It is well known that vitamin A is an essential nutrient required for the maintenance healthy epithelial tissue, for growth and for vision. On the other hand, there is no nutritional advantage to be derived from exceeding the recommended level of vitamin A. The intolerable upper limit of preformed vitamin A rises from 600 micrograms per day for infants to 2,800 for adolescents up to 3,000 for adults. The most usual cause of hypervitaminosis A are prolonged consumption of vitamin A-containing supplements, in the belief that “a little is good: a lot is better”. Furthermore, the physical form of retinol supplements is a major determinant of toxicity: water-miscible, emulsified and solid preparations of retinol are approximately ten times more toxic than oil-based retinol preparations. Unfortunately, some vitamin preparations do contain as many as 25,000 IU of vitamin A. Although the level at which vitamin A becomes toxic varies from one individual to another, a daily dose of 50,000 I.U. for many months can induce toxic symptoms in adults. When taken over an extended period of time, this could be dangerous, especially during pregnancy, producing teratogenic effects in the fetus.
Symptoms often include anorexia, irritability, loss of weight, sparseness of hair. A single dose of a million units of vitamin A can cause severe, acute toxicity. Persons have been known to die from eating large amounts of polar bear liver. Acute manifestations include transient hydrocephalus and vomiting. Chronic hypervitaminosis A has also been observed in infants 3 to 6 months of age. Chronic hypervitaminosis A in children usually results from overzealous parents who are uninformed or believe that high doses will provide beneficial results. A skin disorder, such as acne, for which a remedy is sought, may be a result of excessive dosage of vitamin A. In adults, chronic hypervitaminosis A has been observed in patients receiving large doses (20–30 times RDA) as a treatment for a dermatologic condition. Thus, hypervitaminosis A can be avoided by obtaining vitamin A only from dietary sources or low potency preparations.
The only therapy is to stop the administration of the vitamin or such other drug containing it. If it is necessary to take vitamin A supplements, the vitamin A content of the supplement should approximate the Recommended Dietary Allowance.
Excessive intake of carotenoids can cause hypercarotenosis – yellow or orange discolor-ation of the skin. Some persons do consume unusually large amounts of provitamin A sources, such as the carotenoids but the inefficiency of the conversion of provitamin A to pure vitamin A virtually eliminates the possibility of hypervitaminosis A. The resultant accumulation of the provitamin A pigment causes the yellowing of the skin and the other epithelial layers of the body. Hypercarotenemia has also been documented where there has been prolonged ingestion of large amounts of carrot juice. Where hypercarotenemia has been due to dietary origin, symptoms disappear within a few weeks after withdrawal of the cause.
.It has been suggested that vitamin C plays a role in cholesterol metabolism. Some studies have shown that when large doses of vitamin C was given to hypercholesterolemic subjects, their serum cholesterol levels were decreased. The claim has also been made that doses larger than the RDA could be advantageous in treating respiratory ailments. However, the ingestion of large amounts of vitamin C is not without toxic effects. Reports have indicated that the resultant acid urines may contribute to the formation of renal calculi in those with tendency to gout Furthermore, ascorbic acid is metabolized through the formation of oxalic acid, a substance that also contributes to the production of renal calculi. Thus, chronic intake of vitamin C in excess of the adult tolerable upper limit of 2,000 mg per day can cause diarrhea, kidney stones and excess iron absorption.
While massive doses of vitamin C might reduce the severity of upper respiratory infections in individuals whose tissues are not fully saturated with the vitamin, levels above those necessary for tissue saturation could be harmful, as respiratory infections could increase the amount of vitamin C required for tissue saturation.
There is no evidence that high iron intake, by itself, can lead to secondary iron overload. But excessive dietary iron intake can be detrimental to health, under certain circumstances. The storage form of iron, ferritin, is normally found in the intestine, liver, spleen and bone marrow. If iron is taken into the body parenterally, in amounts exceeding the capacity of the body to store ferritin, it accumulates in the liver as microscopically visible hemosiderin. Furthermore, in certain parts of Africa, traditional fermented beer from maize has been shown to be contaminated by the iron-containing brewing vessels, causing hemosiderosis. Acute iron poisoning causes vomiting, upper abdominal pain, diarrhea, drowsiness and shock. Death may occur in children who mistake iron tablets for sweets. In chronic iron toxicity (hemochromatosis or iron load) affects many organs and tissues. Eventually, diabetes often results in 80% of such patients. The liver becomes enlarged and cirrhotic, and hepatocellular cancer may develop. Cardiomyopathy may also develop, causing heart failure. Mental aberrations and pituitary failure may cause testicular atrophy and loss of libido. Focal hemosiderosis can damage lungs and kidneys.
Sub-Saharan hemochromatosis appears to have a genetic basis, but it is usually associated with long-term diets high in iron derived from cooking pots or steel barrels used in preparing fermented alcoholic beverages. In such patients, portal cirrhosis and diabetes are common.
However, despite associations of high serum ferritin with heart disease, type-2 diabetes, and colon cancer, adverse health effects of moderately elevated iron stores in the general population should be viewed with caution.