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

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    Fiume MZ
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    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
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