From the Archives
In this fascinating article, E V McCollum, a leading scientist of his day, sought to determine the cause of tooth decay. He notes that vitamins A and D help build strong enamel and teeth, and may provide certain immune factors, facts which he tries to meld with the theory that bacteria present in the mouth are the cause of decay. The description of the diet for diabetics is especially interesting—in the days before insulin, the only way to treat diabetes was with a high-fat diet—and this diet also protected these patients against tooth decay. McCollum prescribes such a diet as a sure way to prevent cavities, not because the high-fat diet provides protective vitamins, but because fats “coat the teeth” and thus protect them against bacteria! He also asserts, without evidence, that chewing helps strengthen the teeth. The article provides a good example of how even leading scientists have difficulty determining cause and effect. McCollum was a contemporary of Dr. Price. The article was published in Nature, January 25, 1941, Volume 147, pages 104-108.
The carious lesion in a tooth is caused by acid decomposition of the enamel, and afterwards the dentine, associated with proteolytic destruction of the organic substance of the tooth. Caries of the teeth is restricted to man and other animals which eat liberally of carbohydrate-containing foods. Carnivorous man and animals do not suffer from this disease. Dental caries does not attack the surfaces of teeth indiscriminately, but occurs only at such sites as favour the lodgment of food residues, as in pits or fissures, or on surfaces of the enamel which harbor mucinous plaques. In such sites acid is formed by fermentation of carbohydrate by micro-organisms, and is protected against being washed away by saliva or by neutralization by salivary alkalinity.
Throughout the Americas and Europe, and in most other temperate or torrid parts of the world, almost everyone eats liberally of carbohydrates, so the pabulum for feeding micro-organisms of every kind associated with fermentations is present in abundance at times in every mouth. Yet there is a great variation in the susceptibility of different people to dental caries. Numerous investigations have been devoted to attempts to discover why this great variation exists. Bunting and his associates, and Fosdick and his associates, have been foremost in studies of the microbiology of the oral cavity and its relation to caries of the teeth. A number of distinguished investigators have studied various aspects of the relation of the diet to susceptibility to this almost universal human affliction. I shall limit what I have to say to the nutritional aspects of this problem.
TOOTH STRUCTURE IN RELATION TO DENTAL CARIES
There is almost general agreement that potentially carious areas can be detected by a careful examination of the surfaces of the teeth. Dr. Thaddeus Hyatt, during his long tenure as chief of the dental clinic of the home office of the Metropolitan Life Insurance Company, directed his staff to explore the enamel surfaces thoroughly with a fine tine and when pits were found these were drilled and filled and the surfaces polished, thus eradicating potential food traps, or areas to produce later carious cavities. This system of caries prevention is known as prophylactic odontotomy, and has been found effective by others as a means of preventing the disease. It is fully established, therefore, that developmental defects in the enamel may predispose teeth to decay.
FAULTY NUTRITION AND DEFECTIVE TOOTH STRUCTURE
Experimental work with animals has shown clearly several ways in which dietary deficiencies during the period of tooth development can impair tooth structure. One of these is vitamin A deficiency. In deficiency of this nutrient the epithelia, no matter how they are specialized, as in mucous membranes, glandular secreting structures, and skin, suffer changes in structure and in loss of physiological function. Keratinization and desquamation of epithelia find their counterpart in the enamel-forming organ of the developing tooth, in changes in structure and partial or complete loss of function. The enamel-forming organ is of epithelial origin, being derived from embryonic gum tissue. Each cell of this organ secretes calcium, phosphate, fluoride, magnesium, and carbonate ions in such a way as to cause them to combine and deposit in the form of tenuous enamel prisms. These prisms form a mosaic, which, in the normal tooth, is of great perfection. When, owing to vitamin A deficiency, the enamel-forming cells are injured, prisms which are less dense than normal, or incomplete as to length, and imperfectly fitted together, form defective enamel. In the milder grades of this type there are pits in the enamel. In more severe grades of injury, the surface of the enamel of the greater part of the whole of the tooth may be rough, the enamel thin and deficient in hardness. This is the hypoplastic tooth.
