Physiology of Urea; Nutrition; Diverticulosis; High Points (For-Til B12)
Contents in this issue:
- “The Physiology of Urea,”
- “Tip of the Month (Diverticulosis),”
- “High Points of Standard Process Nutritional Adjuncts (For-Til B12).”
The following is a transcription of the January 1959 issue of Dr. Royal Lee’s Applied Trophology newsletter, originally published by Standard Process Laboratories.
The Physiology of Urea
Urea is chemically a combination of carbon dioxide and ammonia. It is unique as a salt from a physiochemical viewpoint in that it is possibly the only known soluble substance that, when dissolved in water, reduces instead of increases the water’s conductivity of electric current. It probably does this by promoting the polymerization of other salts present into less ionized forms, for urea is known to promote the colloidal state of matter (a state essential to life) from the crystalloid state.
Research by Crile in regard to the part that electrostatic forces play in the cell—and how every living cell is alive only because it has been able to create a potential (electrical) difference between cytoplasm and nucleus—enables us to see how urea can be so important in living tissue. Crile showed that any influence that tended to “short circuit” the potential difference of the cell reduced the cell’s vitality. Urea, if present in pericellular fluid, would reduce the conductivity of the fluid and tend to raise the vitality of the cell.1
It is very likely that urea is necessary to maintain osmotic balances between the semipermeable membranes. “In the elasmobranchs the high urea concentration (2 percent) serves…as a means of increasing the osmotic pressure above that of the external seawater…”2
When water is to be intravenously administered, it must be in the isotonic form of Ringer’s, Tyrode’s, or Locke’s solution, containing enough sodium chloride to afford the same osmotic pressure as normal blood serum or lymph would supply. It seems no one has looked into the possible need for inclusion of urea into such a solution, possibly displacing some of the sodium chloride. Blood normally contains 25 to 50 mg of urea per 100 cc, or about 10 percent of its sodium chloride content.
When adrenocortin is deficient, salt is lost through the kidney, and blood urea rises.3 This is no doubt a compensatory effect. In cortin deficiency it has been shown that the kidney tubules let through more salt and reabsorb more urea. In fact, Kendal found two separate cortical factors—one that controlled the salt elimination, the other the urea.4
Matthews tells us that an average of 40 percent of the urea excreted by the renal glomerulus is reabsorbed by the tubules. This is evidence of the maintenance of a physiological level in the blood. The erythrocyte carries a reserve supply of urea,5 showing that urea must have a physiological significance other than as a metabolic end product. A fact not commonly known is that urea is a normal plant-juice constituent too,6 which would indicate that it may be essential to most cell activity.
Presumably, the moon face of the cortisone user is due to the water retention, secondary to salt retention and low urea, that follows the use of this hormone. The low urea can in part explain the excessive susceptibility to infection of the cortisone user, too, since urea is known to assist antibiotic influences when present in physiological concentrations.6a
It is very probable that the sludged blood phenomena are in large part a consequence of urea deficiency. Clinically, the tendency is characterized by tingling of extremities, dizziness, tinnitus, and danger of thrombus blocks of coronary or cerebral nature. It is significant that a low blood urea is accompanied by a high blood cholesterol and that the administration of urea lowers blood cholesterol.
Klein’s observations of the blood changes that were found to precede coronary thrombosis7 and Knisely’s report on “Sludged Blood”8 are no doubt clinical aspects of this change in the physical properties of blood in which the ionic equilibrium is involved—and in which the use of urea might be helpful.
“In patients with impaired renal function…large doses of water may produce headache, dizziness, vomiting, and cramps, with a marked increase in weight and an increase in the blood pressure…These symptoms can be rapidly relieved by injecting hypertonic salt solution or by giving urea.”7a
Patients on a low-protein diet, particularly in warm weather, may produce so little urea that they develop such symptoms. We have seen urea consistently relieve the tendency to nightmare when given in small doses (one-half teaspoon to a glass of water).
Opiates stop the production of urea, thereby causing kidney inhibition. If urea is supplied with opiates, the mental reactions are not present. In cases of a preexisting urea deficiency, the opiate has highly aggravated, toxic effects.
