What are the symptoms of calcium deficiency?

The calcium level in blood can be moderately low without causing any symptoms. However, if levels of calcium are low for long periods, people may develop dry scaly skin, brittle nails, and coarse hair.

A long-term calcium deficiency can lead to dental changes, cataracts, alterations in the brain, and osteoporosis, which causes the bones to become brittle.

Other symptoms of calcium deficiency include rickets, osteomalacia, scurvy, tetany, parathyroid hyperplasia, stunted growth, laryngospasm.

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

Poor calcium intake affects mostly bone and muscle. Rickets occurs in children when the amount of calcium accretion per unit of bone matrix is deficient.

Hypocalcemia may result in tetany, a condition characterized by intermittent muscle contractions that fail to relax, especially in muscles of the arms and legs. Hypocalcemia is often detected by routine blood tests before symptoms become obvious. Doctors measure the total calcium level (which includes calcium bound to albumin) and the albumin level in blood to determine whether the level of unbound calcium is low.
What are the symptoms of calcium deficiency?

Vitamin D deficiency and rickets

Vitamin D helps child's body absorb calcium and phosphorus from food. Not enough vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones.

Vitamin D (where D represents D2 or D3) is biologically inert and metabolized in the liver to 25-hydroxyvitamin D [25(OH)D], the major circulating form of vitamin D that is used to determine vitamin D status.

In an infant or child this deficiency results in the disease called rickets. Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency. Rare inherited problems also can cause rickets.

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.

Symptoms of vitamin D deficiency rickets include restlessness, lack of sleep, slow growth, a delay in crawling, sitting or walking, soft skull bones, swelling of the skull, bead-like nodules where the ribs and their cartilages join, and a delay in the closing of the skull bones.

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. It is more common in children of Asian, African-Caribbean and Middle Eastern origin because their skin is darker and needs more sunlight to get enough vitamin D.

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 and rickets

Niacin (Vitamin B3)

Niacin is a water-soluble B vitamin important for DNA repair and energy metabolism. Also known as vitamin B3. Niacin is the generic term for nicotinic acid (pyridine 3-carboxylic acid) and nicotinamide (nicotinic acid amide) and the coenzyme forms of the vitamin.

In 1867, nicotinic acid was produced from nicotine in tobacco. In the early 1940s, with its role as a vitamin established, it was renamed “niacin” so people wouldn’t confuse it with nicotine.

Nicotinic acid and nicotinamide are colorless crystalline substances; each is insoluble or only sparingly soluble in organic solvents.

Nicotinamide is the active form, which functions as a constituent of two coenzymes, namely, nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP).

Niacin is part of coenzyme that participates in the production and breakdown of carbohydrates, fatty acids, and amino acids. It involved in at least 200 metabolic pathways. It is also a compound that dilates blood vessel.

A sufficient intake of vitamin B3 (niacin) is important as it helps the body to
• convert food into glucose, used to produce energy
• produce macromolecules, including fatty acids and cholesterol
• DNA repair and stress responses.

Clinical evidence of niacin deficiency includes fatigue, poor appetite, diarrhea, irritability, headache, emotional instability and possible memory loss. These may lead to changes in the skin, mucosa of the mouth, stomach and intestinal tract and the nervous system. These changes are called “pellagra”, which means “raw skin”.

Pellagra is characteristically associated with maize based diets. The disease pellagra has been known since the introduction of corn to Europe in the 1770s. The connection between pellagra and niacin was confirm in 1937 by an American scientist who reaching for the cause of pellagra.

In industrialized country, particularly among alcoholics, niacin deficiency may present with only encephalopathy.

Niacin comes from the diet, but the body can also manufacture it from the amino acid tryptophan, with riboflavin helping out in the process.

Adults require 13-20 mg niacin. In pregnancy, lactation and active muscular work, niacin requirement is further increased by 3-4 mg. Children require 5-16 mg niacin.

Yeast, liver, poultry, lean meats, nuts and legumes contribute most of the niacin obtained from food. In cereal products (e.g., corn, wheat), niacin is bound to certain components of the cereal and is thus not bioavailable.

