IT is not proposed to go deeply into the evidence linking dental caries, and to a large extent periodontal disease, with the consumption of refined carbohydrates, since this is already widely recognized. The author will therefore confine himself to the most important elements of this evidence, and to those having a special bearing on the present work.
Dental caries was for nearly a million years virtually absent from ancient man  as it still is today from a few surviving primitive races and from wild animals. Furthermore, any caries that did occur was of a different type from that occurring in civilized man today, since it usually followed natural attrition of the teeth, or an injury to the dentine or cement, instead of arising as a direct attack on the enamel. [2, 7]
In this latter connexion, it is important to emphasize that the quality of the caries in a skull is almost as revealing as its quantity. Owing to the coarse foods consumed in bygone ages, the natural wearing-down of the teeth took place much faster than it does today, and most of any caries that did occur arose from food driven down into the narrow spaces sometimes appearing between the teeth during this process. Also, as the teeth wore down, the gum margins became more exposed to injury from fragments of bone etc. driven into them during mastication, and, again, caries could arise from food trapped in these areas. In each case the caries tended to occur near the necks of the teeth. The particles of food were too coarse to be trapped elsewhere. Today, however, owing to the refining of foods, caries mainly arises from minute particles trapped in tiny fissures in the enamel, or between the teeth just above their contact points. There is thus a big difference between the type of caries that occurred in former periods and that mainly occurring at the present time.
Though we cannot discuss in detail the very low incidence of caries in the Ancient Britons  (but flanked by a distinctly higher incidence in the more advanced civilizations of Egypt  and Greece  at that time), or do more than mention the rise in the incidence in Britain during the Roman occupation  and the fall that followed it, we must pause to give an illuminating contrast between the teeth in the Anglo-Saxons, after the departure of the Romans, and our own teeth today. Professor J. L. Hardwick  compared 1014 teeth in Anglo-Saxon skulls with the same number of paired teeth in patients in 1957. The result showed an incidence of caries Of 9.5 per cent in the former and 48.6 per cent in the latter. The distribution of the caries was also different, as already explained. The rise in caries since Anglo-Saxon times was relatively slow until the nineteenth century,  and then increasingly rapid, the significance of which will be seen in the next paragraphs.
There are few writers on the history of dental caries who do not consider that, although the disease has borne some relationship to the introduction of the practice of cooking food, its main march has been with the progressive removal of fibre in the refining of carbohydrates,  during the march of civilization itself. The removal of the fibre allows accumulations of carbohydrates to occur in and between the teeth, as we have just seen, in which fermentation by bacteria produces acids that attack the tooth structure. This attack by fermentative acids constitutes the essential caries process.
In the case of cereals it is a mistake to suppose that these refining processes are of a very recent origin. The practice of sieving out the bran from flour dates from quite early times. For example, apart from much earlier evidence from Egypt,  white flour was being produced in Greece at least as early as 500 B.C., and Hippocrates himself recommended white bread for a patient with diarrhoea, as we stated earlier in this work, thereby showing not only that white flour was being made then, but that it was already realized as passing through the gut at a reduced speed.  A quotation from Antiphanes, written before 350 B.C., shows that bakers were by that time producing white loaves in quantity, and by A.D. 50 the production of white flour was geographically widespread,  though socially confined to the higher grades of society in all the countries that produced it. In Britain, from the time of the Roman occupation, the flour was ever more frequently sieved to remove the bran. By the end of the sixteenth century white bread had not yet appeared in the cottages of the poor, but by the end of the seventeenth century some of the poor were eating it, and by the end of the eighteenth century practically all of them were doing so.  In the case of sugar, the refining processes, whereby sugar was first extracted from the sugar-cane and subsequently also from the sugar-beet, are of much more recent origin. Though sugar was produced in small quantities in the countries of antiquity, it did not reach England till the twelfth century,  and then remained a food of the rich for a very long time. The remarkable increase in its consumption, however, since the end of the eighteenth century is shown in Fig. 1 in Chapter II.
