Applied Trophology, Vol. 8, No. 7
(July 1964)

Vitamins (Part I)

Contents in this issue:

  • “Vitamins (Part I),” reprinted from Meyler’s Side Effects of Drugs.

The following is a transcription of the July 1964 issue of Dr. Royal Lee’s Applied Trophology newsletter, originally published by Standard Process Laboratories.

Vitamins (Part I)

“Chapter XXVI: Vitamins” is reprinted in two parts from Meyler’s Side Effects of Drugs, 4th ed. (Part II available here.)

Vitamin A

Acute vitamin A intoxication has been reported after ingestion of 300,000 IU in children and 2–3 million IU in adults.

Chronic intoxication in adults occurred after relatively low dosage with a higher frequency than was formerly recognized. Toxic reactions may arise from prolonged ingestion of vitamin A in daily doses exceeding 50,000 IU.1

Vitamin A intoxication, especially in the child, may cause “pseudo tumor cerebri,” with symptoms of headache, papilledema (with the risk of optic atrophy), and diplopia, but mostly without localizing neurological signs.2 Other features noted in such cases were: dryness, roughness, and desquamation of the skin; fissuring at the corners of the mouth; loss of hair; enlargement of liver and spleen; bone pains; somnolence; mental irritability; anorexia; and hypomenorrhea (in older patients).2

In an infant the diagnosis of hypervitaminosis A was made at the age of four months. Increased intracranial pressure, vomiting, irritability, drowsiness, hyperostosis of the clavicles, tender subcutaneous swellings, and spotty alopecia were the symptoms. Discontinuation of vitamin A intake was followed by prompt improvement. Resumption of excessive vitamin A intake caused a recurrence of all symptoms, which cleared again after definitive withdrawal of the vitamin administration.3

A case of chronic vitamin A intoxication in a 32-year-old man has been described. He received 100,000 IU daily during two months as treatment for acne. When seen he at first denied ingestion of vitamin A. The symptoms were intermittent bone and joint pains, fatigue and insomnia, loss of hair, dryness and fissuring of the lips, anorexia and weight loss. Enlargement of the liver was found. The serum vitamin A level was 250 IU (normal 50–200 IU).4

The administration of an excess of vitamin A to pregnant animals caused malformations in the offspring: micromelia and syndactyly in mice, ectromelia in rats, and syndactyly in rabbits.5

Thiamine (Vitamin B1)

A number of cases of anaphylactic shock after the injection of thiamine hydrochloride have been described.

In the case of a 67-year-old woman, the oral ingestion of one vitamin B1 tablet caused nausea and generalized pruritus. Despite this, next day an injection of vitamin B1 was given intramuscularly. Anaphylactic shock occurred with a loss of consciousness lasting for four hours. This was followed by a phase of angioneurotic edema.6

Anaphylactic shock occurred also in two females after intramuscular injection of thiamine hydrochloride. Both patients had received thiamine injections previously without untoward effects. Intracutaneous skin tests with 0.1 percent thiamine hydrochloride were positive in both patients.7

A 69-year-old female patient developed anaphylactic shock immediately after the first injection of 100 mg of vitamin B1 although she had been previously treated with injections of vitamin B complex without ill effects.

Symptoms noted were intense pruritus on the forearms, incessant sneezing and retching, fall in blood pressure, and dyspnea while the extremities became cold and clammy, and the patient became incontinent of urine and lost consciousness. All these features appeared within three minutes. The administration of adrenaline intravenously and nikethamide led to rapid recovery within an hour.8

The imperative advice is given that to administer vitamin B1 parenterally is both dangerous and unnecessary.

Nicotinic Acid (Niacin)

1. Cardiovascular system: 48 patients treated with high doses of nicotinic acid, namely 3–6 g daily, were questioned about cutaneous flushing. All but four had experienced this effect.

In 29 patients this complaint disappeared before the end of the second week of therapy, in 15 the flushing effect persisted longer than two weeks, and only four patients continued to experience this effect after every dose.9

In a group of 50 patients with angina pectoris studied, 14 patients stated that chest pain was diminishing during therapy with nicotinic acid, two that it was worse, and three that it was unchanged. No conclusion could be drawn.9

2. Liver: Large doses of nicotinic acid administered daily for long periods produced alterations of liver function in a significant minority of patients. In the above-mentioned group of 50 patients9 studied for more than one year, changes in hepatic function tests involving enzymatic reactions (BSP test, alkaline phosphatase, SGOT) were usually not accompanied by histological evidence of hepatic damage. The rapid reversibility of the chemical abnormalities when nicotinic acid was stopped, together with the absence of histological damage, in the presence of markedly abnormal enzymatic tests, suggested that nicotinic acid caused dysfunction of hepatic enzyme systems without cellular damage in the usual sense of the term.

