Unveiling the Vitality of Biotin

Biotin, a pivotal water-soluble member of the B complex vitamin group, orchestrates numerous biochemical processes essential for human health. Primarily, it serves as a coenzyme indispensable in the synthesis of aspartic acid, a critical player in various metabolic pathways including the deaminase system and carbon dioxide fixation.

Despite its significance, biotin's presence in plasma is modest compared to other water-soluble vitamins. Predominantly existing in a free form, it seamlessly integrates into the aqueous phase of plasma, facilitating its vital functions throughout the body.

Deficiency of biotin is uncommon but can manifest under specific circumstances. Consumption of raw egg white, rich in avidin, poses a risk as it binds with biotin, rendering it unavailable for metabolic processes. Furthermore, prolonged usage of certain anticonvulsant drugs may accelerate biotin breakdown, predisposing individuals to deficiency. Infants born with biotinidase deficiency face a genetic anomaly leading to biotin depletion, underlining the necessity of this vitamin from early stages of life.

The repercussions of biotin deficiency are profound, ranging from scaling skin and lesions to nerve fiber degeneration, impeding normal growth and development. Yet, owing to microbial flora in the intestine, there's ambiguity regarding the precise dietary requirement for biotin.

While biotin is ubiquitously present in foods and feedstuffs, its concentrations vary significantly. Liver emerges as a stellar source, with peanuts, peas, beans, and whole cooked eggs also offering substantial amounts. Conversely, fruits and meats typically exhibit lower biotin content, emphasizing the importance of a varied diet for optimal biotin intake.

In conclusion, biotin's multifaceted role in human physiology underscores its indispensability for overall well-being. By understanding its sources and consequences of deficiency, we can ensure adequate intake, thereby safeguarding against potential health implications.
Unveiling the Vitality of Biotin

The Vital Role of Vitamin B in Health and Well-being

Vitamin B encompasses a group of water-soluble nutrients essential for various bodily functions. Within this group are several crucial vitamins, including B1, B2, B3, B5, B6, B12, folic acid, biotin, choline, inositol, and para-aminobenzoic acid. These vitamins play multifaceted roles in maintaining overall health.

One of the primary functions of B vitamins is to support nerve function, appetite regulation, and normal digestion. They are indispensable for growth, fertility, and lactation, underscoring their significance in the human body's fundamental processes.

Moreover, B vitamins are indispensable for optimal brain function. They facilitate the delivery of oxygen to the brain, shielding it from harmful oxidants. Crucially, B vitamins aid in converting glucose into energy within brain cells and help regulate neurotransmitter levels, thereby influencing mood and cognitive functions.

Of all the B vitamins, B6, B12, and folic acid stand out for their profound impact on mood enhancement. Their deficiency can lead to mood disturbances and cognitive impairments, emphasizing the importance of adequate B vitamin intake for mental well-being.

However, despite their critical roles, B vitamins are often lacking in diets due to the destruction of natural sources during food processing. This deficiency can lead to various health issues, including growth retardation, vision impairment, skin disorders, and cardiovascular complications like hypertension and beriberi.

Notably, deficiency in vitamin B1, or thiamine, can manifest as neuritis, forgetfulness, and difficulty in thinking, further highlighting the breadth of its impact on neurological function.

Additionally, inadequate intake of folate, vitamin B12, and vitamin B6 has been linked to an increased risk of fatal heart disease. This association is attributed to elevated levels of homocysteine—a protein-related compound—in individuals with low blood levels of these B vitamins. High homocysteine levels contribute to blood clot formation, arterial damage, and significantly raise the risk of heart attacks and strokes.

In conclusion, Vitamin B is indispensable for maintaining overall health and well-being. From supporting nerve function to enhancing mood and preventing cardiovascular complications, these water-soluble nutrients play a myriad of vital roles in the body. Therefore, ensuring an adequate intake of B vitamins through a balanced diet or supplementation is essential for optimal health and vitality.
The Vital Role of Vitamin B in Health and Well-being

Riboflavin or Vitamin B2

Riboflavin is also known as vitamin B2. The primary form of the vitamin is as an integral component of the coenzymes flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD). Through these two flavoco-enzymes, riboflavin functions as a catalyst for redox reactions in numerous metabolic pathways and in energy production.

