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Abstract
Man is a food-dependent creature. If you don’t feed him, he will die. If you feed him improperly, part of him will die (Cheraskin, 1994).
Dependency is a fact of life. The human body is dependent on food, water, sleep and oxygen. Additionally, its internal chemistry is absolutely dependent on vitamins. Without adequate vitamin intake, the body will sicken; virtually any prolonged vitamin deficiency is fatal. Surely this constitutes a dependency in the generally accepted sense of the word (Heaney, 2003).
A person is said to be vitamin dependent if his requirements for that vitamin are much greater (perhaps 100-fold greater or more) than is the average need for any population. The optimum need is that quantity which maintains the subject in good health, not that quantity which barely keeps him free of disease. From this point of view the Hong Kong veterans have become vitamin B-3 dependent as a result of severe and prolonged malnutrition. It is likely that any population similarly deprived of essential nutrients for a long period of time will develop one or more dependency conditions (Cheraskin, 1994).
The newer concept of vitamin-dependent disease changes the emphasis from simple dietary manipulation to consideration of the endogenous needs of the organism. The borderline between vitamin deficiency and vitamin-dependency conditions is merely a quantitative one when one considers prevention and cure (Heaney, 2003).
The differentiation between deficiency and dependency is the dose. Every patient that was ever helped by high-dose nutrient therapy lends support to the concept of vitamin dependency. By the same token, symptoms resulting from inappropriate and abrupt termination of large doses of nutrients provide equally good evidence for vitamin dependency. While deprivation of low doses of vitamin C causes scurvy, abrupt termination of high maintenance doses may cause its own set of problems. Called ”rebound scurvy,” this includes classical scorbutic symptoms, as well as a predictable relapse of illness that had already responded to high-dose therapy (Cameron, 1991).
There is a certain dependency on ascorbic acid that a patient acquires over a long period of time when he takes large maintenance doses. Apparently, certain metabolic reactions are facilitated by large amounts of ascorbate and if the substance is suddenly withdrawn, certain problems result such as a cold, return of allergy, fatigue, etc. Mostly, these problems are a return of problems the patient had before taking the ascorbic acid. Patients have by this time become so adjusted to feeling better that they refuse to go without ascorbic acid. Patients do not seem to acquire this dependency in the short time they take doses to bowel tolerance to treat an acute disease. Maintenance doses of 4 grams per day do not seem to create a noticeable dependency. The majority of patients who take over 10-15 grams of ascorbic acid per day probably have certain metabolic needs for ascorbate which exceed the universal human species need (Cheraskin, 1994).
In pyridoxine dependent seizures high doses of pyridoxine is needed up to 300 mg daily. In holocarboxylase deficiency, biotin is given in a dose of 20-40 mg daily compared with DRI of 0.3 mg daily (Wilson et al., 2005). Familial hypophosphatemia is treated by vitamin D at levels of 25,000-50,000 U/d (at the lower limit of toxic dosage) (Ariceta et al., 2007).