Vitamins (Part II); Nutritionist Ties Carbohydrates to Atherosclerosis Development; Battle for Life Revealed by Electron Microscope
Contents in this issue:
- “Vitamins (Part II),” reprinted from Meyler’s Side Effects of Drugs,
- “Nutritionist Ties Carbohydrates to Atherosclerosis Development,”
- “An Exciting Story in the Constant Battle for Life Revealed by Electron Microscope.”
The following is a transcription of the August 1964 issue of Dr. Royal Lee’s Applied Trophology newsletter, originally published by Standard Process Laboratories.
Vitamins (Part II)
“Chapter XXVI: Vitamins” is reprinted in two parts from Meyler’s Side Effects of Drugs, 4th ed. (Part I available here.)
Calciferol (Viosterol, Vitamin D2)
Chronic and acute intoxication with vitamin D has been described.
Acute hypervitaminosis D was observed in a 32-year-old previously healthy man after the ingestion of 1,800,000 U vitamin D2. During the first ten days there was excessive vomiting, pains in the back of the head and lower jaw, early signs of renal damage and hypertension (210/110).
On the sixth and seventh day, petechiae on the extremities were observed, and the patient was now admitted to hospital. In the succeeding days, manifestations of nephritis with uremia and myocardial damage developed, and disturbance of the K:Ca ratio in the blood was found. Recovery followed treatment with parenteral fluids.
After four weeks a hypochromic anemia was present, the blood pressure was still too high, and roentgenological changes in the skull bones were demonstrable. Six months later all abnormal findings had disappeared.18
Chronic intoxication with vitamin D is associated with hypercalcemia, calcifications, and renal failure. Several cases were published.19
One patient who took 300,000 U of vitamin D2 daily for 2½ years died under a clinical picture misdiagnosed as multiple sclerosis. Autopsy revealed extensive calcifications.20
A nine-year-old girl with tuberculous lymph nodes was treated with 20 million U vitamin D2 in the space of three weeks. Hypercalcemia (18 mg percent) with vomiting, polyuria, and secondary dehydration developed. Under prednisone therapy the serum calcium decreased to 8.4 mg percent at which point tetanic cramps occurred.21
A 59-year-old woman with chronic rheumatoid arthritis received vitamin D2 90,000 U daily together with salicylates.
In three months the total dose approximated 10 million U of vitamin D2, and at this phase she started to develop physical and mental signs: tiredness, weakness, loss of appetite, general malaise, slight dysphasia, drowsiness and sleepiness. She noticed increased thirst in the last week before admission to hospital, when she also developed disorientation and restlessness, culminating in stupor with hallucinations.
Serum calcium was 14 mg/100 ml, phosphorus 3.1 mg/100 ml, and phosphatase 5 U. There were abnormalities in the EEG, viz. the RT was shortened, and T-waves were depressed. There was hypokalemia but no alkalosis. Cortisone caused a distinct fall in serum calcium to 8 mg/100 ml in a short time, but the level rose again on withdrawal of the steroid. A calcium-poor diet was advised. The patient had one relapse, but finally recovered completely from this intoxication.22
In three patients intoxication developed during treatment of hypoparathyroidism. The first developed vitamin D intoxication with renal insufficiency and nephrocalcinosis, one year after artificial menopause induced by X-ray castration. It was suggested that the lack of estrogens induced the vitamin D intoxication.
The second patient developed hypercalcemia, renal insufficiency, and nephrocalcinosis as during changeover from dihydrotachysterol to calciferol. The nephrocalcinosis lasted for twelve years without further deterioration of renal function.
The third patient developed hypercalcemia and renal failure when spontaneous cure of his hypoparathyroidism occurred. It was probably due to the combined action of “parathormone” and calciferol.23
In 25 patients with lupus vulgaris, treatment with 30–150,000 U of vitamin D2 daily, combined with calcium gluconate 0.5 g. twice daily, leucopenia (46 percent), lymphocytopenia (15 percent), and monocytosis (13–15 percent) were recorded.
In eight patients side effects were reported (central nervous and cardiovascular systems, gastrointestinal tract and kidneys), these disappearing after discontinuation or decrease of the vitamin D2 administration.24
In one article it was advised to give vitamin D2 to children only as treatment or prophylaxis of rickets, and never to give more than 400,000 U in a week’s period.21
Sodium sulphate proved to be effective in lowering the serum calcium level and improving the clinical condition in hypervitaminosis D.