A second situation which may cause defective enameling of the teeth is that seen in the disturbance of calcium and phosphate metabolism seen in the ricketic state. When the diet is complete as regards vitamin A and all other factors which are concerned with the promotion of healthy development, except vitamin D, the enamel-forming organ may be normal in every way, but be unable to withdraw from the blood the necessary structural materials for the formation of normal enamel. In rickets the concentration of phosphate ions in the blood falls below normal, and this interferes with the formation of sound enamel because the solution from which the cells derive their substances is too dilute.
Defects of enamel having their origin in disturbance of calcium and phosphorus metabolism have been most thoroughly studied by Lady Mellanby. She drew the conclusion from her observations that deficiency of vitamin D is of primary significance in predisposing teeth to caries susceptibility. The phosphate ion of the blood is maintained at normal concentration by the provision of this vitamin and, in addition to preventing defective bone growth, likewise has an important role in safeguarding the developing teeth against defects of structure. Lady Mellanby reported extensive experiments with children in Sheffield and Birmingham, all of whom were fed alike. To groups of these she gave generous prophylactic doses of vitamin D over a considerable period, and found that the incidence of dental caries was much lower in these groups than in the controls not receiving the vitamin. She expressed the belief that a diet highly favourable to normal calcification of bones and teeth could in considerable measure lessen the incidence of tooth decay.
McBeath, of New York, has carried out experimental studies with large numbers of school children over a period of several years, along the lines laid down by Lady Mellanby. He finds that there is a seasonal incidence of dental caries, the highest incidence of new cavities occurring in late winter and spring, and the lowest in summer and autumn. These observations he correlates with the amount of ultra-violet light which the children receive at different seasons. He further found that when liberal daily doses of vitamin D were given children during the colder months, the seasonal curve of incidence is flattened out, the incidence during the months of low sunshine being closely similar to that of summer and autumn. This type of experiment places vitamin D, for which suitable doses of ultra-violet light is the equivalent, in the position of playing a significant part in influencing the susceptibility of the individual to dental caries.
It is difficult to see how vitamin D can protect the teeth against decay merely by maintaining the body in a state favourable to calcification. Caries of the teeth occurs as the result of highly localized processes. In an area of stagnating food residues, acid is formed and protected against removal or neutralization, and is able to act more or less continuously in dissolving enamel. There appears to be no possible mechanism for resistance to acid erosion by enamel other than its density, which can be of but minor importance since the most perfect enamel is dissolved by acid when the pH reaches about 4.6, and the quality of enamel is not modified by any known agency after it is once laid down. If it is confirmed that sufficient ultra-violet light or if vitamin D favourably influences the body in its power to resist dental caries, it would seem that we must seek for an explanation in some effect upon the immunological mechanisms, which are of a nature to suppress the growth or functions of the microbial flora ordinarily associated with acid formation in the mouth. This might be exercised through the saliva or mucus, or other agency possessed by the epithelia. There do not appear to have been any studies recorded to test whether ultra-violet rays or vitamin D administration modify the oral flora.
That an immunity to dental caries may be artificially induced is suggested by the success of Bunting and Jay in preparing a vaccine from cultures of Lactobacillus acidophilus which they isolated from carious cavities. Upon intradermal inoculation of caries-susceptible persons there was a cutaneous reaction in nearly all cases, and when the test was applied to a series of caries-immune subjects, the skin reaction was almost always negative. There are in the population a considerable number of people who apparently eat as wide a variety as do most of us, and certainly eat freely of some form of carbohydrate, yet are caries-immune or nearly so. Some are immune to caries of the teeth during a period of years and then become susceptible. There seems much reason to attribute such immunity to a systemic condition of some kind, and the most plausible explanation would seem to be an immunological one—the offending organisms find the mouth environment unfavourable because of the presence of something detrimental, and this something seems to be the product of the living tissues or glands accessory to the mouth.