Riboflavin was first documented in 1879 by Alexander Wynter Blyth as a yellow pigment found in milk and it was called lactochrome or vitamin G. This water-soluble B factor from milk was actually a combination of both thiamine (which is heat labile) and riboflavin (which is heat stable).

Food sources of riboflavin including: legumes (chick peas, lentils, red and black gram and soybean), meat (beef, mutton, chicken, and duck), fish and eggs. Fruits and vegetables are poor sources of riboflavin.

Riboflavin is important for the growth, development, and function of the cells in human body. It also helps turn the food into the energy in the body. Humans require dietary riboflavin for DNA repair, energy production, fatty acid and amino acid synthesis, folic acid activation, and production of glutathione which is a free radical scavenger.

Riboflavin deficiency results in the condition of hypo- or ariboflavinosis, with sore throat; hyperaemia; oedema of the pharyngeal and oral mucous membranes; cheilosis; angular stomatitis; glossitis; seborrheic dermatitis; and normochromic, normocytic bone marrow.
Riboflavin or Vitamin B2

Thiamine deficiency and their symptoms

Thiamine efficiency can cause cardiovascular and neurological signs and symptoms. Beriberi a serious thiamine efficiency disease, usually affects Asians, who subsist mainly on a diet of unenriched rice and wheat.

Among the symptoms of beriberi: chiefly nervous and cardiovascular systems affected; mental confusion, muscular weakness, loss of ankle and knee jerks, painful calf muscles, peripheral paralysis, edema (wet beriberi), muscle wasting (dry beriberi), enlarged heart.

In the United States, although uncommon, it usually occur in alcoholics, malnourished young adults, and infants who are on a low proteins diet or are being breast-fed by thiamine efficient mothers.

Sign and symptoms of infantile beriberi include cyanosis, dyspnea, tachycardia, aphonia (soundless crying), and eventual cardiac failure.

Although whole grains may be rich in thiamine, processing of grains significantly reduces their thiamine content. Likewise, because thiamin is water soluble and heat sensitive, cooking largely results in the loss or destruction of this vitamin especially when chlorinate waster is used.
Thiamine deficiency and their symptoms

Biochemistry of zinc

Nutrition involves the relationship of food and nutrients to health. Biochemistry is the science of the chemistry of living organisms.

Zinc metalloenzymes catalyze approximately 50 important biochemical reactions. Many of these enzymes have been isolated from more than one species, resulting in identification of over 200 catalytically active zinc metalloproteins. Carbonic anhydrase, alcohol dehydrogenase, alkaline phosphatase and steroid hormone receptors are examples.

The functions of zinc in metalloenzymes are catalytic structural, regulatory and noncatalytics. Examples of enzymes in which zinc plays a catalytics role include carbonic ahnydrase, carboxypeptidas, thermolysin, and aldolases.

Excessive intake can cause adverse effects in humans and animals. In human, the effects of acute zinc toxicity are gastrointestinal disturbances giving rose to abdominal pain, nausea and vomiting. Chronic zinc toxicity is associated with changes in copper balance leading to symptoms of copper deficiency.

Zinc deficiency is an important part of protein-energy malnutrition and may limit weight gain during refeeding unless adequate amounts are provided.

The average daily dietary intake of zinc is around 150 umol. It is present in all protein rich foods.
Biochemistry of zinc

What are the causes of vitamin k deficiency in human?

A deficiency of vitamin K is unlikely in healthy adults. The populations groups that appear to be most at risk for a vitamin K deficiency are newborn infants, people being treated chronically with antibiotics, people with severe gastrointestinal malabsorption disorders, and the elderly.

Diseases of the gastrointestinal tract, biliary stasis, sliver diseases, cystic fibrosis, celiac disease, and Ascaris infection can interfere with enteric absorption of vitamin K.

