By Dr. Royal Lee
Summary: In this eye-opening 1952 article, Dr. Royal Lee outlines the basic mechanism behind autoimmune disorders—something that alludes medical science to this day. Under normal circumstances, Dr. Lee writes, growth factors specific to each tissue in the body, which he calls “protomorphogens,” are released into the bloodstream by the tissues’ cells. To keep protomorphogens from causing runaway growth of their corresponding tissue, the body produces antibodies to neutralize them. When a tissue (or organ) becomes overworked, it begins to produce an abnormally high amount of its protomorphogen. This, in turn, causes the body to produce an abnormally high amount of antibodies. If the amount of antibody exceeds the amount of protomorphogen, the excess antibodies begin attacking the actual cells of the tissue—what has come to be known as an “autoimmune reaction.” Not only did Dr. Lee identify and explain such reactions over seventy years ago, he also developed food-based supplements that thwart them, as he describes in this article. With medicine still groping to explain why autoimmune reactions occur and at a loss as to how to stop them, Dr. Lee’s words are nothing short of astounding. 1952.[The following is a transcription of the original Archives document. To view or download the original document, click here.]
Applied Protomorphology: The Physiological Control of Growth and Repair
It may be assumed that the specific growth factors (the cellular blueprints known as protomorphogens (PMGs) that are constantly being secreted by each cell into its surrounding fluids) are prevented from traveling very far by the influence of specific antibodies known as natural tissue antibodies (NTAs). PMGs must be destroyed because if allowed to build up in any concentration, they would promote cell growth and mitosis. Only if any specific organ becomes subject to overwork and consequent inflammation in some degree does this [buildup] occur. (A kidney doubles in size six months after its partner has been removed, for instance, and muscles grow if sufficient demand is made on their ability.)
Where disease has damaged an organ—such as with tuberculosis in the case of the lung—or where the heart has hypertrophied by overwork, the ingestion of heart or lung PMG, as the case may be, may at first create adverse reactions of a toxic nature (malaise, tiredness), apparently by reason of the immediate proteolytic destruction of the ingested PMG by antibodies in the bloodstream, which are present in higher amounts than normal by reason of the longstanding inflammation of the specific organ.
But cardiographic recordings will show that within a few minutes after ingestion of the cardiac PMG, the heart action changes for the better. It is hard to explain this reaction other than by assuming that the excess heart-tissue antibody in the circulating blood has been reduced by combination with the ingested heart PMG. This is probably done without danger of stimulating the formation of more heart-tissue antibody since alimentary ingestion normally does not permit proteins to act as antigens. Parenteral introduction of such materials is another matter. (Note the adverse results that were reported following the injection of eye-lens extracts to treat cataract.)
Other factors that assist in controlling NTAs are allantoin, betaine (probably by a depolymerizing effect), and the hormones of the gonads, thyroid, thymus, and adrenals. Thymus acts by promoting colloidal dispersion that physiologically opposes cortisone, which flocculates antigens into particulate dimensions that permit their ingestion by phagocytes (and then antibody formation). The thymus during the development age prevents this and keeps PMG available for growth stimulation and ultimate enzyme digestion and renal elimination.
Thyroid hormone splits PMG off the chromatin reserves of the cell or from absorbed stores in connective tissue. That is why thyroxin accelerated tadpole metamorphosis [in a study]. It is also the reason why thyroxin increases the metabolic rate. The released PMG stimulates cell activities.
By Dr. Royal Lee. November 16, 1952.