Types and Consequences of Lack of Vitamins

Types and Consequences of Lack of Vitamins

Introduction
Vitamins are organic compounds that perform specific biological functions for normal maintenance and optimal growth of an organism.  An organic chemical compound (or related set of compounds) is called a vitamin when the organism cannot synthesize the compound in sufficient quantities, and it must be obtained through the diet; thus, the term "vitamin" is conditional upon the circumstances and the particular organism. For example, ascorbic acid (one form of vitamin C) is a vitamin for humans, but not for most other animal organisms. Supplementation is important for the treatment of certain health problems (Fortmann et al.,2013). 
By convention the term vitamin includes neither other essential nutrients, such as dietary minerals, essential fatty acids, or essential amino acids (which are needed in greater amounts than vitamins) nor the great number of other nutrients that promote health, and are required less often to maintain the health of the organism (Maton et al.,1993). Thirteen vitamins are universally recognized at present. Vitamins are classified by their biological and chemical activity, not their structure. Thus, each "vitamin" refers to a number of vitamin compounds that all show the biological activity associated with a particular vitamin. Such a set of chemicals is grouped under an alphabetized vitamin "generic descriptor" title, such as "vitamin A", which includes the compounds retinal, retinol, and four known carotenoids
Vitamin by definition are convertible to the active form of the vitamin in the body, and are sometimes inter-convertible to one another, as well.These vitamins cannot be synthesized by the higher organisms including man, and therefore they have to be supplied in small amounts in the diet.Microorganisms can be successfully used for the commercial production of many of the vitamins e.g. thiamine, riboflavin, pyridoxine, folic acid,pantothenic acid, biotin, vitamin B12, ascorbic acid, β-carotene (pro-vitamin A), ergosterol (pro-vitamin D).

                                  TYPES OF VITAMINS
There are 13 essential vitamins. This means that these vitamins are required for the body to work properly. They are:
  Ø  Vitamin A
  Ø  Vitamin C
  Ø  Vitamin D
  Ø  Vitamin E
  Ø  Vitamin K
  Ø  Vitamin B1 (thiamine)
  Ø  Vitamin B2 (riboflavin)
  Ø  Vitamin B3 (niacin)
  Ø  Pantothenic acid
  Ø  Biotin (B7)
  Ø  Vitamin B6
  Ø  Vitamin B12 (cyanocobalamin)
  Ø  Folate (folic acid and B9).

Vitamins are grouped into two categories:

  • WATER-SOLUBLE VITAMINS

These types of vitamins require regular supply in the form of dietary sources or supplements. These are nontoxic and easily absorbed into the body through the gastrointestinal tract and then disseminated in the tissues. Water-soluble vitamins are carried to the body's tissues but are not stored in the body. They are found in plant and animal foods or dietary supplements and must be taken in daily.Any excess quantity of this vitamin consumed does not accumulate in the body. However, with vitamin B12 and B6 as exceptions, these are flushed out during urination. Most B Vitamins act as coenzymes, playing a key role in the breaking down process of carbohydrates, fats and proteins and transforming them to energy. This regulates metabolism, besides promoting healthy digestive and immune system.

Eight of the water-soluble vitamins are known as the vitamin B-complex group: thiamin (vitamin B1), riboflavin (vitamin B2), niacin (vitamin B3), vitamin B6 (pyridoxine), folate (folic acid), vitamin B12, biotin and pantothenic acid. The B vitamins are widely distributed in foods,and their influence is felt in many parts of the body. 

