Report of a Study of the Diet

Report of a Study of the Diet Factor in Relation to Dental Decay in Children and the Most Probably Food Offender

By Waite A. Cotton, D.D.S.

            The Preventive Dentistry Clinic, which is part of the Division of Child Research, Dental School of New York University, was started (as its name indicates) for the purpose of studying ways and means for the best methods of control and prevention of dental decay.

This study has been made from the records of the three hundred (300) children in the clinic.

These children were recruited first from families of the University staff and their friends. At the present time from those who apply. They are accepted at two (2) years or younger and when accepted, it is understood by the parents that they are to bring the children in when called, for a periodic examination until they are eighteen (18). For this they are to receive all dental service at no charge.

A complete examination and history is made by a pediatrician, rhinologist, opthalmologist, dietitian, a physical anthropologist and hygienist with a detailed examination of the teeth and mouth.

We have no very rich children nor extremely poor, but a good cross section of the average child, living in average home conditions, WITH NO suggestions or advice as to what they SHOULD or should NOT eat.

The diets were charted by the dietitian who interviewed each mother each time the diet was taken to determine if the foods and quantities were rightly given and if the diet was an average sample. These diets were taken twice a year for two years. Each child’s diet was charted at to its calorie, mineral and vitamin content and the average taken.

From these averages (which is a fair picture of each child’s food intake over a period of time) we have compiled some sixty (60) or more charts, taking those with the highest mineral, vitamin, acid base and other content, and comparing them with the lowest intake of these factors. To these we have added the caries index, taken from our records, to observe if there were any consistent factors associated either with dental decay or immunity.

The standard used for determining the content of these diets was compiled from Dr. Sherman’s tables, and is sufficiently correct for comparison, as the measure or standard is the same for all.

Among the three hundred sixty-six (366) cases that we have treated in the clinic, there has not been one permanent tooth lost and only one pulp in a permanent tooth even approached by a filling, this was the fault of the mother in not bringing the child in when called, for this is a preventive dentistry clinic, where the children are carefully watched and examined not less than every three months.

A survey made in the schools showed that 12% of children 10 years old had lost one or more of the permanent teeth, and 35% of children 15 years old had lost one or more permanent teeth.

Every pit and fissure is prepared and filled when a fine explorer can enter and catch. Consequently we have no large fillings, and these occlusal, buccal and lingual cavities were not allowed to progress into cavities that might involve the pulp.

I will not show slides of all the charts we have made, as that would take hours; but we will observe the highs and lows in those factors that have been most prominently brought to our attention as of prime importance.

These charts show the case number, the age, the intake in the diet of calcium, phosphorus, iron, copper, acid base balance and the vitamins. The “D” means the deciduous teeth and the “P” means the permanent teeth. The fillings on each surface are given as well as the compound fillings, the total number of cavities, the number of teeth examined, and the average cavity per tooth.


Chart No. 1

On chart No. 1 we have ten (10) cases of highest calcium intake. You will note all have well over the gram required for adequate nutrition, and where the calcium-phosphorus ratio is not always 1 to 1 ½, it is ample for all needs.

In case No. 70, which has the highest intake of calcium, we have the highest caries index both in the deciduous and the permanent teeth.

Case No. 69, only one year younger, had five (5) occlusal cavities in the deciduous and two (2) occlusal in the permanent teeth.

No. 97 (12 years old) had a high caries index on the deciduous, and less than .5 in the permanent.

With this high calcium intake, we have a variation from no cavities to many cavities. The Vitamin D intake is not particularly deficient. We will take that up when we come to the Vitamin D chart.



Chart No. 2

            On chart No. 2. Of the comparatively low calcium intake, you will note that we have three (3) with a caries index over 1.While in the high, we had only one, and two were over .950. You will also observe we have one of 7 years with no cavities. One of 9 with a buccal and mesial in the deciduous teeth and no defects in the permanent teeth. Another of 10 years with no defects in the permanent teeth.

There is also very little difference in the average caries index between the high calcium intake and the low calcium intake.


