Vitamin F

Vitamin F has been identified as linolenic and linoleic acid, or possibly the correct statement is to say that these fatty acids have been given the name of Vitamin F because of their newly discovered vitamin function.

Linoleic and linolenic acids are found in cereals, in especial abundance in flaxseed, but present in all to some extent. (Their abundance in flax is probably a matter of the high oil content of flax, the percentage in the oils of other cereals, rye and oats, probably being higher, but the cost of such oils is fifty to one hundred times that of flaxseed oil). It has been shown that .001 milligram of linoleic acid produces definite improvement in deficient test animals, establishing the “vitamin” characteristic of minuteness of dosage.

In our first discussion of Vitamin F (Vitamin News, Volume 3, No. 8, pages 57-58) we had not become aware of the fact that the investigators of the linolenic acid group were looking at another side of the same picture which we were describing in connection with our findings as to our “Vitamin F.” We were also under the same misapprehension as many others in assuming that linolenic acid was present in larger amounts in common foods (with apologies to those who believe that “any well balanced diet contains plenty of vitamins”).

Matthews has called attention to the resemblance between the oxygen metabolism of linseed oil and protoplasm in the respect that some oxidative accelerator is required in each case, and Plimmer¹ pointed out the fact that the linolenic and linoleic acids present in linseed oil acted as the oxidative accelerator in the cereal oils.

Meyerhof² offers evidence to show that the linolenic acid group of fatty acids is the oxidative catalyst that brings about the oxygen transfers to the muscle cell. This, of course, supplies the theoretical hypothesis that explains the muscular atrophy and malfunction in Vitamin F deficiency, and also throws light on the findings of Zaicsek and Weiser of Budapest, who demonstrated that the feeding of rye to animals caused a muscular development in contrast to the fat accumulation produced by the feeding of wheat.

Our previous approach to the subject through the angle of calcium metabolism is, no doubt, merely another view of the same phenomenon, as oxygen metabolism and calcium metabolism have some important relation, since the control of oxygen metabolism by the thyroid is associated with a parallel control of calcium (when oxygen metabolism is enhanced by the administration of thyroxine, the serum calcium is also lowered) and the thyroid is now considered the physiological controller of tissue calcium content as well as the regulator of oxidation.

Of late some other clinical uses for Vitamin F besides its effect as a reducer of enlarged prostates have become outstanding. One is its action in correcting the common condition of “digestive distress” as characterized by hyperacidity, peptic ulcers, etc. Another is its action in relieving gall bladder trouble. Both of these conditions have been the great mysteries of pathology. It is probable that they both can be explained now on a common ground.

Sajous³ indissolubly connected with oxygen metabolism the metabolic reactions of pepsin and trypsin. Trypsin excess in the bile has been, no doubt, correctly charged with initiating the gall bladder irritation of cholecystitis,⁴ infection, no doubt, being a secondary consequence. So why not consider the same etiology for the irritation that sets the stage for peptic ulcer?

Here are the important facts. Pepsin and trypsin both are protein digesters, acting in series, pepsin in the stomach (in an acid media), trypsin in the small intestine where the reaction is alkaline, (but it will act in either acid or alkaline surroundings), while pepsin will act only in the presence of acids. Now suppose there is a regurgitation of duodenal contents back into the stomach–a common occurrence. Irritation and a sensitiveness to the hydrochloric acid, which, by reason of the irritation, may be overproduced, is the result. This acid now passes into the duodenum, able only to neutralize ordinary quantities, and more irritation results, to say nothing of the proteolytic effect of the excess trypsin on the mucosa.