The synthesis of vitamin K by the intestinal flora meets the requirements of this vitamin. But sterilization of the large intestine by the prolonged use of sulfonamides and antibiotics or diarrheal diseases like sprue, ulcerative colitis and conditions with reduce fat absorption may lead to vitamin K deficiency.

Vitamin K deficiency also occurs in patients with malabsorption and sometimes following prolonged use of broad spectrum antibiotic by mouths (which can destroy the colonic bacteria). Many antibiotics like penicillins, cephalosporins, aminoglycosides, chloramphenicol, amphotericin B, erythromycin are reported to cause vitamin K deficiency and hypoprothrombinemia.

Certain types of drugs can impair vitamin K function. These include warfarin and other 4-hydroxycoumarin anticoagulants and large doses of salicylates, which inhibit the redox cycling of the vitamin.

Newborn are particularly at risk because their food is limited to milk, which is low in vitamin K; their stores of the vitamin are low because inadequate amounts cross the placental and their intestinal tract is not yet populated by vitamin K-synthesizing bacteria.
What are the causes of vitamin k deficiency in human?

Vitamin A deficiency

Where it is the limiting nutrient, vitamin A deficiency causes anemia, growth retardation and xerophthalmia; increase the incidence and/or severity of infectious episodes and reduces childhood survival.

Vitamin A deficiency is a major global problem. Vitamin A deficiency is rare in the US, but it is still a major public health problem in the developing world. It is most often associated with protein/calorie malnutrition and affects over 120 million children worldwide.

Vitamin A affects many physiological systems; it plays a essential role in vision and eye health and it affects growth and susceptibility to infection and anemia in children.

In ancient Egypt it was known that night blindness could be cured after eating liver, which was later found to be a rich source of vitamin A. Vitamin A deficiency contributes to blindness by making the eye very dry, damaging the cornea of the eye (called xerophthalmia), and promoting damage to the retina of the eye.

The consequences of vitamin A deficiency include blindness, poor growth, severe infection and death; it control and prevention are central in child health and survival programs.

Other less well known consequences of vitamin A deficiency include:
*Increases mortality rates among infants 6 months to 6 years of age.
*Augments the severity, complications and risk of death associated with measles.
*Associated with increased infant morbidity, particularly in the severity of disease episodes, such as diarrhea and pneumonia.
Vitamin A deficiency

Vitamin B deficiency

Vitamin B complex helps the body to handle stress and improves all the functions in the cells.

The B complex vitamins are involved in the metabolism of carbohydrates, proteins and fat in the body.

The B vitamins are important for antibody production and red blood cells, and assist with stress related behaviors.

The signs and symptoms of early vitamin deficiency are often more elusive and subtle than those of the major diseases.

Deficiency of certain B vitamins can cause loss of energy, loss of appetite, abdominal pain, depression, numbness and tingling in the arms and legs, muscle cramps, respiratory infections, hair loss, poor growth in children, and birth defects in the fetuses of pregnant women.

It also include digestive disorders, poor muscle tone, sores on the skin and anemia.

If the thiamine or vitamin B1 is deficient in the body, thymus gland and lymph tissue will shrank and the body will reduce antibody response and decrease white blood cell response.

Clinical manifestation of deficiency of some B vitamins such as beriberi, peripheral neuropathies, pellagra, and oral and genital lesions were once major public health probes in some parts of the world. A deficiency of B vitamins also often causes depression.

All the B vitamins working harmony to keep the liver healthy to stabilize brain functions and to metabolize sugar correctly. Consequently, this prevents irritability and fatigue.

Antibiotics deplete the B vitamins and the typical canine diet of processed foods is low in B vitamins increasing the need for supplementation.

Vitamin B deficiency

Deficiency of vitamin A

Vitamin A deficiency is common among children. Night blindness and eye changes are often early sign.

This nutritional deficiency is widespread in developing countries, and the problem is exacerbated by a tendency by some to withhold vegetables from children for cultural or other reason.

