Supplementation of patients with homozygous sickle cell disease with zinc, alpha-tocopherol, vitamin C, soybean oil, and fish oil
Article Abstract:
Sickle cell anemia is caused by an abnormal type of hemoglobin (the protein in red blood cells that carries oxygen), called hemoglobin type S (HbS). The red blood cells (RBCs) in patients with sickle cell disease have a crescent or sickle shape (instead of being round) and their membranes are fragile, which means that the cells break easily. The surface of a sickle cell is sticky, and this causes the cells to adhere to the interior of the blood vessels, which can block the normal flow of blood and cause pain. Irreversibly sickled cells (ISCs) are RBCs that have a sickle shape, a short life span, and a tendency to become trapped in small blood vessels. Studies have examined the effects of vitamins and minerals on ISCs. Zinc has been shown to reduce the number of ISCs in the blood and to increase the survival of RBCs. One study reported that vitamin E reduces the number of ISCs, while another reported that it does not. Vitamins E and C are called antioxidant vitamins because they prevent cell damage caused by highly reactive oxygen atoms. It has been suggested that these vitamins may also help protect RBC membranes from damage. Studies performed on cells grown in culture have shown that fish oils containing omega-3 fatty acids make cell membranes less fragile and reduce the ability of the cells to stick together. Therefore, a study was performed to determine the effects of an eight-month diet supplemented with zinc, vitamins E and C, and soybean oil (diet 1), or the same diet with fish oil substituted for soybean oil (diet 2), in 13 patients with sickle cell disease. The most striking effect was a 38 percent reduction in the number of ISCs caused by zinc with diet 1. Both soybean oil and fish oil increased the amount of fatty acids in RBC membranes, which should make the membranes less fragile. However, more studies are needed to determine if these diets will be beneficial in treating patients with sickle cell disease. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Clinical Nutrition
Subject: Health
ISSN: 0002-9165
Year: 1991
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Zinc toxicity
Article Abstract:
While much research has been done concerning the consequences of zinc deficiency, attention has turned only recently towards the risks of excessive zinc intake. The Recommended Dietary Allowance (RDA) for this essential mineral is 15 milligrams (mg) per day; the RDA includes a margin of safety to cover the needs of virtually all healthy individuals. At extremely high intakes, such as one to two grams of zinc sulfate or 225 to 450 mg of zinc, acute toxicity occurs. Acute toxicity is fairly rare and is usually caused by food poisoning; a food or beverage stored in a galvanized container for a long time may absorb zinc from the container. Somewhat lower intakes, such as 100 to 300 mg zinc per day, are classified as pharmacological doses because they are large enough to function as a drug rather than a nutrient. Physicians may prescribe this level of supplementation for certain conditions such as sickle cell anemia, and individuals may purchase and consume these amounts on their own in the belief that they will derive some benefits. Serious consequences may follow, however. Copper deficiency, iron-deficiency anemia, neutropenia (low level of certain white blood cells), deficient immune function, and undesirable changes in the ratio of low density lipoprotein (LDL) to high density lipoprotein (HDL) cholesterol have all occurred with increased zinc intake. Several of these adverse effects, copper and iron deficiency and reductions in HDL cholesterol, have been reported on even smaller doses of zinc which are closer to the RDA. Persons who choose to take zinc supplements should be informed of the risks involved, which may outweigh any presumed benefits. Many persons may be particularly concerned about adverse effects on blood cholesterol levels and immune function. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Clinical Nutrition
Subject: Health
ISSN: 0002-9165
Year: 1990
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Discovery of human zinc deficiency and studies in an experimental human model
Article Abstract:
Zinc, like many other metals, is needed in small (trace) amounts for proper tissue function. Early studies showed that zinc deficiency in animals caused growth failure, skin changes, and wasting of the gonads (reproductive organs). For many years, however, it was thought that zinc was so ubiquitous that humans could not be deficient. This article recounts the research which established the existence of zinc deficiency in humans and discusses tissue functions in which zinc appears to be important. Zinc deficiency was demonstrated in Middle Eastern subjects who had diets consisting chiefly of cereal with little protein, meat (which contains red blood cells) being a good source of zinc as well as iron. Moderate zinc deficiency was observed to be manifested by growth retardation, poor gonadal development, lethargy, abnormal eye function, and alterations in skin and in wound healing. Some abnormalities in taste were also linked to zinc deficiency. Severe deficiency was associated with particular types of severe dermatitis, diarrhea, baldness, mental dysfunction, and infections. Marginal zinc deficiency was linked to decreased taste, poor dark adaptation by the eye, decreased levels of testosterone and sperm production, increased blood levels of ammonia, decreased muscle mass, and diminished immune function. More recent basic research on zinc in tissue metabolism is discussed, including zinc metabolism, effects on immune system function, effects on regulation of gene function, interaction with copper and other elements, and effects of zinc on free radicals, charged molecules that cause tissue damage. The importance of zinc to normal body function is likely to be demonstrated by ongoing research. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: American Journal of Clinical Nutrition
Subject: Health
ISSN: 0002-9165
Year: 1991
User Contributions:
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