The value of Vitamin F in these cases is, no doubt, explainable by reason of its oxygenizing ability, to combine the findings of Meyerhof and Sajous, by which less trypsin is required. To hypothecate, in the absence of enough Vitamin F an excessive amount of trypsin may be secreted (by reason of the well known compensative physiologic tendencies), and it may not only be responsible for local trouble in gall bladder, stomach and bowel, but may become a blood constituent in excess, with disastrous results. Why should not it start a proteolytic destruction of the vascular intima, and the typical case of arteriosclerosis develop? As corroborative evidence, we cite Joslin’s statement that “The association of gall bladder disease and coronary sclerosis was striking” (among diabetics). He also states that “the amount and extent of coronary sclerosis in diabetic subjects examined postmortem is astonishingly great. Every one with a duration of diabetes of five years or more has shown some degree of coronary sclerosis.”⁵

That is to be expected, according to our new hypothesis. Pancreatic overactivity is known to commonly accompany diabetes, the other pancreatic secretions being overproduced because of excessive sympathetic stimulus that should arouse the insulin-producing cells, too much trypsin thereby being secreted. The great incidence of gall bladder disease among diabetics is another significant point.

This may explain the success of our Vitamin E tablet as a remedy for angina pectoris (usual dosage two or three Vitamin E tablets a day with two or three “Catalyn” tablets). The Vitamin E tablet contains considerable Vitamin F as well as Vitamin E, and the control of the hypertryptic condition may be the reason for its action. (A little “V- P Phosphade” and one Vitamin D tablet daily often helps to hasten results).

Further evidence of the correctness of this hypothesis is the fact that the Vitamin F (linoleic acid) has been shown to have an anti-enzyme action against trypsin,⁶ and linolenic acid has been shown to have an anti-peptic action (no doubt an exhibition of the same characteristic).⁷ This will alter our theoretical assumption above, that in Vitamin F deficiency more trypsin is secreted, but instead the normal quantity present becomes more active. Either way, however, we have a hypertryptic condition to cope with, and we have a new theory to explain some old and puzzling disorders, to say nothing of the results already definitely established in their treatment with Vitamin F.

Keep in mind that Vitamin F can bring about hypocalcemia if Vitamin D and an ample supply of dietary calcium (raw milk) is not supplied, and that the use of the “V-P Phosphade” enables the patient to utilize his own pathological surplus of calcium carbonate.

Pacini⁸ has given the following consequences of Vitamin F deficiency as indicated by animal tests: 

“1. A scaliness of the skin with a general affection of all the epidermal structures in which the hair becomes brittle and splits easily (fragilitans crinium), the finger nails ridge and split and may become eczematous (atrophia ungium) and the skin may become definitely dry with a tendency to exfoliate and later develop distinctly eczematous lesions.

“2. In the rat a swelling of the extremities.suggestive of angioneurotic edema occurs. In the dog urticaria is the counterpart and in the human, giant hives.

“3. The hair fills with scurf and dandruff–a seborrheic dermatitis.

“4. The hair loosens and falls out readily–alopecia.

” 5. Female animals show markedly impaired ovulation together with failures of reproduction and unusually long gestation periods.

” 6. Males display disinclination to want to mate and eventually become completely sterile. Addition of Vitamin F to the diet prevents or relieves this sterility.

“7. Animals eat the same amount of food, but drink twice the usual amount of water suggesting involvement of the pituitary gland.

“8. Pronounced renal irritation as evidenced by the appearance of hematuria and albuminuria occurs.

“9. Growing animals fail to reach the full weight and remain stunted. Males reach about 70% and females about 80% of their adult weight.”

 

References Cited:

1. Plimmer, Organic and Biochemistry, page 163, Longmans Green & Co., 1933.
2. Meyerhof, O., Chemical Dynamics of Life Phenomena, Lippincott, 1924.
3. Sajous, The Internal Secretions and the Principles of Medicine, pages 852-856, F. A. Davis, Co., Tenth Edition, 1922.
4. Waksman and Davison, Enzymes, page 71, Williams & Wilkins, 1926.
5. Joslin, Treatment of Diabetes Mellitus, page 339, Lea & Febiger, 1935.
6. Jobling, Jol. Exp. Med., 19:239, 1914.
7. Velluz, Bull. Chim. Biol., 9:483, 1927.
8. Pacini, Brochure on Vitamin F, Pharmaceutical Specialties Co., 1936.