The Menace of the Microbe, Part I
The following is a transcription of the May 1959 issue of Dr. Royal Lee’s Applied Trophology newsletter, originally published by Standard Process Laboratories.
Also in this issue:
- Tip of the Month (Aspirin in Gastric Ulcer)
- Dental Erosion Caused by Soft Fruit Drinks and Ices
- High Points of Cataplex E2
The Menace of the Microbe, Part I
(See Part II in the June 1959 issue of Applied Trophology.)
We believe the hypothesis is well established that explains infectious disease by saying it is due to the lowered resistance that follows malnutrition. Most Americans lose their teeth by reason of periodontal infection, entering at the gingival margin. Test animals on cooed food always lose their teeth in this way, but if fed raw foods never do.
To cure periodontal infection, once it is well established, is not by any means as easy as to create it. A rigid exclusion from the diet of all cooked and refined food is essential. However, few people will take the trouble to try to reverse the trend. It is easier to progressively replace the lost teeth with artificial ones.
But there is a lot more to the situation. May we quote from Dr. Weston A. Price:
“I found…in my analysis of conditions in the flu epidemics that the incidence of systemic complications…was about two and a half times greater among patients with extensive dental infections than in those without dental infections.”1
What else does this mean other than that the same cooked food program that predisposes to the loss of teeth also predisposes to the virus of flu?
Degenerative disease—often considered as separate from infectious disease—also can be an end result of periodontal inaction. According to Dr. Price:
“If the placing of an infected tooth beneath the skin of a rabbit can in weeks, months, or a year…develop a typical nephritis in a rabbit where the tooth was taken from a patient suffering from nephritis….it becomes a matter of great concern…that in the groups of individuals with most focal dental infections, the incidence of these degenerative diseases is greatest.”2
A case report by Dr. Price shows the remarkable selectivity of germs toward specific organs even though they are taken from diseased teeth:
“One of our experiences of years ago convinced us that there was danger in some of these pulp involvements to a degree far exceeding that which we had expected. A boy of fifteen years presented with a very acute rheumatism; he was brought by a nurse from a Visiting Nurse Association. The history showed that four weeks previously he was compelled to leave school because of an acute toothache definitely located in the left mandible. This acute pain lasted only a few hours; then it entirely disappeared.
“About a week or ten days later, it was found that he could not get up from his seat in school and had to be carried home with acute rheumatism that kept him in bed for two weeks, after which he was hustled back to school. The teacher reported that he did not seem to care to play with the other children and seemed very tired, which she and the visiting nurse interpreted as being due to the lingering rheumatism. To our amazement we found a very bad endocarditis, with the heart greatly enlarged and already some cyanosis.
“Examination of his mouth revealed deep caries without pulp exposure in the lower left first molar. The tooth was extracted, and the boy was ordered to bed under strict control of the district physician, which directions were not properly carried out, and he was buried in about seven months as a result of a complete breakdown of this heart.
“Before the tooth was extracted, it was determined that the pulp responded nearly normally to irritation and thermal change. After extraction the tooth was sterilized externally, including the pulp cavity, and after the removal of the caries, culture was made from the pulp, which macroscopically was nearly normal except that it showed slight congestion.
“Of thirty rabbits inoculated from this culture, 93.3 percent, or twenty-eight rabbits, developed acute endocarditis within a few days, and 100 percent developed acute rheumatism. This, along with many other experiences, made us very suspicious of the pulps of teeth with deep caries and prompted these special studies.”3
And Dr. Price discusses this matter further:
“Problem: Do diseased organs and tissues modify bacteria growing in the distant focus or create in them a capacity for elective localization for those diseased tissues?
“Experimental and Discussion: This is an exceedingly difficult but very important problem, for if it is true, it not only removes from the organisms some of the culpability but furnishes an explanation for some of the phenomena that develop by transferring the organisms from that focus to another host. An analysis of our clinical records and experimental data throws some direct light on this problem. In the second chapter preceding, I reviewed a case in which the bacteria from the dental infection of a patient suffering from acute involvements in the cervical and dorsal regions, when inoculated into experimental animals, developed acute involvements in the ovaries, tubes, and uterus—a lesion that is so rare that not one percent of experimental animals develops such a lesion from dental cultures of ordinary patients. Indeed, it had not been revealed in the taking of the physical history that this woman had had operations, a secret which she carefully guarded. After the development of the lesions in the rabbits, I asked her specifically regarding the history of disturbance in the pelvic organs, whereupon she gave me the history that one ovary and tube had been removed some years previously at one operation, and at a later time the other ovary, tube, and uterus. In this case, then, there were no such tissues to be involved.
“In Chapter 62, ‘Primary and Secondary Sex Organ,’ we report a case with a very similar history. The woman presented had a heart involvement and quite severe rheumatism. The inoculation of the rabbits developed acute involvements in the ovaries, tubes, and uterus, with an unusually severe involvement of the uterus, with extensive suppuration. I sent for the patient and asked her if she had given me the history correctly. She said she had not and that she did not wish to think about it, let alone talk about it, since a purulent uterine discharge had been becoming more severe for six months, and her physician had advised her that it was probably malignant and at her age an operation would not be justified. In this case, as shown in that chapter, this purulent discharge completely subsided with the removal of her infected teeth and has not recurred in two years except for a couple of days at the time that an infected sequestrum was giving trouble after one of the extractions. Had the infected uterus been the primary lesion, we would not suspect that the removal of the dental infection would have seriously modified the primary focus, which is very important.
“In that same chapter, we recite the case of a man from whose dental infection cultures were taken and inoculated into rabbits, which produced acute infections in the testes of each of three male rabbits, the cultures being taken from three different teeth. On being questioned, his reply was, ‘Can’t a person have any secrets?’ and confessed that he had had a recent severe involvement of the testes, and that he had had gonorrhea twenty years previously, which had been treated and supposedly cured.