Where it is the limiting nutrient, vitamin A deficiency causes anemia, growth retardation and xerophthalmia; increases the incidence and/or severity of infectious episodes.

Reduced survival is the most severe and potentially the most widespread consequence of vitamin A deficiency, and the one that has generated the most interest.

It is also common knowledge that an adequate levels of vitamin A is essential for animal vision and that prolonged low levels of vitamin A can lead to xerophthalmia and ultimately, blindness.

Vitamin A deficiency decreases resistance to infections and increases the severity, complications and risk of death from various diseases.

When vitamin A deficient, the epithelial cells of growth skin, oral cavities and respiratory, genitourinary and gastrointestinal tracts become dry and flat, hardening so that absorption of nutrients is reduced.

Moreover, vitamin A deficiency may increase the risk of bacteria colonization or delay recovery.

Deficiency of vitamin A

Calcium deficiency

99% of this major mineral is found in bone and teeth but it is also important for blood clotting, muscle contraction and nerve conduction.

Diet deficient in calcium affect the human body’s functions of bone formation and maintenance, transmission of nerve impulses, muscular contraction, and abilities for blood coagulation.

The symptoms of calcium deficiency includes rickets, osteomalacia, osteoporosis, scurvy, tetany, parathyroid hyperplasia, stunted growth, laryngospasm.

One of the first signs of a deficiency is a nervous affliction called tetany, which is characterized by muscle cramps, numbness and tingling in the arms and legs.

While ‘rickets’ is a condition when bone is malformation due to a softening of the bones.

Other symptoms include: curvature of the spine and ribs, loss appetite, and lameness. In the case of more prolonged deficit of calcium, ‘leaching’ of this element from the bones causes increased absorption of lead from polluted environments and its incorporations into bones and teeth.

Deficiency of calcium lowers the body resistance and for the children become as easy prey to respiratory and intestinal infections.

Calcium deficiency

Factors of vitamin K deficiency

Human intake of vitamin K comes from two main sources - our diets and synthesis from intestinal bacteria.

Vitamin K deficiency is rare among humans and most other animal species. This is due to the wide occurrence of vitamin K in plant and animal foods and to the significant microbial synthesis of the vitamin that occurs in the intestines.

Vitamin K deficiencies can be caused by a variety of factors. These include:
*Not consuming enough vitamin K from one's diet can contribute to a deficiency. Dietary vitamin K is highest in leafy green vegetables such as lettuce, kale, broccoli and collard greens.

*A diet with high intakes of salicylates can block vitamin K. Salicylates are found in foods such as nuts, fruits, spices and mints. Aspirin is a salicylate. Blocking vitamin K is why aspirin can "thin" the blood - it basically keeps blood from coagulating. This is why too much aspirin can cause stomach and intestinal bleeding.

*Antibiotics can cause bleeding problems from vitamin K deficiencies. Antibiotics drugs can virtually sterilize the lumen of the intestine, thus removing an important source of vitamin K. Prior to surgery, a patient’s vitamin K status is often tested to assess the risk hemorrhaging because antibiotics are frequently part of the treatment regimen.

*Candida (systemic yeast) infections have been linked to vitamin K deficiencies. An overgrowth of Candida albicans or other kinds of yeast can crowd out the helpful bacteria in the digestive tract that make vitamin K. People who eat a lot of sugary foods, an unusually high proportion of alkaline foods and/or take antibiotics tend to be at high risk for Candida infections.

*Lipid malabsorption. Whenever lipid absorption falters, as occurs when bile production falls, vitamin K absorption diminished. Diseases of the gastrointestinal tract, biliary stasis, liver disease, cystic fibrosis, celiac disease and Ascaric infection can interfere with the centric absorption of vitamin K.

*Certain types of drugs can impair vitamin K function. Anticoagulants like Warfarin block the action of vitamin K. In turn, vitamin K blocks the action of anticoagulants. That could block blood vessels leading to the heart or brain.

*Megadoses of vitamins A and E counteract the actions of vitamin K. Vitamin A appears to hamper intestinal absorption of vitamin K and excess vitamin E seems to decrease the vitamin K dependent clotting factor, thus promoting bleeding.

