Reference Information

Term descriptions

AVITAMINOSIS is total depletion of all vitamins in the body (total vitamin deficiency). Avitaminosis develops certain clinical symptoms which are characteristic of all vitamin deficiencies. C-avitaminosis (scurvy, Barlow´ s disease), B1-avitaminosis (alimentary polyneuritis, Beriberi), PP-avitaminosis (pellagra), B2-avitaminosis (ariboflavinosis), A-avitaminosis (hemeralopia, xerophthalmia), D-avitaminosis (rickets, osteoporosis).

Deficiency of vitamins see appendix p. 126- 127.

ANTIVITAMINSare the compounds which lessen or negate the chemical action of vitamins in the body metabolism by breaking up, inactivating vitamins or preventing their assimilation. Antivitamins are divided into two groups:

a) the structurally similar antivitamins (competitive inhibitors; they compete with vitamins or their derivatives in the corresponding biochemical metabolic processes). They include sulfanilamides, dicumarin, megafen, isoniaside, etc.

b) the structure modifying antivitamins (natural antivitamins; they destroy or decrease the effect of a vitamin by modifying the molecule itself or by building complexes with the metabolite). They include thiaminase, ascorbic oxidase, avidin, etc.

VITAMINS are low molecular weight and highly biologically active organic compounds required for living. They are synthesized (or insufficiently synthesized) in the body and supplied through food. The biological role of water-soluble vitamins consists in the fact that they are involved in making coenzymes; the biological role of fat-soluble vitamins is to control the functional condition of cell membranes and subcellular structures.

VITAMINS ANTAGONISTS: B1 and B2; A and D; nicotinic acid and choline; thiamine and choline (a long-term therapy with one vitamin results in the deficiency in another vitamin).

SYNERGY VITAMINS: C and R, R, C, K; B12 and folic acid; C, K, B2; A and E; E and inositol (they can increase the biological effect of each other when used together in multivitamin medications).

HYPOVITAMINOSISis a sharp decline in vitamin supply. is an initial stage of avitominosis. Hypovitaminosis is caused by insufficient consumption of vitamins that need to be included in the diet during a certain period of time.

LATENT FORM OF VITAMIN DEFICIENCYoccur when the body does not have a steady supply of vitamins in the diet. Latent forms of vitamin deficiency does not have any clinical manifestations. They are considered to be a preclinical stage of vitamin deficiency and are characterized only by biochemical disorders.

However, it has a negative effect on working capacity and resistance of the body to various unfavourable factors. It also makes recovery after a disease longer.

DIETARY FIBERS are macro molecular carbohydrates (cellulose, hemicellulose, pectin, lignin, chitin, etc.), mainly of plant origin that are indigestible and non-absorptive in the small intestine, but subject to full or partial fermentation in the large intestine.

MAJOR CAUSES OF HYPOVITAMINOSES AND AVITAMINOSES are as follows:

1. Inadequate intake of vitamins from food:

1.1. Low contents of vitamins in the diet

1.2. Reduced food intake as a result due to low energy expenditures of a modern person.

1.3. Loss of vitamins during improper processing, storing, and cooking.

1.4. Imbalanced diet (a high carbohydrate diet requires more vitamins; inadequate intake of native vitamins С, РР, В 1 results in the situation when they are rapidly excreted with urine without being involved in metabolic processes. It also inhibits transformation of carotene into vitamin A).

1.5.Anorexia

1.6. Presence of vitamins in a form that cannot be utilized in some foods (inositol in the form of phytin in cereals).

1.7. Effects of antivitamin agents that are found in food.

2. Suppression of intestinal flora producing a number of vitamins.

2.1.Diseases of the gastrointestinal tract.

2.2. Aftermaths of chemotherapy (dysbacterioses).

3. Malabsorption of vitamins.

3.1. Disorders related to malabsorption of vitamins in the gastrointestinal tract (diseases of the stomach, liver, gallbladder, intestinal diseases; old age disorders such as impaired bile secretion which is important for absorption of fat-soluble vitamins).

3.2. Most vitamins are utilized or broken down in the human body by intestinal parasites or pathogenic intestinal microflora (deficiency in B12 in case of broad tapeworm invasion).

3.3. Disorders of vitamin metabolism and formation of their biologically active forms (coenzymes) associated with various diseases, effects of toxic and infectious agents, chemotherapy, old age disorders.

4.Increased vitamin requirements

4.1. Special physiological states (intensive growth, pregnancy, lactation).

4.2. Special climatic conditions (vitamin requirements increase by 30-60%due to higher energy expenditures at low temperatures in the northern climatic zone).

4.3. Intense physical activity.

4.4.Psychological and stress loads.

4.5. Effects of harmful occupational factors (People working in hot shops and exposed to high temperatures (32 degrees) require twice as much vitamins C, B1, B6, pantothenic acid than those doing the same job at 18 degrees).

4.6. Infectious diseases and intoxications (In severe sepsis daily requirements for vitamin C reach 300-500 mg).

4.7. Internal diseases and diseases of endocrine glands.

4.8. Increased excretion of vitamins.

5. Congenital, genetic disorders of vitamin metabolism.

5.1. Congenital disorders of vitamin absorption.

5.2. Congenital disorders of vitamin transport in blood and across cell membranes.

5.3.Congenital disorders of vitamin biosynthesis (nicotinic acid from tryptophan).

5.4. Congenital disorders of conversion of vitamins into their coenzyme forms, prosthetic groups and active metabolites.

5.5. Disorders related to the failure to bind vitamins to the active site of an enzyme.

5.6. Impaired structure of an apoenzyme impeding its interaction with a coenzyme.

5.7. Impaired structure of an apoenzyme resulting in complete or partial enzymatic activity loss regardless of its interaction with a coenzyme.

5.8. Boosted vitamin catabolism.

5.9. Congenital disorders of renal reabsorption of vitamins.

Table 2