It would thus seem that the slow rise in the incidence of caries from the Bronze Age onwards was chiefly due to the refining of flour, but the much faster rise in recent times has been due to the refining of sugar. Though the starch in flour is converted by bacterial fermentation into sugar fast enough, any sugar eaten as such is clearly still more quickly fermentable into the final acids. Refined flour, however, through the removal of the bran, becomes much more sticky, owing to the concentration of the protein, and the resulting adherence to the teeth not only increases any fermentation from the flour itself, but also binds to the teeth any sugar eaten at the same time, and so increases the fermentation from that, too. Observing the soluble nature of sugar, such fermentation could not otherwise take place to the same extent. In connexion with the foregoing one might add that, owing to different ratios in the proteins present, refined rice when moistened does not become sticky like refined flour (which is the main reason why bread is not made from it), and therefore those races living on milled rice and very little else are singularly free from caries.
As an example of the shocking prevalence of caries in Westernized countries today, it may be stated that in Great Britain during 1963 there were provided to young people of 20 years of age and under no less than 5440 sets of full upper and lower dentures (including 640 replacements), and 84,330 courses of treatment which included the provision of partial dentures. To this total of some 90,000 dentures must be added dentures, mostly partial, supplied to 11,320 pupils by the School Dental Service, and still further dentures supplied under the Hospital and Specialist Services and a few under private contract. 
As an example of this evidence, the author in his first paper  drew attention to the remarkable deterioration of the teeth that has taken place in the inhabitants of the remote island, Tristan da Cunha, since 1932,  consequent on the arrival of refined carbohydrates in the island, which deterioration has been increasingly documented ever since. The Royal Navy has always had exceptional opportunities for medically observing the inhabitants of Tristan da Cunha.
The racial evidence in dental disease may also be exemplified by two quotations nearly 20 years apart.
In 1946: Professor J. C. Middleton Shaw:  'The native [of South Africa] in his natural state is not prone to dental disease, and there is little doubt that the primary cause of these diseases is the highly refined foods and sugars... .'
In 1964: Professor A. B. MacGregor,  after a recent survey of dental disease in Ghana, which showed the very close association between dental caries and refined carbohydrates, stated in his concluding remarks: 'The significance of the survey lies in the fact that, while it has been postulated for many years that dental caries is associated with the consumption of refined carbohydrates, there is little direct evidence, and the evidence here presented was obtained from people living on the traditionally normal diet, some being able to afford refined carbohydrates and others not, so that reasonably controlled conditions could be obtained.'
The loss of teeth from periodontal disease (so-called 'pyorrhoea') may, in some sectors of the community, rival the loss from caries itself, and often it seems that where the build of the teeth makes them more resistant to caries, the build of the gums makes them more prone to periodontal disease. This latter condition, also, is widely recognized as linked to the consumption of refined carbohydrates. As Sir Wilfred Fish  puts it in his work on this disease, the soft pappy nature of these foods does not provide sufficient friction to keep the gum margins hard and keratinized; any more than clerical work gives a person the hands of a bricklayer.
Considerable care, however, is needed in expressing the above view on the causation of periodontal disease. It is perfectly true that refined carbohydrates are a prime cause, but it does not necessarily follow that unrefined carbohydrates can not be a cause. It all depends on the form these unrefined carbohydrates take. If they take the form of stale, coarse, wholemeal bread, and hard fruits and vegetables, such as the raw apple, the fresh salad, and the fibrous vegetable, no periodontal disease will follow their consumption. But if they take the form of boiled whole grains, such as soft porridges of maize or oats, and various vegetable mashes, with little other food eaten, then periodontal disease may still supervene. This happens in many natives in India and Africa, where the diet is of just this type, whereas Eskimoes and Australian Aborigines, who eat little carbohydrate but much tough meat, escape. It is clear from the above that, where periodontal disease is concerned, unrefined carbohydrates have every advantage over refined carbohydrates, but some of them should be eaten in the raw state. To summarize, those who eat unrefined carbohydrates are candidates for salvation over periodontal disease; those who eat refined carbohydrates never are.