*The bacteria that synthesize vitamin K thrive in an acidic digestive environment. Antacids, if taken in sufficient quantity, may cause a vitamin K deficiency, as well as irritable bowel syndrome and various nutritional deficiencies, because they neutralize the hydrochloric acid in a person's stomach. Hydrochloric acid is needed to digest food and create the acidic environment in which the beneficial bacteria thrive.

*Some drugs disrupt vitamin K’s synthesis and action in the body: antibiotics kill the vitamin K-producing bacteria in the intestine, and anticoagulant drugs interfere with vitamin K metabolism and activity. When vitamin K deficiency does occur, it can be fatal.

Factors of vitamin K deficiency

Deficiency of essential fatty acids

Essential fatty acids are as important to human health as oxygen and water. Research links a deficiency in essential fatty acids to most illnesses and diseases.

There are three important functions of essential fatty acids, the most important is as part of phospholipids in all cellular membranes.

Secondly, this type of fatty acids act as precursors of prostanoids which are only formed from essential fatty acids and the last functions is of course as energy source.

The clinical manifestations of essential fatty acids deficiency in human include dry, scaly skin, usually erythematous eruptions, diffuse hair loss, poor wound healing failure of growth and increase metabolic rate.

It is also associated with capillary fragility, abnormal liver and kidney function and neurologic damage. During pregnancy, the fetus relies on material circulation and transfer of these essential fatty cods across the placenta. In case the growing tissues requirements are not met, the fetus is at increase risk for essential fatty acid deficiency.

In essential fatty acids deficiency, oleic acid can be dehydrogenated to yield polyunsaturated fatty acids that are non essential and do not substitute for the essential fatty acids. The end products of non-essential fatty acids extension cannot however, function in cell membranes or in eicosanoid precursors.

Malnutrition is a common cause of essential fatty acid deficiency. American Heart Association and the FDA both recommended essential fatty acid supplements for cardiovascular benefits.

The National Institute on Aging proposes a correlation between Alzheimer’s diseases and a deficiency on essential fatty acids.

Deficiency of essential fatty acids in adults is rare, but has been seen in children fed virtually fat-free diets.

Deficiency of essential fatty acids

Niacin deficiency

First documented in 1735 by a Spanish physician named Gaspar Casal the niacin deficiency disease pellagra was originally named ‘mal de la rosa,’ or ‘red sickness.’ Its due to the telltale redness that appears around the necks of people with the disease.

Pellagra means ‘rough skin’ in Italian. The great pellagra epidemic in America’s South did not emerged until the early twentieth century.

Because the niacin coenzymes NAD and NADP are involved in just about very metabolite pathway, niacin deficiency wreaks havoc throughout the body. It also that the depressive psychosis is assumed to be because of inadequate formation of the neurotransmitter serotonin as a result of tryptophan deficiency.

The classical features of endemic pellagra are dermatitis, inflammation of the mucous membranes, diarrhea and psychiatric disturbances.

The dermatitis often appears after exposure to sunlight and resembles sunburn.

Pellagra condones to plaque people living in Southeast Asia and Africa however, whose diet lack sufficient niacin and protein.
Niacin deficiency

Vitamin D deficiency rickets

In an infant or child this deficiency results in the disease called rickets, in which the rapidly growing bones grow soft and eventually bend under the weight of the body.

It’s a defect in the mineralization of bone matrix with increase bone mass.

Affected children lack the exposure to ultraviolet light necessary for the dermal synthesis of vitamin D and have a poor diet in vitamin D in which the component (high fiber and high cereal) probably contribute to the excessive breakdown of vitamin D.

In adults, the same disorder is called osteomalacia or adult rickets. It is to be distinguished from osteoporosis where bone mass is decreased from hypophosphatemic osteopeniaof premature infants, and from renal osteodystrophy.

The name rickets is from the Old English wrickken, to twist. The more technical medical term, rachitis, which comes from Greek, the spine , was suggested by Francis Glisson in 1650.