Chart No. 3. In high Vitamin D, we have one with a caries index over 1, and the lowest with only one (1) occlusal pit. One with fifteen (15) and one with thirteen (13) cavities in the permanent teeth, and yet the Vitamin D and calcium are adequate.



Chart No. 4. In the low Vitamin D, we have (2) with a caries index above 1. One of 10 years has no cavities in the permanent teeth. One of 11 years has eighteen (18) cavities, and one of 11 years has only two (2) occlusal pits, and another of 11 years has four (4) occlusal pits. These compared with the high D do not show any striking difference.

Children who had Rickets


Chart No. 5

            Chart No. 5. Rickets, which is a disease caused by a deficiency of both calcium and Vitamin D, should show mouths reeking with decay if these two factors controlled decay; but that is not what we find.

We have one of 9 years old with a high caries index. We find one a year younger with only one (1) occlusal pit, and of 7 years has had no caries at all. So we cannot conclude, at least in these children, that the deficiency of these factors causes decay.

Chart No. 6. In high Vitamin C, you will note No. 66 with the highest intake of C has a high caries index of the deciduous teeth and a considerably lower index of the permanent. It might be that the deciduous teeth decayed and the youngster was given Vitamin C and thus reduced the decay in the permanent; but if we look at No. 88, we will see the decay reversed. The deciduous teeth have the lowest caries index and the permanent the most even after the addition of Vitamin C as the child grew older.






Chart No. 7. In low Vitamin C, we have a higher caries index of both the deciduous and permanent teeth.

In the high Vitamin C, we find 137 carious cavities in the deciduous and 75 carious cavities in the permanent teeth. While in the low C, we have 170 carious cavities in the deciduous and 93 in the permanent teeth. Not such a startling difference at that. Of course, in the low C, we have two (2) children of 7 years of age. It will be interesting to see if decay develops in the next three years to compare with the children of 10 years.



Chart No. 8

            Chart No. 8. Our attention has been called to the acid base balance.

Here we have ten (10) of the highest in base intake, and we find only one with a caries index over 1, and cavities varying in the deciduous teeth from one lingual pit in one case to 24 cavities in another, and from no cavities on 12 permanent teeth to 16 cavities on 28 permanent teeth.






Chart No. 9

            Chart No. 9. In the low base balance, we also have one with a caries index over 1. We also have a child 9 years old with only one distal cavity in the deciduous and none in the permanent. Another with two (2) occlusal pits in the deciduous and none in 8 permanent teeth.

Here is a 38 acid -37 base, with 6 cavities in the deciduous and only two (2) occlusal pits in the permanent.

It may be in some localities a low base and high acid produce decay; but, with these children, we have not found it so.



Chart No. 10

            Chart No. 10. We have been led to believe that a quart or more of milk per day would certainly give an adequate diet and prevent decay. Yet, in this group, we have three (3) with a carious index of over 1.

We have all the way from two (2) cavities to thirty (30) in the deciduous teeth, and (25) to none in the permanent teeth.

Chart No. 11. Those children taking from less than a pint to no milk –we have four with a caries index over 1.

In the deciduous teeth, we have a variation of from 9 to 33 carious cavities, and in the permanent teeth a variation of from no cavities to 36.

On the average, we have a little less decay on a quart or more of milk; while we also have no decay with no milk.


Chart No. 12. Salads have been suggested as a primary factor in controlling decay.

In these 10 children who eat plenty of salads, we have two with a caries index over 1. We find one with 25 cavities in 16 permanent teeth –most of them on the occlusal surface. We also find no cavities on 12 permanent teeth.






Chart No. 13. Those eating no salads – we have three (3) with a caries index over 1. We have one with 36 cavities in 28 permanent to five (5) occlusal pits on 12 permanent teeth. No startling difference.



Chart No. 14

            Chart No. 14. In high iron, there seems to be less decay. With an adequate supply, the highest caries index we get is .780 for both sets, and no 11-year old with a perfect score in the deciduous and only two (2) occlusal pits on the 22 permanent. Only three (3) compound cavities on the permanent teeth in the ten (10) children.



