the unprocessed bran for future prevention. He wrote a second letter on this subject to the British Medical Journal in 1962 [30] and a third as recently as 1972. [31] He is glad to see that the use of this substance is at last spreading in the United Kingdom, but with at least 15 per cent of the population on habitual purgatives, as already stated, this spreading has a very, very long way to go yet. And of course the same applies to the substitution of a true wholemeal bread for white bread.
It may be added that the author has by no means confined the prescribing of unprocessed bran to cases of simple constipation. He has used it in other saccharine manifestations, ranging from haemorrhoids to the diverticular disease described above; and as regards the latter, Mr. N. S. Painter has recently employed this treatment on a much larger scale, with most satisfactory results. [32]
It is important to add that the taking of unprocessed bran should not be accompanied by the eating of any bread that is not truly wholemeal. It would be senseless to take such bran on the one hand, but exclude it from the bread on the other. Indeed, the author [31] has argued that, far from reducing the natural amount of bran incorporated in a true wholemeal loaf, as is so often done, it is usually much wiser to add 10 per cent of extra bran to the loaf, so as to help atone for some of the fibre lost in the refining of flour. In short a '110 per cent extraction' flour is far better than a 90 per cent extraction flour. To this effect, some 5 years ago, the author succeeded in getting a 'bran-plus' loaf of this type introduced into the heart of London, where it is now being baked in increasing quantities (Messrs. Cranks, Marshall Street, London, W.1).
The extra bran has proved no deterrent whatever to the demand for such bread, and the bran-plus loaf can also easily be baked in the home, by using the simple Grant method (Grant, Doris (1973), Your Daily Food. London: Faber & Faber). (Grant loaf recipe.)
Finally, as regards the actual taking of unprocessed bran, although this substance has the advantages of cheapness and unimpaired vitamin content, the former being of decisive importance in hospital and other institutional use, there are a few precautions to be noted:
a. There is a tendency to the production of flatulence for the first two or three weeks, until the gut becomes acclimatized, but this is an indication for a temporary reduction in the dosage, never for an abandonment of taking this most natural material. The author can understand that old or frail people require a longer and more gradual habituation, but this is rarely necessary in younger people -- and was never necessary in the Navy.
b. As regards the dosage, which is set out in the diet card at the end of the present book, this depends entirely on how much other fibre is taken in the diet. Wealthy people, who can afford plenty of fruit, will not need bran at all. But the poorer members of the community may need a great deal -- anything from one tablespoonful morning and evening to one or two tablespoonfuls at meal times.
c. The bran should be taken before meals, so as to prevent any indigestion from overloading of the stomach. The taking before meals also has the effect of reducing the calorie intake, as the bran itself has very few calories. This effect becomes valuable in cases of obesity.
d. Unprocessed bran cannot be swallowed dry. It is best taken in a thick fluid -- for example, a jug of pea soup can be made up and kept in a refrigerator: a little at a time mixed with the bran gives an easy and pleasant descent. Or the bran can be taken in porridge, Shredded Wheat, or other whole cereal, with milk. Or, of course, the bran can just be washed down in some water, as it usually was in the Navy.
e. Finally, unprocessed bran is now being sold inside Cellophane wrappers. However aesthetically desirable this is, it is essential that those poorly off should realize that Cellophane wrappers are no more a necessity with bran than they are with, let us say, ordinary apples. The author has found that bran bought from any of the shops specified above is perfectly safe, as long as it is reasonably fresh from the mills and has been kept throughout under cover to protect it from mice, etc.
Finally, constipation is especially liable to occur in old age, because the loss of teeth makes it difficult to bite up the coarse fruits and vegetables which supply the vital fibre. Thus, in one of the most beautiful, and certainly one of the most famous, pieces of English ever written, the 12th chapter of Ecclesiastes, the Bible tells us that in old people 'the doors shall be shut in the streets, when the sound of the grinding is low' (the grinders being the teeth). This trouble with the bowel rivals in importance the other troubles of old age so magically described in the above chapter, such as the frequency of passing water, due to the shrinking capacity of the bladder, which is rendered in the famous (but seldom appreciated) metaphor, 'the grasshopper shall be a burden' (i.e., the male organ of generation) -- and there are few old men who would not agree with these dramatic words.