EFFECTS OF EATING SUGAR ON CARIES INCIDENCE
The eating of sugar and sweets has long been popularly believed to cause the teeth to decay. This view is supported by the observations of Bunting and his co-workers, who, by means of dietary control, reduced the incidence of dental caries in an orphanage to a very low level. Upon permitting a group of children, whose mouths were free or nearly so of Lactobacillus acidophilus, and who were classed as caries-immune, to eat about three pounds of candy per week, they found that they soon became caries-susceptible, and that the oral environment returned to the caries-producing type.
It is difficult to explain why eating sugar should be more likely to induce dental caries than cooked starch. Sugar is so easily soluble that it tends to be swallowed promptly as fresh quantities of saliva are secreted. Cooked starch, on the other hand, is pasty and is easily lodged in pits and fissures. Mixed with saliva and acid-forming organisms, starch would continuously undergo diastatic conversion into maltose, a fermentable sugar, thus furnishing an uninterrupted supply of nutriment for acid formation. Yet it is concluded by Bunting that this is not the case. Human experience confirms the findings of Bunting that people may eat freely of starchy foods and yet remain free from dental caries, or nearly so. An example are the people of the Island of Tristan da Cuhna, who consume potatoes as a staple food. The primitive Pacific Islanders, before the era of exploration, ate largely of starchy foods, yet they were almost free from dental caries. Sugar, therefore, seems on the basis of scientific observations now available, to be far more of a menace to the health of the teeth than are the starchy foods.
A dietary study of outstanding interest in relation to the caries problem was reported in 1926 and 1928 by Bodd and Drain, of the University of Iowa. They made repeated routine examinations of the teeth of the patients in the pediatric clinic over a period of some years, and encountered many teeth which had large cavities, which ordinarily, would have an area of softened dentine surrounding the zone of destruction, but in these patients were found to have uncommonly dense and hard dentine walling off the cavities and arresting the progress of the carious processes. These cases of arrested caries, in which a secondary deposit of dentine had occurred, which formed an effective barrier against further invasion of the tooth, were found to be without exception diabetic patients. The arrest of dental caries appeared to have occurred as the result of their having been restricted to the low-carbohydrate high-fat type of diet now generally used by diabetic patients. This type of diet does not seem to have been further studied as a means of controlling dental caries, and is worthy of most careful consideration. If replacement of a considerable fraction of the carbohydrate moiety in our daily diets by fat will protect the population in great measure against dental caries, the fact should be made known, and such a diet recommended for non-diabetics.
But human experience appears to afford fairly numerous examples of peoples who in great measure escaped the ravages of dental caries, who did not eat low-carbohydrate highfat diets. Chinese students in America appear to have a lower incidence of caries of the teeth than do persons of similar ages who have grown up in America. I have been repeatedly told by Chinese students that they experienced markedly increased incidence of tooth decay after spending a few years in the United States. The great majority of Chinese people have from very early times eaten freely of starch-rich vegetable foods. They eat various vegetable foods which have a detergent action on the teeth, which may be a factor of considerable importance in preventing stagnation areas.
Experimental studies on the effects of deficiency of ascorbic acid (vitamin C) on the teeth indicate that the dentine-forming organ, the odontoblastic membrane, is peculiarly susceptible to injury in this deficiency state. The odontoblastic membrane lines the pulp cavity, and from its cell filaments (Tomes fibrils) permeate the dentinal tubules, which permeate the dentine to the base of the enamel. It seems certain that it is through the functioning of these fibrils that secondary dentine can be laid down near the outer border of dentine whenever irritation arises. This is a peculiar repair process, which, when the state of nutrition is near the optimum for calcification, can be called into being so as to arrest caries by a walling-off process. In this respect the perfection of function of the odontoblasts, which is influenced profoundly by the ascorbic acid supply, becomes an agency in the prevention of the extension of dental caries, but not of its incidence.