Chart No. 15. In the low iron intake, we have three (3) with a caries index of over 1, and cases of very high caries index for the deciduous and three (3) fairly high for the permanent teeth.

In the high iron, we have 18 compound cavities in the deciduous and three (3) compound cavities in the permanent.

In the low iron, we have 36 compound in the deciduous and four (4) in the permanent.






Chart No. 16

            Chart No. 16. In the 11-12 year age groups, we have taken ten with the highest caries index, and with the exception of two cases, they have an ample calcium intake.

The phosphorus (except for one case) is also ample.

The acid base balance is fair.

The vitamins are fairly uniform –none very high, and three (3) fairly low; yet the low-ones do not have the most decay.

Chart No. 17. In the low caries index, the intake of the calcium and phosphorus runs a higher in most cases. The iron and copper are no better. The acid base is very little better. The vitamins also run higher, but the spread in all these factors is not great enough to account for the difference in the caries index.

Of course, the diets of those in the low caries index are better diets that those in the high caries index; but we also have many cases with an adequate amount of all known nutrition factors, and still we have much decay.







Chart No. 18. This chart shows ten (10) children with a high caries index with their urine analysis.

The pH varies from 5 to 7 and

The calcium elimination from ½ grain to 5 ½ grains.

The sodium chloride from 24 grs. to 330 grs.

Phosphorus from 3.57 grs. to 23 grs.

We find nothing consistent in this.

Chart No. 19

            Chart No. 19. In the low caries index and urine analysis, we have much younger children, with no caries in the deciduous teeth and only one buccal pit.

The pH varies from 5.8 to 7.2.

The calcium from .61 of a grain to 2.19 grains.

The sodium chloride from 70.5 grs. to 175 grs.

The phosphorus from 5.75 to 10.92.

The variation in this group seems to be nearly as wide as in the high caries index.

From the study of these charts, it would seem that an adequate diet, as a rule, will produce a less carious mouth than a deficient diet; but we still have those receiving an adequate diet with many cavities, and many with deficient diets and no cavities. Evidently, the adequacy or inadequacy of a diet does not furnish the answer to dental decay.

In searching for an explanation to what these charts show us, it might be well to review what we do know of the causes of caries.

It is commonly accepted that decay starts from the outside of the tooth due to the acid produced by the fermentation of carbohydrates or starch retained in contact with the teeth. This acid is probably lactic acid, produced by certain bacteria acting on solid or liquefied starch in a similar was as a diastase. This conversion is probably doe to an enzyme secreted by a micro-organism.

With this view of caries, how does diet fit into the picture? Time will not permit discussion of the subject in detail, but we can present some of the most salient points.

Chart No. 20. There are three factors always present in decay: first –bacteria, second –food debris, and third –stagnation; and every tooth has a liability to these factors.

FIRST: Liability of form which are pits and fissures or any fissures or any surface defect which includes a roughness of the enamel which would favor the stagnation of food debris. When these pits and fissures are filled and any roughness of the enamel polished, particularly between the teeth, there is less likelihood of stagnation and the formation of placques on a polished surface. When this has been done, we have removed the possibility of stagnation at these points of the liability of form.

SECOND: The liability of position exists in the irregularities of position where food debris can stagnate. This can usually be corrected by Orthodontia.


THIRD: This is the liability of environment which includes the gum tissue, the secretions, and the warmth of the mouth which makes it an ideal incubator for bacteria.

When the gum tissue is normal, it does not permit stagnation. When it is abnormal, it does permit stagnation and may lead to decay.

Of the secretions we have three:

The serous glands which are well distributed over the membrane and are for lubrication.

The saliva is a digestive secretion, containing a digestive enzyme. The composition and quantity of the secretion is controlled principally by the chemical stimulus is received from food. It moistens food, helps in swallowing, is absent during sleep, is neutral or slightly acid at rest, has no germicidal qualities for inhibiting bacterial action; and, if it were the protecting secretion of the mouth, we should find the least decay where saliva is the most abundant, and the most decay where we have the least saliva. This does not seem to be in accord with the facts; for we have the most decay in the lower first molar and the least in the labial surface of the centrals.