Knisely tells how common the sludged blood phenomena are. He found them in a high majority of cases of infectious and degenerative disease, no doubt as a complication that aggravated the severity of the disease. This complication is probably due to malnutrition and harmonic imbalances.8
Salt deprivation can aggravate the situation where urea is low. Any patient put on a salt-free diet may need supplementary urea regularly. Most patients considered candidates for a salt-free diet are of the high cholesterol type, and it may be more important for them to get more urea than to get less salt.
Sex hormones indirectly maintain urea output. The symptoms of urea deficiency are those of menopause and of the later periods of life. These symptoms are stubborn and fail to respond to measures other than the right one, as is the case in all deficiency reactions.
Testosterone, for example, caused an increase in kidney arginase of 600 percent in thirty days.9 We believe this was the result of mobilizing tissue determinants for gonad use, with a consequent increase in metabolic waste products to be eliminated by the kidney.
Nephrosis seems to be the result if kidney arginase fails to be produced to cope with the need for waste elimination. In nephrosis the use of Arginex (the Standard Process brand of arginase in tablet form) has been phenomenally successful in restoring kidney function, as indicated by the disappearance of albuminuria. The relief is very prompt. Arginex also has found much use as a headache remedy in headaches of the auto-intoxicative type (those caused by missing a meal, allergic headaches, and those caused by milk allergy being the commonest).
The Pharmacopeia recognizes the value of urea as a diuretic but in the heavy dosage of 20 grams per day—about twenty times the amount we consider necessary to correct a deficient state. This is the usual difference between physiological doses and pharmacological doses. It is of great importance to keep this difference in mind, for if we retain our physiological balances, we will never need pharmacological assistance.
Knisely’s blood sludging may be considered a reaction to toxic metabolites that are not properly or promptly eliminated. A patient with second degree burns was found to be low in urea;10 another with uremic poisoning also had low blood urea. This is evidence that the urea supply had been exhausted in osmotically eliminating poisons.
It seems highly probable that sodium chloride and urea are both essential factors in promoting osmotic elimination of toxic metabolites from the body through both the kidneys and sweat glands.
Salt is an electrolyte and urea anti-electrolyte, with one thing in common: both are required in the proper proportion to maintain osmotic pressure for eliminative functions. This no doubt is true of other internal balances between semipermeable membranes.
Salt increases the conductivity of body fluids (an undesirable characteristic), while urea reduces this conductivity, yet both substances raise osmotic pressure. Thus it is clear that the balance between salt and urea is one of physiological equilibrium as much as it is of isotonic balance, which considers osmotic pressure alone. This is a factor overlooked by Ringer and all investigators who followed him. It is well to note too that urea prevents the formation of blood clots in the vascular system.11
This is another example of the unique nature of urea in promoting the colloidal state of matter. If flowers of sulfur are boiled in a solution of urea, colloidal sulfur is produced.12 The crystalloid sulfur is converted into a colloidal suspension of molecular particles, comparable to the colloidal carbon in India ink. A grain or two of salt will precipitate the carbon in a bottle of India ink, by discharging the electrical charges on the carbon molecules so that they no longer repel each other and drop to the bottom of the bottle.
Blood sludging is in all probability a parallel process. No wonder there is a general furor over excess salt in the diet, just as there is concern over too much cholesterol in the blood or too much calcium in the tissues of the victim of hypertrophic arthritis. But let us find the cause of the disorder.
The arthritis sufferer will be found to have calcium deficiency symptoms along with his calcified joints, for he has lost the ability to keep calcium in solution. He often has osteoporosis to go along with his deposits of calcium where it is not wanted. By correcting hyperalkalinity, his bones will get more calcium and his tissue deposits will disappear. This transportation system is restored in function as regards calcium, which no longer falls out of the bloodstream on its way to its destination.
We can, therefore, attribute three important physiological functions to urea:
- It helps maintain osmotic pressure, by which water-soluble toxic metabolites are eliminated via the kidneys and sweat glands.
- It opposes the effect of salt by decreasing the electrical conductivity of body fluids. (Urea reduces conductivity of water by its presence.)