At this point a few lines must be devoted to the subject of dental plaque. If, in the presence of a refined diet, the teeth are not cleaned with a toothbrush for several days, many people can actually sense a film forming over the teeth. This film, or dental plaque, a large part of which in Nature is kept removed by the friction of hard fruits and vegetables, has sinister dental implications. Not only does it harbour to a dominant extent the bacteria responsible for caries, but it also plays a big part in the initiation of periodontal disease, just described.
As regards caries, some micro-organisms in dental plaque are capable of producing from sucrose various extracellular polymers, largely dextrans, which, being sticky, favour the extension of the plaque. These extracellular deposits also act as a reservoir of fermentable material for the organisms, with consequent maintenance of the carious process over longer periods of time. And as regards periodontal disease, such a chain of events in dental plaque, when occurring near the gum margins, produces a direct inflammatory effect on the gums themselves, which is aggravated by any mechanical injury arising from roughened enamel surfaces, or the sharp edges of cavities, due to the carious process. This gingivitis is the essential initiator of periodontal disease.
The author here wishes to record his gratitude to Professor J. L. Hardwick for his great assistance over the subject of dental plaque and the origin of periodontal disease.
Fluoridation of Drinking Water
It is not intended to discuss this issue, except to point out that the prevention of dental caries is no more important than the prevention of the dreaded periodontal disease, or, for that matter, of most of the other saccharine manifestations set out in this work. And however useful fluoridation is in the prevention of caries, it can do nothing for the prevention of periodontal disease or of these other manifestations. Therefore, the prevention of caries, by removal of the cause, alone appears to hold out any hope of success in this wider sense. And that means educating the public to the dangers in eating refined carbohydrates, so that their consumption is drastically reduced, especially in school tuckshops, as referred to in the final chapter.
What can, indeed, be achieved by removal of the cause in the case of the dental diseases discussed here is well seen in the two-year study, 1955-7, by G. L. Slack and W. J. Martin,  in which schoolchildren were given slices of apple after meals. These children, as long as they were given the slices of apple, not only got significantly less caries than the control children did, but they got much less gum disease, too. To the purely dental result could be added the reduction in potential other disease that follows from the evidence presented in this work. It is into educative channels of this type, plus some subsidization of school tuckshops to sell fruit, nuts, raisins, etc., instead of sweets, that fluoridation costs would seem better directed.
1. National Research Council, Washington, D.C. (1952), Survey of the Literature of Dental Caries, 127. Publication 225.
2. Colyer, J. F., and Sprawson, E. (1953), Dental Surgery and Pathology, 9th ed., 383-384. London: Butterworth.
3. Ibid., 317-318.
5. Kirkos, A. (1935), Trans. Amer. Dent. Soc. Eur., 174, 7.
6. Hardwick J. L. (1960), Brit. Dent. J., 108, No. 1, 9.
7. Ibid., 11, 12.
8. Ibid., 13, 14.
9. Colyer, J. F., and Sprawson, E., Op. cit., 386-391.
10. McCance, R. A., and Widdowson, E. M. (1956), Breads, White and Brown, 2. London: Pitman Medical.
11. Ibid., 9.
12. Ibid., 6.
13. Ibid., 46.
14. Hardwick, J. L., Op. cit., 12.
15. From figures kindly procured for the authors by G. W. Marshall, British Dental Association, from the Ministry of Health.
16. Cleave, T. L. (1956), J. R. Nav. Med. Serv., 42, No. 2, 55.
17. Gamblen, F. B. (1953), Ibid., 39, No. 4, 252.
18. Shaw, J. C. Middleton (1964), S. Afr. Dent. J., 20, No. 8, 238.
19. MacGregor, A. B. (1946), Ann. R. Coll. Surg. Engl., 34, 179.
20. Fish, E. W. (1946), Paradontal Disease, 18. London: Eyre & Spottiswoode.
21. Slack, G. L., and Martin, W. J. (1958), Brit. Dent. J., 105, No. 10, 366.
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