The mucous secretion is derived from the buccal glands in the cheek and the labial glands in the lips and the glands on the edge of the tongue dipping down into the floor of the mouth. It is a thick, vacid, sticky secretion, discharged directly upon each and every tooth, does not mix easily upon each and every tooth, dos not mix easily with either water or saliva, and is not easily washed off the teeth. It is continuous in its secretion during all of the twenty-four hours, and is not intermittent like saliva, and has germicidal properties which inhibited, they cannot act on carbohydrates to form lactic acid.

The secretions of the body that have bacteria inhibiting properties are the secretion of the skin, wax of the ear, lachrymal secretion, nasal mucous vaginal secretion and the mucous secretion of the mouth. These secreting areas are all derived from the ectoderm. This sterilizing property of the oral mucous has not been sufficiently investigated.

Chart No. 22. Here we not that the buccal and labial glands discharge their secretion on the buccal and labial portions of the teeth, and the mucous glands on the edge of the tongue discharge their secretion on the lingual side of the teeth. There are no glands in the gum tissue.

In my endeavor to learn if there were any difference between the mucous membrane of a caries-susceptible mouth and an immune mouth, I obtained fresh specimens of the buccal mucosa, the labial mucosa, and the edge of the tongue. The slides were made under the direction of Dr. Darlington. About 55 slides were examined, and they showed a definite microscopical difference between the glands in an immune mouth and one full of caries. Of course, two cases do not prove anything. We should examine many cases before passing an opinion. I tried to obtain more specimens, but was unable to do so.

Chart No. 23. This is taken from the work of the University of Illinos. Different areas of the mouth were seeded with B. prodigiosus, and smears taken as shown, and the colonies counted. You will note that there was no reduction of colonies from the gum tissue, but there was a marked reduction in the buccal gland area and on the edge of the tongue where the mucous glands are most numerous.




The galactans are the mucilaginuous substances which make a wheat flour paste possible. I have never heard of a paste being made from carrots, turnips or string beans; they do not contain galactans.

Polysaccharides,   Starch,          Found in the vegetable kingdom.

(C8H1003)     Dextrine      A soluble starch, produced by a diastase, enzyme, acid, or heat.

Cellulose      Forms the cell wall.

Galactans     Occurs in seeds, legumes, cereals, Alge, Litchens and Mosses.

Pentosans   Fibrous tissue and gummy exudation of plants.


Diaccharides,         Sucrose,       Cane Sugar.

(C12H22012)                        Maltose        Reduced From starch by enzymes, heat, acid.

Lactose         From Milk Sugar.

Monosaccharides,Grape Sugar, Dextrose, Glucose

-These rotate polorized light to the right.

Fruit Sugar, Fructose, Levulose,

-These rotate polorized light to the left.

Lactic Acid,              Galactose, From Milk Sugar.

-Produced during Lactose fermentation. Also produced as a side product in the fermentation of sugars and starches in the presence of protein.

Chart No. 28.

You will also note that lactic acid is the product of fermentation of lactose, and is also formed as a side product of fermentation of dextrines, starches and sugars in the presence of protein.

Wheat contains the most galactans: Rice and corn much less and only half as much protein as wheat. If either of these factors have any bearing on dental decay, we would expect less decay among those peoples who eat corn and rice and no wheat, which is true.

In seeking for the causes of dental decay, we have followed many clews. Among those clews that have been partially successful are the reparative measures which have inhibited decay from progressing, while all efforts up to the present time of preventing decay from starting have not met with any startling degree of success. We have investigated and practiced prophylaxis with some degree of success, we have added to deficient diets those minerals and vitamins no necessary to life, and, in spite of all these measure, decay still persists.

In following clews, it may be possible that instead of WHAT WE DO NOT EAT CAUSING decay, it may be WHAT WE DO EAT that has a greater bearing on the problem.