Vitamin D deficiency rickets occurs in underprivileged populations throughout the world, particular in the northern hemisphere.

Women in United States usually take multivitamins and eat vitamin D dairy foods so rickets and vitamin D deficiency is less a problem than in developing countries and northern Europe.
Vitamin D deficiency rickets

Potassium deficiency

Potassium deficiency is a proven contributing cause for many illness including: arthritis, kidney stones, atrial fibrillation, adrenal insufficiency, celiac disease, high blood pressure, coronary artery disease, ulcerative colitis, hypothyroidism, irritable bowel syndrome, Alzheimer’s disease, multiple sclerosis, myasthenia gravis, Crohn’s disease, lupus, atherosclerosis, diabetes and stroke.

A lack of potassium first affects the muscles and nerves. There is muscle weakness, irritability, mental confusion and rapid heartbeat.

Other sign of potassium deficiency includes abnormally dry skin, acne, chills, cognitive impairment, constipation, depression, diarrhea, diminished reflex function, edema, nervousness, insatiable thirst, glucose intolerance, growth impairment, high cholesterol levels, insomnia, low blood pressure, nausea and vomiting, periodic headaches, proteinuria, respiratory distress and salt retention.

Sweating associated with regular or extend periods of exercise can lead to potassium deficiency. Because potassium helps the body covert glucose into energy, early signs of potassium deficiency in athletes are muscle weakness and great failure.

Potassium deficiency is another cause of kidney failure, though it is uncommon. Kidney function decreases in severe potassium deficiency and may never recover.

Cortisol is reduced during potassium deficiency and this reduction accounts for many of the symptoms of rheumatoid arthritis. Cortisol shuts down most of the copper’s enzymes when it declines so that excretion of copper is increased and Lysyl oxidize inhibited.
Potassium deficiency

Iodine deficiency disorder

The importance of iodine as an essential element arises from the fact that it is a constituent of the thyroid hormones thyroxine and triiodothyronine.

These hormones are essential for normal growth and physical and mental development in animals and man.

Iodine deficiency occurs worldwide and is a public health problem in 130 countries.

Deficiency arise when dietary iodine intake does not meet requirements. The diet is likely to be deficient whenever the soil content of iodine is low, which is often the case in mountainous regions.

The most severe deficient soils are those of the European Alps, the Himalayas, the Andes and the vast mountains of China.

Iodine deficiency leads to inadequate production of thyroid hormone that indispensible for brain growth and development.

The iodine deficiency disorders consist of wide spectrum, including mental retardation, impaired physical development, increased prenatal and infant mortality, hypothyroidism, cretinism and goiter.

The most visible manifestation of iodine deficiency is goiter. Goiter is defined as an enlargement of the thyroid gland and cretinism is a term used for a severe form of iodine deficiency characterized by severe mental retardation.

The most severe damage due to iodine deficiency occurs from the fetal period to the third month after birth, during which iodine deficiency can produce cretinism, an irreversible form of mental retardation.
Iodine deficiency disorder

Biotin deficiency

Biotin is a water soluble vitamin that is generally classified in the B complex group. This B complex vitamin used in the formation of enzymes that fuel the human body.

Biotin is a key factor in metabolizing and utilizing fats an glucose for energy.

Deficiency of this compound is unusual, but can be demonstrated by the feeding of raw egg white, which contains the substance, avidin, which ties up biotin.

Because some anticonvulsant drugs breakdown biotin, people who take then for long periods also risk a deficiency.

Biotin deficiency also has been clearly demonstrated in biotinidase deficiency. This due to several process which involved gastrointestinal absorption, salvage of biotin at cellular level and renal loss of biocytin.

Infants born with biotinidase deficiency suffer from a rare genetic defect that leads to biotin depletion.

Decreased levels of biotin cause the metabolism to become severely impaired. When enzymes aren’t available to breakdown and build up protein, every biochemical process of the body suffers since protein are the essential building blocks of cellular composition.