(Incidentally the whole of the medical significance of the 12th chapter of Ecclesiastes was documented and set out in 1952 by 0. H. P. Pepper, [33] at that time Emeritus Professor of Medicine at the University of Pennsylvania in Philadelphia, to whom the author was indebted for valued personal communications on this subject.) However, to refer again to the constipation of old age, it must be repeated that though the unprocessed bran will supply the fibre here in a most practicable manner (and also the constituents of the vitamin-B complex often sadly deficient at this age), the bran needs to be introduced very gradually, because the preliminary flatulence, which is of little importance in younger people, can be very important indeed in older ones. Incorporation in a suitable vehicle to facilitate swallowing, as in (d ) above, is also essential in old people.
As pointed out to me by Mr. Conrad Latto, Shakespeare in Coriolanus (Act I, Scene 1 speaking for the human belly, says, in brief, 'I am the storehouse of the whole body, and what I receive I send through the blood to the heart, the brain and even the small inferior veins, and all I am left with for myself is the bran from the flour'. It is feared that in Westernized countries today this latter is far from being the case, the belly usually being left with no bran at all, and as a consequence the serious maladies set out above are needlessly incurred. It is hoped that what has been written may help to correct this state of affairs, and meanwhile we pass on to a study of these same inferior veins.
References
1. Cleave, T. L., and Campbell, G. D. (1968), Brit. Med. J., 1, 579.
2. Campbell, G. D., and Cleave, T. L. (1968), Ibid., 3, 741.
3. Manousos, O. N., Truelove, S. C., and Lumsden, K. (1967), Ibid., 3, 760.
4. Burkitt, D. P., Walker, A. R. P., and Painter, N. S. (1972), Lancet, 2, 1408.
5. Morris, J. N. (1941), Ibid., 1, 5 1.
6. Connell, A. M., Hilton, C., Irvine, G., Lennard-Jones, J. E., and Misiewicz, J. J. (1965), Brit. Med. J., 4, 1095.
7. Lancet (1964), 2, 631.
8. Wells, C. (1949), Brit. J. Radiol., 22, 449.
9. Carlson, A. J., and Hoelzel, F. (1949), Gastroenterology, 12, 108.
10. Spriggs, E. I., and Marxer, O. A. (1925), Quart. J. Med., 3, 1.
11. Lewis, J. H. (1942), The Biology of the Negro. Chicago: University of Chicago Press.
12. Painter, N. S., and Burkitt, D. P. (1971), Brit. Med. J., 2, 450.
13. Cleave, T. L. (1956), J. R. Nav. Med. Serv., 42, No. 2, 55.
14. -- and Campbell, G. D. (1966), Diabetes, Coronary Thrombosis, and the Saccharine Disease, 1st ed. Bristol: Wright.
15. Painter, N. S. (1967), Brit. Med. J., 3, 434.
16. Cleave, T. L., Campbell, G. D., and Painter, N. S. (1969), Diabetes, Coronary Thrombosis, and the Saccharine Disease, 2nd ed. Bristol: Wright.
17. Painter, N. S. (1964), Ann. R. Coll. Surg., 34, 98.
18. -- and Truelove, S. C.(1964), Gut, 5, 201.
19. Kaye, M. D., and Kern, F. (1971), Lancet, 1, 1228.
20. Parks, T. G. (1969), Brit. Med. J., 4, 639.
21. Latto, C., Wilkinson, R. W., and Gilmore, O. J. A. (1973), Lancet, 1, 1089.
22. Schowengerdt, C. G., and Hedges, G. R. (1969), Arch. Surg., 98, 500.
23. Harvey, R. F., Pomare, E. W., and Heaton, K. W. (1973), Lancet, 1, 278.
24. Cleave, T. L. (1973), Ibid., 1, 1443.
25. -- (1960), On the Causation of Varicose Veins, 35. Bristol: Wright.
26. Gorbach, S. L., Laila Nahas, Lerner, P. I., and Weinstein, L. (1967), Gastroenterology, 53, 845.
27. Walker, A. R. P. (1971), S. Afr. Med. J., 45, 377.
28. Burkitt, D. P. (1971), Cancer, 28, 3.
29. Cleave, T. L. (1941), Brit. Med. J., 1, 461.
30. -- (1962), Ibid., 1, 191.
31. -- (1972), Ibid., 2, 409.
32. Painter, N. S., Almeida, A. Z., and Colebourne, K. W. (1972), Ibid., 2, 137.
33. Pepper, O. H. P. (1952), Am. J. Med. Sci., 223, 589.
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