From what we know of dental conditions of the different people, we have observed that not all races have decay. For instance, the Esquimaux, who do not eat the grain products of civilized peoples, have very little, if any, decay. The Arab living on milk, meat, dates and tigs has almost no decay. The Hawaiians living on their natural foods (no grain products) have excellent teeth. The vegetable eating tribes are also in the same class –no decay, in Tristan de Cuna where fish, potatoes and vegetables are eaten, and no grains, the teeth are also good. The American Indians living on corn had less than 3% of decay. Those living on rice have about 40% to 50% of decay, and those eating whest and wheat  products have from 80% to 100% dental decay. Herein is suggested another clue; it would seem that those peoples who eat seeds or grains that grow above the ground have the greatest susceptibility to dental decay. Then the question arises, are grain and grain products a natural food for man? Is this digestive tract designed and suited for digesting and assimilating seeds such as wheat, rye, corn and rice?

We know that nature, during millions of years, has developed living things that will thrive in certain environments; such as fish in the sea and birds in the air. One fish can live near the surface of the water and another must live at a great depth. Over millions of years, nature has developed the legs of a deer to run and a kangaroo to jump. The physical body has thus been developed to function best in different ways.

There also have evolved in digestive tracts a specialization for each class of work. Some, like the tiger’s with an intestine three times the length of the body, will digest meat best. Another, as in the sheep, with an intestine approximately ten times the length of the body, will digest grass best. Hummingbirds live on the sweet water of flowers and the juice of sweet fruits; this food needs very little digestion, so the intestine is only twice the length of the body, or about two inches long. The ostrich, which lives on fruit, vegetation and vegetables with no teeth to massurate the food, requires fifty (50) fee of intestine, twenty (20) times the length of the body. Man’s intestine varies from twenty-two (22) to thirty-five (35) feet.

As food undergoes progressive modification as it passes through the digestive tube, as might be expected, we also find the tube itself shows a difference in its structure and secretions for these varied tasks. Time does not permit us to observe the changes that take place in the food during its modification.

There are some species of birds that can and do live on seeds. Occasionally grain seeds will be found in the stomach of ground squirrels and some other rodents. I can find no other forms of life to which seeds are a natural food. Man eats them, but is his digestive tract adapted to them? Cows and horses eat grains when fed by man, but if they are turned loose in a field of ripening wheat or oats, they eat only the green part preferably, and any ripened grain ingested is merely by accident, unless they are starving.

There are two ways in which the ingestion of seed foods, particularly wheat, can have an influence on dental decay. As you will note in this slide, the grain carbohydrates contain galactans, and these galactans furnish the mucilage that assists in the stagnation of food debris not only in pits and fissures but on rough surfaces of the teeth. The second may be either an allergy or the effect of toxic material produced during the digestive process, or both. In the field of allergies, wheat is one of the worst offenders.

Commercial sugars eaten with grain starches often interfere with digestion and produce a large number of digestive disturbances. The increase of toxic substances thus formed puts an extra load on the liver and kidneys, and if not thrown off by the kidneys but accumulates, this acid-forming, toxic material often causes acne, as the skin tries to eliminate it. It also causes a catarrhal condition of all mucous membranes, and the mucous membrane of the mouth is often affected, probably lowering its germicidal properties, allowing decay to take place.

Chart No. 30

Chart No. 30. This slide shows the formation, shape and comparative size of the starch granule of potato, wheat, arrowroot, corn, and rice. You will not the potato granule is a different formation and is between two and three times larger than the wheat granule. The corn is much smaller and the rice considerably smaller.

Chart No. 31. This slide gives us the average content of water, protein, carbohydrate and cellulose in the different foods.

Wheat has 13.4% of water, 13.6% of protein, 69.1%of carbohydrate and 2.5% cellulose. Compare this with potato, for instance, with its 75% of water, only 2.08% protein, 21% of carbohydrate and only 8% of cellulose. We can readily see that potato would digest much more easily than wheat. Potato takes about 1 ½ hours and wheat takes 3 to 5 hours. Note that difference in the water content.