Prolonged use of nicotinic acid could occasionally result in histological changes in the liver, including fibrosis and cholangiolitis, but in the three patients so affected it was not certain that these changes were caused by the nicotinic acid.9,10

From another quarter two cases of jaundice in patients treated with nicotinic acid on account of hypercholesteremia were reported.11

In the case of a 58-year-old man receiving 3 g nicotinic acid daily, hypoalbuminemia, edema, and abnormal liver function tests were observed. The BSP test showed a retention of 30.5 percent. Hanger’s test was 4+ and alkaline phosphatase was 9.5 U (Bodansky). After discontinuance of the therapy all symptoms disappeared within a month.12

Out of 61 patients on long-term treatment with nicotinic acid (1.5–6 g daily), 23 exhibited at least one abnormal result in a test of hepatic function. Jaundice occurred in two patients, a histological picture similar to that of viral hepatitis has been found.13

3. Gastrointestinal system: In seven out of 14 patients with preexisting complaints of heartburn and indigestion, these complaints became worse during therapy. Nausea was reported in three cases. Activation of peptic ulcer was noted in seven patients. A tendency to diarrhea was reported by three patients.9

Gastrointestinal disturbances experienced after taking substantial doses (3–7.5 g) of nicotinic acid were exemplified also in the histories of five other patients. In addition to the underlying vascular disease, present in every case, three patients were known to have had peptic ulcers before and two had had other upper gastrointestinal symptoms. After prolonged administration (up to 124 weeks in one case) of nicotinic acid, all developed symptoms and signs of active ulcers. When the nicotinic acid was administered in the form of tablets containing a buffer the gastrointestinal disturbances subsided promptly. The use of buffered preparations of nicotinic acid is suggested when long-term treatment is necessary.14

4. Skin: Dryness of the skin was reported in 21 patients out of a group of 50.9

Localized rough brown pigmentation was reported by four patients, all males (in three patients this involved the axillae, and in one the sides of the neck). In a similar case the only significant histological change in the involved skin was found to be marked thickening of the stratum corneum.

5. Metabolism: Activation of fibrinolysin was reported, but only after parenteral administration of nicotinic acid, or sublingual or buccal administration of potassium nicotinate.9

An effect upon the glucose tolerance was reported. Glucose tolerance was probably decreased in many patients taking large doses of nicotinic acid for long periods, but diabetes was not aggravated, nor could the development of diabetes be attributed to nicotinic acid therapy.9

Serum uric acid levels tended to be increased slightly by nicotinic acid therapy. Clinical episodes of gout or renal calculi have not been observed.9

Pyridoxine (Vitamin B6)

In two of 21 patients with acne rosacea treated with 50 mg of pyridoxine intramuscularly daily for 30–40 days, treatment had to be discontinued on account of severe headache.16

Folic Acid

Folic acid may correct the anemia of patients with pernicious anemia and thereby mask and interfere with correct diagnosis. This is dangerous because folic acid does not prevent the neurological deterioration that is related to avitaminosis B12.

Two cases were reported in which the first manifestations of pernicious anemia were those of spinal cord degeneration. The absence of hematological failure had to be attributed to the ingestion of folic acid incorporated in multivitamin preparations. It is urged that folic acid be omitted from multivitamin preparations.16

Ascorbic Acid

It is not quite certain if the administration of excessive doses of vitamin C is completely innocuous.

Guinea pigs on a diet deficient in vitamin C died significantly sooner if before their normal laboratory diet had contained an additional 0.5 g daily of vitamin C.

It was reported that during the siege of Leningrad scurvy was observed in 67 percent of the people, but among those who had received large doses of vitamin C beforehand the incidence was 81 percent. The possibility was suggested that, on a higher intake, the excretion and the oxidation assume a higher level.17


  1. Med., 65, 402, 1961.
  2. A.M.A., 173, 1802, 1960.
  3. Pediat., 59, 260, 1961.
  4. New Engl. J. Med., 265, 369, 1961.
  5. Lancet, 2, 599, 1962.
  6. Presse Méd., 68, 2058, 1960.
  7. Harefuah, 62, 121, 1962.
  8. Practitioner, 185, 820, 1960.
  9. Intern. Med., 107, 639, 1961.
  10. Intern. Med., 107, 653, 1961.
  11. A.M.A., 177, 546, 1961.
  12. A.M.A., 175, 137, 1961.
  13. J. Med., 31, 24, 1961.
  14. A.M.A., 173, 1466, 1960.
  15. Voprosy fiziologii i Patologii Organov Pishchevareniya (Trudy I Med. Inst.), 8, 129, 1960.
  16. Med., 125/4, 233, 1960; New Engl. J. Med., 264, 1339, 1961.
  17. Schweiz. Med. Wschr., 90, 726, 1960.
  18. Sov. Med., 126, 1960.
  19. Ann. Intern. Med., 53, 1250, 1960.
  20. Conn. Med., 26, 428, 1962.
  21. Dtsch. Gesundh.-Wes., 17, 35, 1962.
  22. Acta endocr. (Kbh.), 31, 282, 1959.
  23. Nord. Med., 65, 405, 1961.
  24. Zh. Biol., abstr. nr. 85211, 1958.
  25. Pediatrics, 21, 1004, 1961.
  26. Rev. Franc. Etud. Clin. Biol., 6, 431, 1961.
  27. Acta Paediat. Belg., l6, 73, 1962.
  28. J.A.M.A., 502, 1960.

Danielle LeBaron

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