They function as coenzymes that help the body obtain energy from food. The B vitamins are also important for normal appetite, good vision, and healthy skin, nervous system, and red blood cell formation.
THAIMINE
is a vitamin of the B complex. it was eventually assigned the generic descriptor name vitamin B1. Its phosphate derivatives are involved in many cellular processes. The best-characterized form is thiamine pyrophosphate (TPP), a coenzyme in the catabolism of sugars and amino acids. In yeast, TPP is also required in the first step of alcoholic fermentation.
All living organisms use thiamine, but it is synthesized only in bacteria, fungi, and plants. Animals must obtain it from their diet, and thus, for humans, it is an essential nutrient. Insufficient intake in birds produces a characteristic polyneuritisThiamine deficiency has a potentially fatal outcome if it remains untreated ( Mahan and  Escott-Stump,  (2000). Thiamine is a colorless organo-sulfur compound with a chemical formula  C12H17N4OS. Its structure consists of an amino pyrimidine and a thiazole ring linked by a methylene  bridge. The thiazole is substituted with methyl and hydroxyethyl side chains. Thiamine is soluble in water, methanol, and glycerol and practically insoluble in less polar organic solvents. It is stable at acidic pH, but is unstable in alkaline solutions.
 Sources of Thaimine include peas, pork, liver, and legumes. Most commonly, thiamin is found in whole grains and fortified grain products such as cereal, and enriched products like bread, pasta, rice, and tortillas. The process of enrichment adds back nutrients that are lost when grains are processed.
. In mammals, deficiency results in Korsakoff's syndrome, optic neuropathy, and a disease called beriberi that affects the peripheral nervous system (polyneuritis) and/or the cardiovascular system. Thiamine derivatives and thiamine-dependent enzymes are present in all cells of the body, thus a thiamine deficiency would seem to adversely affect all of the organ systems. However, the nervous system is particularly sensitive to thiamine deficiency, because of its dependence on oxidative metabolism.
Thiamine deficiency commonly presents subacutely and can lead to metabolic coma and death. A lack of thiamine can be caused by malnutrition, a diet high in thiaminase-rich foods (raw freshwater fish, raw shellfish, ferns) and/or foods high in anti-thiamine factors (tea, coffee, betel nuts) and by grossly impaired nutritional status associated with chronic diseases, such as alcoholism, gastrointestinal diseases, HIV-AIDS, and persistent vomiting (Butterworth et al.,2006).
RIBOFLAVIN (VITAMIN B2)
Riboflavin (vitamin B2) is part of the vitamin B group.It was formerly known as vitamin G,
As a chemical compound, riboflavin is a yellow-orange solid substance with poor solubility in water compared to other B vitamins. Visually, it imparts color to vitamin supplements (and bright yellow color to the urine of persons taking a lot of it).
The name "riboflavin" comes from "ribose" (the sugar whose reduced form, ribitol, forms part of its structure) and "flavin", the ring-moiety which imparts the yellow color to the oxidized molecule. The reduced form, which occurs in metabolism along with the oxidized form, is colorless.
Riboflavin is the common name of 7,8-dimethyl-10-(D-19-ribityl)isoalloxazine, also known as vitamin B2, colorant E101, lactoflavin, lactochrome, or ovoflavin. The latter names referring to the source the vitamin was derived from. The compound is naturally synthesized by plants and most microorganisms, but not by higher eukaryotes. Starting from GTP and ribulose 5-phosphate
the riboflavin biosynthesis pathways of fungi and bacteria are similar, albeit the order of two consecutive biosynthetic steps, the reductase and deaminase reactions, is inversed. The genes encoding the riboflavin biosynthetic enzymes are well conserved among bacteria and fungi. Vitamin B2 has key functions in energy metabolism, maintenance of healthy skin and muscles, support of immune and nervous system, and promotion of cell growth and division. Riboflavin is the precursor for the coenzymes FMN (flavin mononucleotide) and FAD (flavin adenine dinucleotide), which are both important electron carriers in biological redox  reactions.

 Furthermore, the two flavo-coenzymes participate in nonredox phenomena like bioluminescence, light sensing, phototropism, DNA protection against UV, and in resetting of the circadian clock. Light sensitivity and poor resorption makes riboflavin deficiency recurrent, as suggested by worldwide surveys on nutritional status, and supplementation is often recommended. Overdosing due to dietary supplementation does not occur owing to the direct excretion of riboflavin in the urine. In industrialized countries processed food is often fortified by the use of riboflavin as a colorant or vitamin supplement. The main application (70%) of commercial riboflavin is in animal feed, since productive livestock, especially poultry and pigs, show growth retardation and diarrhea in case of riboflavin deficiency.
Sources of riboflavin are milk, cheese, eggs, leafvegetables, liver, kidneys, legumes, mushrooms, and almonds.
The milling of cereals results in considerable loss (up to 60%) of vitamin B2, so white flour is enriched in some countries such as US by addition of the vitamin. The enrichment of bread and ready-to-eat breakfast cereals contributes significantly to the dietary supply of vitamin B2. Polished rice is not usually enriched, because the vitamin’s yellow color would make the rice visually unacceptable to the major rice-consumption populations. However, most of the flavin content of whole brown rice is retained if the rice is steamed (parboiled) prior to milling. This process drives the flavins in the germ and aleurone layers into the endosperm. Free riboflavin is naturally present in foods along with protein-bound FMN and FAD. Bovine milk contains mainly free riboflavin, with a minor contribution from FMN and FAD. In whole milk, 14% of the flavins are bound noncovalently to specific proteins (Kanno et al.,1991).Egg white and egg yolk contain specialized riboflavin-binding proteins, which are required for storage of free riboflavin in the egg for use by the developing embryo.
Riboflavin is added to baby foods, breakfast cereals, pastas and vitamin-enriched meal replacement products. It is difficult to incorporate riboflavin into liquid products because it has poor solubility in water, hence the requirement for riboflavin-5'-phosphate (E101a), a more soluble form of riboflavin. Riboflavin is also used as a food coloring and as such is designated in Europe as the E number E101.

