I BECAME INTERESTED in adrenal physiology almost two score years ago and my interest has never waned. The reason is simply that adrenal function remains a major area of unexplored potentials.
When I began my research in the metabolic aspects of psychoses, the adrenal seemed to pop up at me from almost every direction. Let's take one simple case in point. It was in the late 402 when the Worchester group postulated an adrenal deficit in schizophrenia on the basis of a reduced adrenal reserve. Having spent some years with patients in a female disturbed service, the concept of an asthenic catatonic schizophrenic was simply unreal. Also, having wrestled for physical integrity with a 90-pound patient who had bitten the ears and nose of other patients, it was clear that what was being confused was total current adrenal output with residual reserve. There were a whole range of other clues, including, but not limited to, a remarkable absence of the common cold and other viral diseases, psychosomatic disorders, such as ulcerative colitis, peptic ulcer, as well as asthma and hay fever in patients during an active psychotic episode.
We soon began to appreciate that patients high tolerance to pain, high tolerance to histamine, thyroid, and other substances could have major significance. This was borne home to us by both our clinical findings and our counter-experiments involving extirpation of thyroid, gonads, adrenal, and thymus. Incidently,I should comment that one result was our report that the thymus was an important endocrine gland-a report made some 30 years ago.
You may therefore appreciate why I pass on to your, as an interesting comment, in view of the current concern with Reye's syndrome, a letter we just received from Robert F. Cathcart III, M.D.
The quandary facing physicians wishing an antipyretic for children with flu or chickenpox but not wanting to risk the increased incidence of Reye's syndrome with aspirin administration is easily resolved by administering large doses of ascorbic acid orally or sodium ascorbate intramuscularly.
Ascorbic acid administered orally to bowel tolerance (just short of producing diarrhea) has a definite antipyretic effect. Two to 4 cc of a 25% solution of sodium ascorbate (without preservatives) administered IM to small infants will usually have a dramatic effect on elevated temperatures. Repeat doses can be given if the temperature elevates again.
It is interesting that the common childhood diseases which increase bowel tolerance to ascorbic acid the most are influenza and varicella. Mononucleosis is champ among teenagers.
I think that this increased bowel tolerance is a sign that the metabolic processes are utilizing the additional ascorbate so that it does not reach the rectum and cause diarrhea. This increased utilization of ascorbate puts at risk all metabolic functions of the body dependent upon ascorbate.
Since some of the symptoms of aspirin toxicity are perhaps not coincidentally some of the symptoms of ascorbate deficiency, it may be that aspirin increases the body's utilization of ascorbate. Perhaps there is an accumulatively induced deficiency of ascorbate which has something to do with the increased incidence of Reye's syndrome in profoundly ill children administered aspirin. (Cathcart RF: Vitamin C: Titrating to bowel tolerance, anascorbemia, and acute induced scurvy. Medical Hypotheses 7:1359-1376, Nov, 1981.)
Before signing off, I think I should call attention to two points:
1. Robert F. Cathcart III is the brilliant originator of the Cathcart hip prosthesis.
2. For those following ascorbic acid in the literature, its relationship to adrenal function and implicitly also to thymic function, as well as to immune responses, to collagen formation, to phagocytosis, to mucosal integrity, etc., does not come as a surprise nor would this be new to the growing number of physicians who share my respect as well as affection for one of the greatest living scientists: Linus Pauling.