Vitamin D intoxication in a 15-month-old boy after parenteral administration of 6,000,000 U of vitamin D2 was treated with milk containing sodium sulphate 1 percent. This caused a gradual decline in the calcium levels. As soon as treatment with sodium sulphate was stopped, calcium levels rose again, only to decrease when the administration was resumed.25
Excessive vitamin D administration during pregnancy might be able to induce prolonged gestation. It could be responsible for increased deposition of calcium in the skull, kidneys, and other soft tissue parts of the fetus.26
Increased sensitivity to vitamin D may occur under certain conditions. Three patients, aged between eight months and two years, developed signs of vitamin D intoxication though moderate doses of vitamin D had been used. The two-year-old child had myxedema and presented generalized calcification of the arteries, renal insufficiency, osteosclerosis and hypercalcemia.27
Vitamin K Group
Kernicterus in premature infants, which develops as late as the end of the first week of life, may result from our excessive administration of vitamin K.
Hypoprothrombinemia due to severe liver disease cannot be corrected by vitamin K administration analogously to the manner, whereby anticoagulant drugs induce hypoprothrombinemia, and the administration of vitamin K may be even harmful.
The case was described where a patient with advanced cancer received vitamin K. This resulted in liver function disorders, including hypoprothrombinemia, with return to normal only after discontinuation of the vitamin K treatment.
Side effects due to the administration of vitamin K in massive doses included anemia, pancytopenia of renal tubular degeneration, albuminuria, porphyrinuria, vomiting, depression of prothrombin activity and the provoking of focal hemorrhages.
It is advisable to stop vitamin K administration if no improvement of prothrombin activity occurs within forty-eight hours.28
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- A.M.A., 173, 1802, 1960.
- Pediat., 59, 260, 1961.
- New Engl. J. Med., 265, 369, 1961.
- Lancet, 2, 599, 1962.
- Presse Méd., 68, 2058, 1960.
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- Voprosy fiziologii i Patologii Organov Pishchevareniya (Trudy I Med. Inst.), 8, 129, 1960.
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Nutritionist Ties Carbohydrates to Atherosclerosis Development
Carbohydrates as well as saturated fats may be dietary villains in atherosclerosis, Dr. Margaret J. Albrink, a West Virginia University physician-nutritionist, considers refined sugar particularly undesirable.
She contends that a large carbohydrate intake is more characteristic of the modern diet than is a large consumption of fats. Dr. Albrink also feels that the excessive caloric intake from all sources corresponds more closely with the increased incidence of coronary heart disease than does any change in fat consumption.
Further, serum triglyceride levels may total serum cholesterol levels, Dr. Albrink reported to the Federation of American Societies for Experimental Biology.
Whenever caloric intake is excessive, whether from carbohydrate or fat, the surplus calories are stored as lipids. The increased fat levels and fat transport show up as an increase in blood triglycerides, Dr. Albrink said.
The West Virginia nutritionist added that serum triglyceride concentration profoundly affects the physical form of cholesterol, whether circulating as normal lipoproteins or as giant low-density atherogenic particles.
An Exciting Story in the Constant Battle for Life Revealed by Electron Microscope
For generations medical scientists knew there were forces within the human body that helped man fight off attacking germs.
But no one understood how these “defenders” did their work.
Ordinary microscopes, which magnify only 2,000 times, were powerless to pierce this hidden universe. What mysteries lay beyond the barrier?
After years of research, one of America’s leading companies developed a microscope using electrons instead of light waves—a microscope that magnified from 50,000 to 200,000 times!
Man entered a strange land of giants—human hairs as large as the Washington Monument…corpuscles the size of two-foot sofa pillows…tuberculosis germs as big as sausages.
With the electron microscope, scientists first saw the actual destruction of enemy bacteria pictured above!
[This article includes four images with the following captions:]
Research worker examining bacteriophage (bacteria-destroying agents) through a microscope.
Bacteriophage (small black dots) attacking Bacillus coli. This is an actual photograph magnified 8,500 times.
After twenty minutes of attack, the bacteria begin to disintegrate. Magnified 17,200 times.
Thirty minutes later, bacteria are destroyed. Debris litters the “battlefield.” Magnified 8,300 times.