Starches are hydrolized in three ways: first –by enzymes, second –by acids, and third –by heat. At temperatures from 178 to 212 degrees F. all starches are changed to soluble forms when suspended in water. If the starch is merely moist, the change is markedly less. It takes 400 degrees F. to convert dry starch to a soluble form.

It is generally believed that baking or toasting of bread converts a large portion of the starch to a soluble form. It does convert a small amount in the crust, but not the inside, for the 400 degrees of heat necessary does not reach the inside.


Chart No. 31


Chart No. 32. The following table of the U. S. Department of Agriculture shows that more than 2 or 3% of starch in bread is converted to sugar or soluble starch.

Chart No. 33. From this chart taken from Professor Pavlov’s “Work of the Digestive Glands,” we note that each food takes a definite amount of juice and a definite amount of digestive power. It is obvious that weak digestions would be improved by eating only one type of food at a time. I have always maintained that course meals were “curse” meals. Where, of course, we need a balanced diet, it does not seem wise to balance each meal, but to maintain that balance through a number of meals.

Stomachs, intestines and their digestive glands are the products of a development over millions of years, and would, therefore, function best with the type of food on which they were developed.

Now note the glands of the seed eating bird at the proventriculus. (G) They are somewhat different and probably have a different secretion. The rest of the glands look very much the same.

In the meat eating, the muscular discs, horny lining and pebbles are missing; the duodenal opening is also lower down –more like an animal’s stomach.

I wish to again call your attention to this point, that the seed eating bird retains its food in the crop or cardiac portion of the stomach, which acts not only as a storage for food, but the food is also mixed there with the crop secretion which seems to have the capability of softening the cellulose content and adding water to the starch granule making it easier to hydrolise the starch. It is then mixed with the fundus or gastric juices and passed on to the muscular stomach to be masticated.

How does man eat these grain foods? He first takes all the water out by baking, depending upon the high heat to convert the starch to sugar and break down the cellulose; or he makes a mush of it, frequently adding a fermentable, refined sugar. He then makes a poor bluff at mastication, which should mix it with the primary digestive juice, saliva; he then swallows it, believing that the short cut he has taken will be supplemented by the other juices along the way.

Birds which are natural grain eaters, mix the digestive juice with the grains and then masticate them. Man, even if he so desired, is not able to eat his grains in this manner. As it is, he won’t even chew them.

The seed digesting apparatus of birds was evolved before the advent of civilized man.



Slide No. 37. This is the digestive tract of man and has the same divisions, namely, oesophagael, cardiac, fundus and pyloric, and that is about as far as the resemblance goes. We would be justified in believing that nature had evolved and developed each digestive tract to function best on the food eaten by that particular animal. Man has been eating grains for 3,000 or 4,000 years, and has not as yet developed a crop or gizzard. He is also not the physical being he was 4,000 years ago.

Slide No. 38. Cats, as you know, are meat eating animals, not grain eaters. This is an X-ray of a cat’s stomach fed on bread and milk mixed with bismuth. As a cat’s stomach is not designed for the digestion of grains or seeds, we find, at the end of seven hours, portions, of such a meal still remain in the stomach; where meat to which it is adapted should digest in 3 hours.

I wish again to call your attention to the fact that in our clinic children we have found comparatively little difference in the caries index between those receiving an adequate diet and those receiving an inadequate diet. There are highs and lows in each group. I also wish to remind you that it is quite possible for dental decay to take place as a result of what and how we DO eat, rather than what we DO NOT eat.

I have presented the facts as I have found them, and am drawing no definite conclusions.

The work yet to be done will undoubtedly reveal to us what effect such factors as foods, particularly the grains, worry, nervous conditions, confusion while eating, fear, anger, hurried eating, overeating, have on the digestive secretions. This influence frequently extends to the oral mucous secretion reducing its germidical inhibiting property, then when stagnation of food debris occurs, micro-organisms can flourish with decay as a result.

241 West 71st. St., New York, City.