The clinical findings and biochemical abnormalities caused by biotinidase deficiency are quiet similar to those of biotin deficiency: common finding include periorificial dermatitis, conjunctivitis, alopecia, ataxia, and development delay.
Biotin deficiency

Deficiency of manganese

A deficiency of manganese (which is extremely rare) may lead to atherosclerosis, confusion, eye problems, hearing problems, heart disorders, high cholesterol levels, hypertension irritability, memory loss, muscle contradiction, pancreatic damage, profuse perspiration, rapid pulse, teeth grinding, tremors and a tendency towards breast ailments.

Although people who consume normal varied diets do not appear to be at risk for manganese deficiency, certain disorders may cause suboptimal status.

Manganese deficiency has been shown to lead to bone demineralization and impaired growth in children, decreased serum cholesterol levels and a transient skin rash in young men, and mildly abnormal glucose tolerance in young women.
Deficiency of manganese

Vitamin B12 Deficiency

Vitamin B12 or cobalamin is a very complex chemical compound. Cobalamin is referring to the group of cobalt containing vitamer compound, this include cyanocobalamin, hydroxocobalamin, 5-deoxyadenosylcobalamin and methylcobalamin.

This vitamin required for the normal development of red blood cells, and a deficiency it causes acute pernicious anemia and a variety of other disorders. The exact requirement of Vitamin B-12 is yet unknown, since some B12 is synthesized by bacteria in the intestine. The organs of animals are excellent sources of Vitamin B12 and the muscles of warm-blooded animals and fish are good sources.

Vitamin B12 deficiency is commonly asymptomatic, but can also present as anemia characterized by enlarged blood corpuscle, so called megaloblastic anemia. However in serious case deficiency can potentially cause severe and irreversible damage to the nervous system.

Since body stores of vitamin B12 are adequate for up to five years, deficiency is generally the result of failure to absorb it. In older people, is also caused by inadequate intake of impaired absorption.

Megaloblastic anemia, Crohn's disease and other intestinal disorders are the most frequent causes of vitamin B12 deficiency.

Symptoms are attributable primarily to anemia, although glossitis, jaundice, and splenomegaly may be present. Vitamin B12 deficiency may cause decreased vibratory and positional sense, ataxia, paresthesias, confusion.

Apart from anemia due to vitamin B12 deficiency, the neurologic symptom of vitamin B12 deficiency include numbness and tingling of the arms and more commonly the legs, difficulty walking, memory loss, disorientation and dementia with or without mood changes.

Neurological or psychiatric symptoms occurs in about 40% of patents with vitamin B12 deficiency, in association with progressive damage to the spinal cord, peripheral nerves and cerebrum.
Vitamin B12 Deficiency

Vitamin E Deficiency

Vitamin E was discovered in 1922, but not until 1983 that vitamin E was demonstrated to be dietary essential for human beings.

Vitamin E deficiency was first describe in children with fat malabsorption syndromes, principally abetalipoproteinemia, cystic fibrosis, and cholestatic liver disease.

They have been reports of vitamin E deficiency symptoms in person with protein calories malnutrition.

The frequency of human vitamin E deficiency is very rare, deficiency is usually associated with disease of fat malababsorption such as cystic fibrosis.

In individual at risk, it is clear that vitamin E supplements should be recommended to prevent deficiency symptoms.

Without vitamin E, the red blood cells break open and spill their contents, probably due to oxidation of the polyunsaturated fatty acids in their membranes.

The classic sign of vitamins E deficiency, known as erythrocyte hemolysis, is seen in premature infants, born before the transfer of vitamin E from the mother to the infant that takes place in the last week of pregnancy.

The primary human vitamin E deficiency symptoms is a peripheral neuropathy characterized by the degeneration of the large caliber axons in the sensory neurons.

Other vitamin E deficiency symptoms observed in humans include spinocerebellar ataxia, skeletal myopathy, and pigmented retinopathy.

Prolonged vitamin E deficiency also can causes neuromuscular dysfunction involving the spinal cord and retina of the eye.
Vitamin E Deficiency