Vitamin F and Carbamide in Calcium Metabolism
The following is a transcription of the February 1961 issue of Dr. Royal Lee’s Applied Trophology newsletter, originally published by Standard Process Laboratories.
Also in this issue:
- Carbamide in Glaucoma
- High Points of Cardiotrophin PMG
Vitamin F and Carbamide in Calcium Metabolism
Address by Royal Lee, DDS, to Florida Osteopaths, November 14, 1945.
Carbamide, otherwise known as urea, is a physiological constituent of all body fluids that has heretofore been mistakenly considered a waste product. Its presence in urine in considerable amounts has been responsible for this conclusion. Sodium chloride, too, is a constant constituent of urine and is no more a waste product than carbamide. Both are necessary blood and lymph salts, but carbamide is made by the cells for use as an osmotic regulator, and either carbamide or sodium chloride must be available to promote water output in kidneys or sweat glands, where an aqueous solution of waste products is to be thrown off by osmosis. A deficiency of salt in hot weather is a serious matter for the body, but a deficiency of carbamide has heretofore not been recognized as possible or probable. I believe the evidence is clear to show that such may be and often is the case.
Carbamide is made only in the liver and is a product of the splitting of arginine by arginase to yield ornithine and carbamide. Arginine is available, of course, from protein digestion; it is one of the commonest amino acids. Arginase is present in male liver in higher amounts than in female, according to Tauber, and in highest concentration after sexual maturity.1
Carbamide denatures proteins, according to various investigators. That means that it alters the affinity of the protein molecule for any mineral salts that may be conjugated with it, and we know that the calcium in the blood that is destined for bone or tooth use is carried as a nondiffusible molecule of calcium phosphate attached to a protein carrier.
Vitamin F promotes the release of calcium bicarbonate in the blood and its consequent diffusion into the tissues. How? Apparently in this way: Vitamin F is known to promote the action of the sex hormones. The extra activity of the male hormone may cause the increased promotion of arginase activity, with consequent increased blood carbamide. The carbamide denatures the protein-calcium complex, releasing into the blood free ions of calcium phosphate, which react with sodium bicarbonate always present to afford calcium bicarbonate and sodium phosphate. It is probably this same protein-calcium complex that is built up in the bloodstream by the action of vitamin D. It is obvious that without the aid of vitamin F this calcium cannot be unloaded after it reaches its destination.
The rise in blood urea also would account for the great relief sunstroke victims experienced from the use of vitamin F, for their distress is known to be due to two reactions: 1) a stoppage of perspiration that we can now see is a consequence of depletion of both salt and carbamide, without which no sweat can be osmotically secreted, and 2) a high blood calcium from too much vitamin D, which acts as a tissue poison until brought under control. We must recall that the only way excess vitamin D can cause harm is by its boosting of the blood calcium levels.
It also explains why older persons, especially women, can tolerate less sunshine than younger persons.
Chemically, carbamide is carbon dioxide combined with ammonia. As such, it must be considered a buffer salt, for while neutral in itself, it can release ammonia for neutralizing acids if urease (an enzyme that catalyzes this reaction) is present. Now, significantly, urease is found in the stomach mucosa. As such, it should be expected to act as a protection against the tendency of the gastric acid to irritate the stomach wall, by locally providing ammonia to neutralize acid. Suppose the carbamide levels were lowered by reason of sex hormone deficiency? The natural reaction would very possibly be a tendency to gastritis and ulcers, for peptic ulcer is definitely a result of uncontrolled gastric acidity. It is not strange that one important clinical use that has developed for vitamin F is in gastritis now that we see this connection.
Vitamin F has never been actually isolated and identified. It is an associated factor found in certain unsaturated fatty acids. Its highest potency is found in arachidonic acid of kidney fat or the fat of other mammalian glandular organs. Some fish oils are 40 percent arachidonic acid, but they fail to have a vitamin F potency in proportion. It is probably the synergistic association of vitamin F in fish oils that affords the better effect of vitamin D from that source, and it is probably the high sex hormone content of the blood in pregnancy that, by its stimulation of carbamide production, prevents vitamin D from raising the blood calcium to toxic levels, it being an established fact that in pregnancy the female is immune to vitamin D toxicosis.
Do not forget that both sexes make use of both the female and male hormones; the difference is in the proportions. One of the best commercial sources of estrogen is stallion urine. It is probable that an increased intake of vitamin F promotes a normal balance between male and female hormones. It is a common clinical result of vitamin F administration for a woman patient to report a falling off of a masculine hair growth. The effect seems to be a disintegration of the hair shaft at the skin surface. It seems to indicate that the female grows hair, but the shaft cells are friable. Otherwise, how explain this sudden dropping off of hair? Sometimes children and even adults report numerous hairs dropping off on their pillows when arising. That is a disorder of the endocrine system that usually responds to a multiple vitamin treatment. Often it is ascribed to a spirochetal infection, but many cases are seen where this explanation is not probable and which promptly respond to vitamins.