The amino acid tryptophan contributes as much as two thirds of the niacin activity required by adults in typical diets. Important food sources of tryptophan are meat, milk and eggs.
Niacin (Vitamin B3)

Deficiency of vitamin K

Human intake of vitamin K comes from two main sources - human diets and synthesis from intestinal bacteria. The dietary essentiality of vitamin K was discovered as the result of a series of experiments carried out by the Danish nutritional bio9chemcist Henrik Dam (1895 – 1976), working at the University of Copenhagen.

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.

*The vitamin is lipid soluble and is absorbed primarily in the small intestine. A healthy patient usually has a 30-day body store. Vitamin K deficiency occurs with anatomic lesions that bypass the small intestine, malabsorption, intrahepatic or biliary obstruction, hepatic disease, and rarely with inadequate intake.

*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.

*A variety of antibiotics interferes with intestinal bacteria growth and can impair vitamin K synthesize or interferes with intracellular role of vitamin K.

*The most common cause of fully functional vitamin K deficiency is the therapeutic use of oral anticoagulant drugs of the coumarin family, such as warfarin. Warfarin blocks 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.

*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.

*Vitamin K is furnished by dietary intake of plant foods and synthesis by intestinal flora. 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.
Deficiency of vitamin K

Manifestation of iodine deficiency

Iodine is an essential constituent of the hormones of the thyroid gland, namely, triodothyronine (T3) and thyroxine (T4). These hormones are essential for normal growth and physical and mental development in animals and man.

Iodine deficiency is the result of insufficient dietary iodine intake, which can lead to inadequate production of thyroid hormones and many adverse effects at all life stages, collectively known as iodine deficiency disorders.

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.

WHO recommends that the daily intake of iodine should be 90 μg for preschool children (0 to 59 months), 120 μg for schoolchildren (6 to 12 years, 150 μgfor adults (those older than 12 years) and 200 μg for pregnant and lactating women.

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. Thyroid function is dependent upon the availability of iodine and several other trace elements, The relationship between the iodine intake level of a population and the occurrence of thyroid disease is U-shaped, with an increase in risk associated with both low and high iodine intake.

Iodine deficiency during pregnancy remains a common cause of preventable cognitive of impairment worldwide. 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.
Manifestation of iodine deficiency

Food sources and deficiency of ascorbic acid

Ascorbic acid was recognized as early as 1734 as the factor in fresh fruit and vegetables that prevent the development of scurvy.

Vitamin C has been implicated in the hydroxylation of proline to form the hydroxyproline required in the formation of collagen.

It helps in the healing of wounds fractures, bruises and bleeding, gums and recues liability the infection.

Excellence sources of vitamin C are citrus fruits, berries, guava, capsicum and green leafy vegetables. Tomato juice, if it has been processed properly, is a fair source of this vitamin. Green peppers, cabbage, broccoli, and sprout are excellent to good sources of vitamin C.

Deficiency of vitamin C causes scurvy (spongy gums, loose teeth, swollen joints, hemorrhages in various tissue, etc) and impaired healing of wounds. Orange juice is an excellent source of vitamin C.
Food sources and deficiency of ascorbic acid

Protein deficiency in human body

Protein is one of the three ‘macronutrients’ (protein, carbohydrates, and fats) that human bodies need in balanced amounts.

Proteins are constantly being turned over in body tissues as old cells die and are replaced by new ones. Approximately 300 g of new protein is made each day in the human body.

The disease syndrome of kwashiorkor first described in 1933 is believed to be due to protein deficiency, but it occurs to varying degrees in conjunction with calorie deficiency. The dramatic clinical picture of kwashiorkor (edema, hypoalbuminemia, and a fatty lover with or without skin and hair changes) represents acute decompensation of a relatively long-standing deficiency state, usually precipitated by infection.

The disease syndrome is variable source the degree in both calorie and protein malnutrition, as well as the nutrients, will influence the biochemical and clinical changes.

MYOGLOBIN

The term protein deficiency can be defined as state of relative or absolute deficiency of body proteins or one or more of the essential amino acids. The deficiency can result from a protein-deficient due to other disease and in general can also result from a global deficit of food.

