Vitamin Deficiency

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Vitamin Deficiency


a morbid condition brought on by the complete absence, inadequate intake, or increased destruction of vitamins in the organism. Vitamin deficiency was experimentally reproduced for the first time in the world in white mice by the Russian physician N. I. Lunin in 1880. In 1912 the Polish scientist C. Funk named the substances discovered by Lunin “vitamins,” and the illnesses caused by their absence in nutrition “avitaminoses.” A letter and numerical designation of vitamins is appended to the word “avitaminosis” for a more precise identification of vitamin deficiencies—for example, avitaminoses A, B1, B2, B6, C, D, E, K, and PP. Hypovitaminoses—obliterated forms of vitamin deficiency that can linger for years—are observed when the organism receives inadequate amounts of vitamins. Monoavitaminosis, or monohypovitaminosis, develops from a deficiency of one vitamin, and polyavitaminosis, or polyhypovitaminosis, occurs when two, three, or more vitamins are absent. Normally vital activities require a certain amount of vitamins, which enter an organism with the ingestion of food or are synthesized (some vitamins) by the bacteria of the intestines. The need of the human organism for vitamins is greatly increased during severe physical stress, pregnancy, and breast feeding and in the presence of infectious and endocrine diseases. In this connection, a vitamin deficiency can develop even when an organism receives an adequate amount of vitamins.

There are two types of vitamin deficiency, exogenous and endogenous. Exogenous, or alimentary, deficiencies are associated with inadequate amounts of or absence of vitamins in food. This rarely occurs in times of peace. This form of vitamin deficiency is most often caused by the improper storage of food products and gross violations in preparing and cooking food, which result in the destruction of most of the vitamins. The disturbances in vitamin exchange brought about in the exogenous form of vitamin deficiency are reversible; they may be eliminated by the vitaminization of food. The endogenous form of vitamin deficiency is encountered most frequently. It is produced by two groups of causes. The first group includes diseases that lead to the increased destruction of vitamins in the gastrointestinal tract, improper vitamin absorption, and suppression of vitamin synthesis in the intestines. This is observed in the presence of helminthiasis, lambliasis, and several liver diseases. The second group includes a variety of factors resulting in the increased vitamin requirements of an organism or improper exchange between vitamins and the cleavage products of proteins, fats, and carbohydrates (for example, during infectious and toxic processes). Vitamin deficiency develops gradually, and the clinical indications of its existence are not immediately apparent, since the adaptational resources of the human organism are rather great. The symptoms and treatment of vitamin deficiency depend on which vitamin the organism is lacking.

Measures for preventing vitamin deficiency are of especial importance in cases of exogenous avitaminosis and consist of increasing the production of food products rich in vitamins, an adequate consumption of vegetables and fruits, and the proper storage of food products and efficient food processing at food industry enterprises, public eating establishments, and the home. Vitamin deficiency requires supplementing diets with vitamin compounds and with vitaminized food products intended for mass consumption.


Efremov, V. V. Vazhneishie avitaminozy cheloveka. Moscow-Leningrad, 1939.
Ryss, S. M. Gipovitaminozy i bolezni vitaminnoi nedostatochnosti (C i gruppy B). Moscow, 1948.
Bicknell, F., and F. Prescott. The Vitamins in Medicine, 3rd ed. London, 1953.


Vitamin deficiency in farm animals often appears in the form of hypovitaminoses and, less frequently, avitaminoses. It may be associated with inadequate amounts of vitamins and provitamins in the ration, difficulty in (or absence of) the absorption of vitamins in the intestines, poor assimilation of vitamins by cells and tissues during sickness, and the action of antivitamins (thiaminase, sulfanilamides, certain antibiotics, and so forth). It develops primarily when live-stock is housed in stables. Vitamin deficiency is often ob-served in young animals during growth, in pregnant females, and in very productive animals.

Vitamin deficiency in animals causes reduced productivity and fertility, increased morbidity, especially of young stock, and shortened periods of economic use of male and female breeding stock. Vitamin-deficient animals yield biologically inferior foodstuffs (milk, dairy products, meat, and eggs) and poor-quality raw materials for industry (wool, leather, and fur).

The prevention and treatment of vitamin deficiency in animals are based on improving zoohygienic housing conditions, providing full-value rations containing vitamin-rich feeds, and administering vitamin compounds orally or through intramuscular injections. Important also is the dissemination of information on vitamin deficiency to workers involved with livestock breeding.


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