The fact which has been thoroughly established by the work of Bunting with institutional groups of children, all of whom were provided with the same food, is that there are individuals in whose mouths Lactobacillus acidophilus grows profusely, and forms the principal flora, whereas the mouths of other individuals contain principally organisms of other types. This would seem to demonstrate that the character of the oral flora depends greatly on conditions other than the character of the food eaten day by day, especially when a mixed diet, affording a fairly wide variety, is eaten. The most plausible explanation for the observed facts would seem to be found in the humoral defence mechanisms of the mucous surfaces, the mucous secretions of the saliva. We have one outstanding example of the relation between the state of nutrition and the character of the oral flora. At one time it seemed that Chittenden and associates at Yale University, and also Goldberger, in Washington, were dealing with the same state of malnutrition in their experimental dogs, both believing that the condition produced by their different faulty diets was the analogue of human pellagra. At Yale the dogs were cured by the administration of butter or boiled carrots, both of which are sources of vitamin A. At Washington what appeared to be the same disease could not be cured by butter or carrots, but responded well to yeast administration, which did the dogs no good. In 1937 Smith and his co-workers at Duke University repeated both experiments and found that in the one case the dogs were in a severe state of vitamin A deficiency, and in the other of nicotinic acid deficiency. In both cases the earlier experiments had depended greatly on the mouth condition for making their diagnosis. The oral flora in both groups of animals was of the fusospirochaetal type seen in Vincent’s angina. This is an abnormal and pathological mouth flora, and overgrows the oral cavity when the tissues are debilitated. It appeared in the dogs as the result of two quite distinct types of malnutritional deficiency states. In these two conditions the overgrowth of the mouth by a pathological flora would seem to be best explained on the basis of a lack of some humoral factor or factors which the normal mouth contains, and which serves to suppress the growth of certain abnormal types of micro-organisms. Perhaps the decided differences in the oral cultures found in many individuals may be accounted for on the same basis, namely, the failure of the oral structures to produce some humoral factor of immunological significance.
The recorded experimental data seem to warrant the acceptance of the following conclusions: If the nutrition of the individual is optimal during the development period of the teeth, their structure will be safeguarded, and freedom from structural defects such as pits, fissures, hypoplastic enamel, may be expected. It would seem that dense, thick, hard enamel must afford some degree of protection against dental caries.
A state of optimum nutrition appears to afford marked protection against dental caries. It seems certain that such protection is in considerable measure due to some property of the mucous secretions or of the saliva or both, which tends to suppress the growth or functions of microorganisms whose presence in large numbers would be inimical to the health of the teeth.
Subsistence throughout life on a strictly carnivorous diet will prevent dental caries. This would be impractical in most parts of the world, and if practicable, would be less satisfying than is a mixed diet. The presence of considerable carbohydrate in the diet is necessary for the development of carious teeth. There seems to be good evidence in support of the view that the regular consumption of a diet in which all the essential nutrients are present in adequate amounts, and in which the ratio of fatty acids to total carbohydrates (including the sugar which may arise from protein and glycerol) is not less than 1.5:1, prevents dental caries. This is equivalent to saying that a diet suitable for the diabetic is so constituted as to afford protection against dental caries, and even makes possible the arrest of the carious process in open cavities. This protective action of excessive fat in the diet may possibly be due to greasing the tooth surface and the cavity surface, thus waterproofing it and preventing access of water-soluble acids (for example, lactic acid) to the enamel surface.
There seems to be good evidence that the elimination of sugar from the diet, and the provision of carbohydrate in the form of starch, affords a less favourable oral medium for the development of acid-forming organisms, and so protects the teeth against acid decomposition.
It appears probable that the provision of an abundance of vitamin D, either taken directly, or derived from the action of ultra-violet rays on the skin, exerts a favourable action on the immunological mechanisms in the oral secretions or on the epithelia of the mouth, and makes for preventing the growth of excessive numbers of acid-forming organisms.
The dentist can supplement the protection against dental caries which right eating can give, by early eradication of potential sites of decay.
The food should always supply certain things which require vigorous chewing, since teeth which are not exercised do not retain optimum health. Every meal should end with some food such as raw fruit or a raw vegetable, which requires thorough mastication, both because of the exercise afforded the teeth, and for the detergent effect of chewing foods which do not have a tendency to adhere to the enamel surface.
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Winter 2015