- It promotes colloidal dispersion of materials insoluble in water. (This effect causes urea to cooperate with heparin in preventing nonphysiological blood clotting).
Vitamin B12 and heparin both contribute to the control of hypercholesterolemia and to the elimination of the xanthomatous skin lesions accompanying blood cholesterol excess in some cases.12a
This involvement of urea in the common problem of sludged blood and thrombosis disease brings us to the recently published finding that the clinical effect of vitamin K deficiency is a greatly increased tendency to coronary thrombosis.13
The use of deep-freeze foods was found to bring about a vitamin K deficiency by reason of the oxidative destruction of the vitamin in vegetables stored for too long a time.
It is likely that low-protein diets and refined cereal foods were important contributory factors, with low urea resulting as a consequence.
Urea (“carbamide” to the chemist) is used as a food factor in cattle feeding, since a considerable part of the protein component in the feeding ration can be displaced by the urea: the cow’s intestinal flora synthesizes protein from the urea. But certainly a refined or crystalline substance is no substitute for a natural food protein complex with its vitamins and trace minerals.
- Crile, G.W., MD. The Bipolar Theory of Living Processes. Reprinted by the Lee Foundation.
- Sumner and Myrback. The Enzymes, Vol. l, Part II, p. 898. Academic Press, 1951.
- Svirbely and Kendall. Jol. Physiol., 116:187–193, 1936.
- A.M.A., 105:1486, 1935.
- Rolls, J.O. Biol. Chem., 151:2, 529, 1943.
- Reifer and Melville. Biol. Chem., 178:715, 1949;
6a. Ann. Rev. Biochem., p. 453, 1943.
- Klein, Ernest, MD. Lee Foundation Reprint No. 96 (reprinted from Prevention);
7a. Macleod’s Physiology in Medicine, 9th Ed., p. 1082.
- Knisely, Bloch, Eliot, and Warner. “Sludged Blood.” Lee Foundation Reprint No. 35 (reprinted from Science, November 7, 1947).
- Vitamins and Hormones, Vol. X, p. 336, 1952.
- Bowman et al. Lab. & Clin. Med., p. 706, August 1945.
- Rev. Physiology, p. 178–179, 1954.
- Van Klooster. Experiments in Physical Chemistry, p. 162. The Chemical Publishing Co., 1925;
12a. Nutrition Reviews, Vol. 14, p. 47, 1956.
- Doles, Hunter, McGuire. Lecture, Norfolk Cosmopolitan Club, February 1957; Vitamin News, p. 215, July 1957.
What the Journal of the American Medical Association has to say about diet and degenerative diseases:
“When we learn to eat day after day, month after month, year after year all the essential nutrients, a higher degree of health will result. There will be a marked decrease in the degenerative diseases, and a prolonged, healthy life span will follow. Progress of the science of nutrition and growing knowledge of vitamins, minerals, and enzymes place the physician in possession of facts that enable him to prevent and control the ever-increasing danger of degenerative diseases in geriatric patients. Food intake should be based on what materials the body needs for its health and efficient function, rather than on present-day, perverted taste habits. The diet should be low in carbohydrate, low in fat, high in protein, and high in foods that contain natural vitamins and minerals, such as whole grain products, in the form of breads and cereals, and fruit and fresh vegetables; and the intake of refined foods and sugars must be restricted or eliminated.”
—W.C. Martin, MD, “Essential Nutrition in Geriatrics,” International Record of Medicine, September 1953
Tip of the Month (Diverticulosis)
Recent tests on rats indicate that diverticulosis (intestinal) can be overcome through the use of bulk-forming foods such as fresh whole wheat products.
High Points of Standard Process Nutritional Adjuncts
For-Til B12: A geriatric product containing tillandsia and fortified with a fermentation type of vitamin B12. Tillandsia supplies vitamin E-chlorophyll complex factors that have been observed to clinically counteract some of the effects of degenerative conditions in the aged.
For-Til B12 also seems to reestablish delayed sexual development and has been clinically observed to support the growth of underdeveloped breasts in some young women.