“In that chapter we refer to cases of ovarian cysts that have been operated and in in which cases the cultures from dental infections developed ovarian cysts in the rabbit.
“It is not possible to state from these clinical cases to what extent either the dental infection was originally causative in the involvement of these special tissues or to what extent these special tissues influenced the organisms growing in the focus. In the first case mentioned, however, it was seven years since the last operation. In other words this individual did not have in her body primary sex organs to be related directly to the dental infection. It is true, however, that the dental infections that were removed had been of probably twenty years standing, and her first operation had occurred fifteen years previously.”4
It is quite evident that infective processes can be almost as irreversible as cancer. It is a matter of history how Dr. Price, when he realized that the basic cause of disease was malnutrition, closed up his dental practice and took a trip around the world to gather the evidence he presents in his monumental book Nutrition and Physical Degeneration.
It is evident that the streptococcus has a selective action on specific organs. This can be accomplished only by some mechanism that makes use of the tissue protomorphogen, for it is the protomorphogen that confers specificity on any organic substance.
We know from clinical evidence that certain strains of the streptococcus organism have specific enzymes that attack heart tissue, causing rheumatic heart disease. The heart disease appears fourteen days after the initial attack of streptococcus infection. Fourteen days is the period required for the development of any natural tissue antibody, and the heart symptoms are due to this antibody, we are sure, not to the primary effect of the streptococcus organism.
Suppose the patient having a tooth abscess had become infected with a streptococcus that had been trained in its previous environment to enzymatically digest the wrapping layer off of heart protomorphogen.
We have ample evidence to show that the blood carries protomorphogens from all specialized tissue (necessary to the function of gonads and parotid, if not pancreas).
Suppose the nest of streptococcus in the apical tooth abscess proceeds to unwrap and release these free circulating protomorphogens into the bloodstream. Phagocytes pick up free protomorphogens as a normal thing and carry them to the reticuloendothelial tissues (spleen, etc.), where natural tissue antibody will then be elaborated. (This antibody reaction is normally not activated to this extreme degree, except to combat a microbic invasion.)
Then we have a full-blown case of rheumatic heart disease or other specific breakdown of some organ, as described by Dr. Price.
A case of exophthalmic goiter promptly recovered after abscessed teeth were extracted, and a rabbit inoculated with a culture from the infected teeth promptly developed exophthalmos.5
References
- Price, Weston A. Dental Infections—Oral and Systemic, 1, p. 583. Penton Publishing Co., 1921.
- Ibid., p. 622.
- Weston A. Dental Infections and the Degenerative Diseases, Vol. 2, p. 55. Penton Publishing Co., 1923.
- Price, Weston A. Dental Infections—Oral and Systemic, 1, pp. 318–319. Penton Publishing Co.
- Ibid., p. 565.
Tip of the Month (Aspirin in Gastric Ulcer)
Aspirin shown to aggravate hemorrhage in gastric ulcer (“Gastrointestinal Hemorrhage and Salicylates,” J.A.M.A., pp. 179, 643, February 7, 1959).
It would seem the logical approach here would be to use Anti-Gastrin [Gastrex] or Comfrey Pepsin E3 [Okra Pepsin E3] as indicated, to promote healing, rather than to aggravate with antacids.
Dental Erosion Caused by Soft Fruit Drinks and Ices
“Mellanby and coworkers (British Dental J., 104:305, May 6, 1958) stated that soft fruit drinks, carbonated beverages, fresh fruit juices, candies known as ‘acid drops,’ and frozen synthetic fruit drinks sold as ‘iced lollies’ cause dental erosion. Carbonated beverages are less harmful than the others. Most of the observations were carried out on the teeth of rats and dogs, but some were made on extracted human teeth. Many children suck iced lollies for long periods, and in this way citric or tartaric acid comes in direct contact with the teeth for long periods, causing marked erosion. Sucking fruit-flavored candies, which also contain these acids, is also harmful to the teeth.”
—J.A.M.A., June 28, 1958
High Points of Standard Process Nutritional Adjuncts
Cataplex E2: This is the specific anti-angina fraction of the E complex in its natural form. It is probably the real active principle of the E complex. The tocopherols seem only to be useful as an antioxidant, to protect this specific factor from destruction. E2 seems to be the fraction that actually prevents the sudden death from coronary attack that follows if vitamin E is omitted from the diet, as reported in Science, Vol. 104:2701, p. 312.
Clinical experience in the use of high unit dosages of the single tocopherol factors for cardiac involvement has been disappointing. This is due, we believe, to the fact that natural forms of vitamin E complex lose up to 99 percent of their potency when separated from their natural synergists (Ann. Review Biochemistry, p. 38, 1943). These synergists include tannins, fatty acids (vitamin F complex), phospholipids, and other synergistic factors.
Further, chemically purified vitamin E (tocopherols) in high unit dosages reverses its effect and produces the same symptoms (bone decalcification) as a deficiency (Vitamins in Medicine, Bicknell and Prescott, p. 735).
The inference here is that you cannot measure a vitamin by one of its fractions, which, when isolated, cannot act as the vitamin and may actually cause a reversal of vitamin action by exhaustion of essential synergists.
Vitamin E2 is a natural phospholipid concentrate, prepared from mammalian tissue high in chromatin material and including trace elements from green leaf source. This concentrate is particularly high in vitamin E2 but includes natural tocopherols, but only to the extent that they appear in the natural vitamin E complex as protective antioxidants.
Indication for possible need: Angina pectoris, coronary disease, and hypertension.