One of the first indications of vitamin F deficiency is nephritis. If carbamide is necessary to osmotic discharge of toxic substances in solution (along with sodium chloride), and its production is dependent on vitamin F, then it is apparent that serious embarrassment of the kidney will inevitably result from F deficiency. It is significant that in sunstroke not only the sweat glands but also the kidney function is paralyzed more or less. This shows, I believe, that there is a severe deficiency of carbamide, and a vicious circle of symptoms is present, which is broken by the vitamin F. The use of carbamide along with salt as a hot weather aid to the osmosis of perspiration would seem desirable.
A mixture of salt and carbamide, equal parts, added to drinking water in small proportions seems to add thirst-quenching properties that the plain water lacks. About a quarter level teaspoonful is ample, to the glass of water.
In allergic conditions a deficiency of calcium is usually considered a contributory factor, and the tissue fluid content of diffusible calcium is usually demonstrably low. Clinically, the use of the vitamin G complex is the most successful of the schedules we have seen tested. A clue is seen here in that pyridoxine deficiency is known to cause tetanic convulsions, and pyridoxine, plus an unknown B factor, has been found interchangeable with vitamin F in the treatment of controlled F deficiency in animals.2
I consider allergies a result of a combination of circumstances that includes a deficiency of vitamin G complex, a lowered level of blood carbamide (common after middle age), and reduced pancreatic activity in which proteins are incompletely digested and antigenic fractions can get into the bloodstream and produce some specific sensitization. I think carbamide is a vital link in this chain, since where it is deficient, there is a great enhancement of the tendency to sensitization. That is because carbamide in itself is a mild denaturant of proteins and probably acts as a first line of defense against sensitizing agents by destroying their antigenic power. Since the carbamide level is secondary to the sex hormone level, the beginning of allergy trouble at middle age is obviously natural. But do not forget that nutritional deficiencies of the G complex and calcium greatly enhance the development of symptoms.
Most patients who need calcium do not respond to its administration in the usual forms. That is no doubt because their condition is due more to their inability to assimilate the element than to its actual absence in the food. It is known that an alkaline intestine will prevent the assimilation of calcium.3
A deficiency of hydrochloric acid in the gastric secretions will definitely inhibit calcium assimilation. Probably one of the benefits of lactobacillus acidophilus or lactic acid yeast is the reduction of intestinal alkalinity and the promotion thereby of calcium absorption.
High phosphorus diets, which may be created by an excess of cereal foods, are stated by the same authority to exert an unfavorable effect on calcium absorption. And calcium phosphate, commonly sold for nutritional purposes, is totally useless nutritionally, according to investigators of the Ohio Experiment Station, reported in Bulletin 347, at least for promoting bone growth in pigs and cows.
The calcium of plant cells and cereal germ is in the form of phytate, an organic combination that also carries inositol, a factor of the vitamin B complex. This calcium compound is soluble in acids and is no doubt normally dissolved by the gastric juice. It also can be rendered soluble with citric acid, so that its assimilation is not dependent on the presence of gastric juice and it can then be taken without other foods. Calcium is best assimilated on an empty stomach because it tends to combine with foods, especially fatty foods, and remain in the intestinal tract if foods are present. So it appears that we have a complicated situation with respect to the assimilation of calcium, and it is easy to see how a patient can develop a condition of acute deficiency in spite of the universal presence in foods of at least some form of calcium.
References
- Enzyme Chemistry, p. 114. John Wiley, 1937.
- Schneider et al. Biol. Chem., 133:LXXXIII, 1940.
- Cantarow, Hare. Calcium Metabolism and Therapy. Lea and Febiger, 1933.
Carbamide in Glaucoma
The Wall Street Journal (Vol. XXVI, No. 106) in an article on new discoveries in eye treatment tells us that urea (carbamide) is a “sight saver in sudden onslaughts of glaucoma”—a “dramatic discovery.” We have pioneered carbamide as a commonly deficient organic substance in the human body for several years. The foregoing article and “The Physiology of Urea,” in the January 1959 issue of Applied Trophology, will verify this.
Glaucoma is most prevalent in warm countries, where the sweat glands are more active, and where the diet is low in proteins to afford the formation of urea as an end product of nitrogen metabolism. Urea in some instances has been defined as a waste product because of its presence in the urine, but it is not a waste product any more than is vitamin C or sodium chloride, which are also thrown out by the kidneys when in excess. We know that both are required to facilitate osmotic transfer of fluids in the body, especially in the kidneys and sweat glands and, it now appears, in the eye.
The vitamin G complex is an essential synergist in the nutritional pattern of the glaucoma patient, we are convinced. Its action as a vasodilator is, no doubt, the important effect.
High Points of Standard Process Nutritional Adjuncts
Myotrophin [Cardiotrophin PMG]: Myotrophin (same as Cardiotrophin) is an extract of beef muscle that acts as a general muscle tonic. It increases the muscle tone and thus increases the capacity for exertion in all muscular tissue. Myotrophin is also used as a supplement for the diabetic because it activates blood sugar pickup by muscle. It may aggravate hyperinsulin tendencies by reason of this.
