Applied Trophology, Vol. 10, No. 8
(August 1966)

“Immunity and Hypersensitivity as Factors in Etiology of Mesenchymal Diseases” and “Acidophilus Milk in the Therapy of Infantile Diarrh”

The following is a transcription of the August 1966 issue of Dr. Royal Lee’s Applied Trophology newsletter, originally published by Standard Process Laboratories.

(Editor’s note on “A Doctor’s Viewpoint of Whole Food”: This article was originally published in two parts in the July and August 1966 issues of the Applied Trophology newsletter. For your convenience, we have presented the article in its entirety in the July 1966 Archive issue, available here.)

Immunity and Hypersensitivity as Factors in Etiology of Mesenchymal Diseases

Excerpts from Postgraduate Medicine, Special Issue, Connective Tissue Diseases, by Peterson and Good, p. 422, May 1962.

Hypersensitivity associated with the production of cross-reacting antibodies may be the basis for many diseases. So-called autoimmune diseases, characterized by the presence of antibodies against the patient’s own tissues, may involve cross-reacting antibodies in some instances. For example, in lupus erythematosus the antibodies directed against the host cell nuclei may have been elicited by an exogenous antigen rather than the host’s cell nuclei.

Auto-Antibodies to Isolated Antigens

There are tissues in the body that are essentially isolated from immunologically competent cells under normal conditions. If such tissues are exposed by trauma or disease, antibodies against them may be produced. Such antibodies may merely reflect this unusual exposure and may have no other significance, or they may result in damage to the tissue.

Sympathetic ophthalmia is a disease that seems to illustrate this type of auto-antibody.12 A penetrating injury to one eye exposes tissue previously well isolated from the rest of the body. Such tissue is not recognized as “self” by the antibody-producing cells, but rather is considered foreign material. Antibodies and hypersensitivity are therefore produced, which in turn may damage the other eye. Such a situation may also obtain where other auto-antibodies are found, e.g., antibodies against the heart following a myocardial infarction or after cardiotomy,13 antibodies against thyroglobulin following thyroid infection or surgery, and antibodies against the pancreas in patients with cystic fibrosis of the pancreas or chronic pancreatitis.14 There are many similar examples.

In experimental animals, central nervous system disease or peripheral neuritis simulating post-infectious leuko-encephalitis or Guillain-Barre syndrome may be produced by injecting brain or peripheral nerve tissue along with immunologic adjuvants at a parenteral site.15,16 In these latter instances, the role of the antibody in causing the disease is seriously questioned; whether or not antibody perpetuates disease is even more difficult to answer. It has been suggested that cellular immunity, rather than circulating antibody, is responsible for some of these diseases.17

Auto-Antibodies Resulting from Altered Antigenicity of Host Tissues

Although the body generally will not make antibodies against its own tissues, it appears that slight modification of the antigenic character of tissue may cause it to appear foreign to the immune system and thus a fair target for antibody production. Schwentker and Comploier18 proposed that the streptococcal toxin causes damage to renal tissue and consequent release into the general circulation of a protein which acts as a foreign protein, thereby stimulating production of an antibody to kidney protein. Circulating anti-kidney antibodies have been related to both clinical and experimental renal disease; they are present in the serum of patients with various renal conditions19 and have been shown to result in experimental renal disease.20 Whether or not such a mechanism causes human renal disease is unknown, but the immunologic implications of existing data are strong.

Infections in the colon may alter the gastrointestinal mucosa sufficiently to induce formation of the anti-colon antibodies found in patients with ulcerative colitis.

From these considerations, it seems entirely possible that certain human diseases have as their basis an immunologic reaction to host tissues made antigenic by infectious processes.

We are here discussing the infinite complications and ramifications of disease that can develop. To remedy the ravages of such malnutrition, ill-advised drugs and poisons in huge dosages are used, which are often injected directly into our long-suffering bloodstream by medical doctors. Patients “would be healthier if drugs had never been discovered,” to quote the famous Boston physician, Oliver Wendell Holmes, and who also said: “If all the medicines were thrown into the sea, it would be better for mankind, but all the worse for the fishes.”


The references below apply only to quoted excerpt from Postgraduate Medicine, May 1962.

  1. Theodore, F.H., and Schlossman, A. Ocular Allergy. Baltimore: Williams & Wilkins Company, p. 347, 1958.
  2. Gery, I., Davies, A.M., and Ehrenfeld, E.N. “Heart-Specific Antibodies.” Lancet 1:471–472, 1960.
  3. Murray, M.J., and Thal, A.P. “Clinical Significance of Circulating Pancreatic Antibodies.” Int. Med., 53:548–555, 1960.
  4. Waksman, B.H., and Adams, R.D. “Allergic Neuritis: An Experimental Disease of Rabbits Induced by the Injection of Peripheral Nervous Tissue and Adjuvants.” Exper. Med., 102:213–236, 1955.
  5. Kabat, E.A., Wolf, A., and Bezer, A.E. “The Rapid Production of Acute Disseminated Encephalomyelitis in Rhesus Monkeys by Injection of Heterologous and Homologous Brain Tissue with Adjuvants.” Exper. Med., 85:117–130, 1947.
  6. Waksman, B.H. “A Comparative Histopathological Study of Delayed Hypersensitive Reactions.” In Wolstenholme, G.E.W., and O’Connor, M. (Editors). Cellular Aspects of Immunity, Boston, Little, Brown & Company, pp. 280–322.
  7. Schwentker, F.D. and Comploier, C. “Production of Kidney Antibodies by Injection of Homologous Kidney Plus Bacterial Toxins.” J. Exper. Med., 70:223–230, 1939.
  8. Kramer, N.C., Watt, F., Howe, J.H., and Parrish, A.E. “Circulating Antihuman Kidney Antibodies in Human Renal Disease.” Am. J. Med., 30:39–45, 1961.
  9. Masugi, M., Sato, Y., Murasawa, S., and Tomizuka, Y. “Ueber die Experimentelle Glomerulonephritis durch das Specifische Antinierenserum.” Jap. Path. Soc., 22:614–628, 1932.
  10. Broberger, O., and Perlman, P. “Auto-Antibodies in Human Ulcerative Colitis.” Exper. Med., 110:657–674, 1959,

Acidophilus Milk in the Therapy of Infantile Diarrhea

In the paper are presented the results achieved in the application of acidophilus milk in dyspeptic infants infected with pathogenic E. coli G.E.I. In 21 out of 28 cases dealt with from the University Children Hospital in Zagreb has been isolated E. coli O111 seven strains proved resistant to all antibiotica of the daily praxis; two strains were poorly resistant (+) only to aureomycin; one strain (+) to aureomycin and terramycin; two strains (+) to aureomycin and chlormycetin; and one strain (+) to chloromycetin. Besides two strains that were poorly sensitive (+) to aureomycin and chlormycetin, all the other serotypes of E. coli O86–O114 and O127 proved sensitive (+ +) to one antibioticum at least.

The pathogenic E. coli G.E.I. disappeared from the lumen of the gastrointestinal tract of the dyspeptic infants within one to five days after application of acidophilus milk. Owing to the rich contents of the acidophilus milk in vitamins and other soluble lactates of phosphor, calcium and iron, easily resorbed by the organism, the infants recovered rapidly and—as observed by clinicians—gained weight quicker and more copiously than other infants of a control group.

—Von K. Tomic-Karovic and J. Famiek, Aus dem Immunologischen Institut., Zagreb. Translation of summary reported in Ann. Pediatric., 199: 625–634, 1962

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