SIGNS AND SYMPTOMS

In humans

Mild deficiencies can exceed 50% of the population in third world countries and in refugee situations. Deficiency is uncommon in the United States and in other countries that have wheat flour, bread, pasta, corn meal or rice enrichment regulations. Flour, corn meal and rice have been fortified with B vitamins as a means of restoring some of what is lost in milling, bleaching and other processing. For adults 20 and older, average intake from food and beverages is 1.8 mg/day for women and 2.5 mg/day for men. An estimated 23% consume a riboflavin-containing dietary supplement that provides on average 10 mg. However, anyone choosing a gluten-free or low gluten diet should as a precaution take a multi-vitamin/mineral dietary supplement which provides 100% DV for riboflavin and other B vitamins.
Riboflavin deficiency (also called ariboflavinosis) results in stomatitis including painful red tongue with sore throat, chapped and fissured lips (cheilosis), and inflammation of the corners of the mouth (angular stomatitis). There can be oily scaly skin rashes on the scrotum, vulva, philtrum of the lip, or the nasolabial folds. The eyes can become itchy, watery, bloodshot and sensitive to light (Sebrell 1939)Due to interference with iron absorption, even mild to moderate riboflavin deficiency results in an anemia with normal cell size and normal hemoglobin content (i.e. normochromic normocytic anemia). This is distinct from anemia caused by deficiency of folic acid (B9) or cyanocobalamin (B12), which causes anemia with large blood cells (megaloblastic anemia). Deficiency of riboflavin during pregnancy can result in birth defects including congenital heart defects (Smedts et al.,2008) and limb deformities (Robitaille et al.,2008).
The stomatitis symptoms are similar to those seen in pellagra, which is caused by niacin (B3) deficiency. Therefore, riboflavin deficiency is sometimes called "pellagra sine pellagra" (pellagra without pellagra), because it causes stomatitis but not widespread peripheral skin lesions characteristic of niacin deficiency (Sebrell and Butler.,1939).
Riboflavin has been noted to prolong recovery from malaria,despite preventing growth of plasmodium (the malaria parasite) (Das et al.,1988).

In other animals

In other animals, riboflavin deficiency results in lack of growth ( Patterson and  Bates., 1989), failure to thrive, and eventual death. Experimental riboflavin deficiency in dogs results in growth failure, weakness, ataxia, and inability to stand. The animals collapse, become comatose, and die. During the deficiency state, dermatitis develops together with hair loss. Other signs include corneal opacity, lenticular cataracts, hemorrhagic adrenals, fatty degeneration of the kidney and liver, and inflammation of the mucous membrane of the gastrointestinal tract. Post-mortem studies in rhesus monkeys fed a riboflavin-deficient diet revealed about one-third the normal amount of riboflavin was present in the liver, which is the main storage organ for riboflavin in mammals (Waisman and Harry.,1944). Riboflavin deficiency in birds results in low egg hatch rates (Romanoff et al.,1942).  

REFERENCES
  • 1.      Fiume MZ (2001). "Final report on the safety assessment  of biotin". International Journal of Toxicology 2: 45–61.
  • 2.      Maton, Anthea; Jean Hopkins; Charles William McLaughlin; Susan Johnson; Maryanna Quon Warner; David LaHart; Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. ISBN 0-13-981176-1
  • 3.      Brigelius-Flohé R, Traber MG; Traber (1999). "Vitamin E: function and metabolism".FASEB J. 13 (10): 1145–1155.
  • 4.      Smedts HP, Rakhshandehroo M, Verkleij-Hagoort AC, de Vries JH, Ottenkamp J, Steegers EA, Steegers-Theunissen RP (Oct 2008). "Maternal intake of fat, riboflavin and nicotinamide and the risk of having offspring with congenital heart defects". European Journal of Nutrition 47 (7): 357–365.
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