In uncomplicated protein deficiency, for example, protein catabolism should be minimal when total energy is the limiting factor, however, protein catabolism must increase to cover energy needs.

Severe marasmus or choric starvation , is characterized by growth retardation , loss of body fat, and muscle wasting. Studies of mass starvation during World War II and in chronically deprived populations suggest that severe deficits of calories and protein result in decreased fertility, in a deceased in the length and weight of the newborn, and in increased rates of neonatal mortality.

When total caloric intake has been adequate or nearly adequate, as is possible when starchy low protein foods are dietary staples, the symptoms are more toward changes associated with protein deficiency pellagra-type dermatitis, fatty liver, changes in texture and pigmentation of hair, gastro intestinal disturbances and diarrhea with resulting loss of electrolytes.

Protein deficiency in human body

Manganese deficiency in human nutrition

The total amount of manganese in the adult human is approximately 15 mg. relatively high concentrations have been reported in the liver, pancreas, intestine and bone. The pancreas and liver have the highest concentration and about 25% is in the skeleton.

Manganese deficiency is rare, but it has been reported in cases of diabetes and pancreatic insufficiency and in protein-energy malnutrition states such as kwashiorkor.

Symptoms include impaired growth, skeletal abnormalities, depressed reproductive function and defects in lipid and carbohydrate metabolism.

In human, manganese deficiency generally does not develop unless the mineral is deliberately eliminated from the diet. It has been reported that prolonged manganese deficiency is associated with osteoporosis in man and that osteoporotic subjects have low serum manganese levels.

Other problems associated with manganese deficiency include the occurrence of ataxia, loss of equilibrium, cell ultrastructure abnormalities, compromised reproductive function and abnormal glucose tolerance.

Low serum manganese levels have been reported in some diabetic and epileptic children, and a negative manganese balance has been observed in children with pancreatic insufficiency.
Manganese deficiency in human nutrition 

Fat soluble vitamin deficiency in infants

Infants and young children are particularly at risk of vitamins deficiency. It starts with the fact that vitamin deficiencies are present throughout life cycle, and an infant born to a mother with vitamin deficiency will have lower stores some nutrients at birth.

Although it is often difficult to isolate the effects of nutritional deficiencies from other socioeconomic complications, severe vitamin deficiencies have a direct influence on the developing brain.

Fat soluble vitamin deficiency is more common and can be detected biochemically before clinical symptoms, which are obvious only when severe deficiencies appear.

Hypo or hypervitaminosis A can lead to developmental and learning disabilities as well as problems with motor, balance, eye problems and mood and emotional disturbances.

The classical presentation of vitamin D deficiency in infants is rickets. Clinical and radiological rickets may take several months to develop depending on the growth rate.

Deficiency of vitamin E leads to hemolysis, peripheral neuropathy and occasionally visual loss. Vitamin E deficiency can occur in infants with severe forms of fat malabsorption.

Vitamin K deficiency may result in vitamin K deficiency bleeding. Bleeding usually occurs from the umbilical stump or after minor procedures, but serious events such as gastrointestinal and cerebral hemorrhage are also possible.
Fat soluble vitamin deficiency in infants

Vitamin A is important for vision and eye health

Vitamin A affects many physiological systems; it plays an essential role in vision and eye health.

This vitamin is a fat soluble antioxidant vitamin present in supplements preformed or as beta-carotene (provitamin A), which the body then coverts to vitamin A.

Vitamin A is essential for normal vision and eye health because it is involved in the perception of light and because it is needed for normal cell differentiation.

Cell differentiation is the process whereby immature cells change in structure and function to become specialized.

Vitamin A help human see because retinal is part of rhodopsin. Rhodopsin is alight sensitive pigment. When light strikes rhodopsin, it initiates a series of events that’s result in a nerve signal being sent to the brain, which allows human to see.

Vitamin A also requires for producing iodopsins, the light sensitive pigments for daylight or color vision.

The first sign of the breakdown of rhodopsin is the loss of night vision. The eye no longer distinguishes colors. Such deficiency calls for vitamin A.  The cornea is also damaged when this vitamin is lacking, but the greatest damage is to the retina.
Vitamin A is important for vision and eye health

Protein deficiency symptoms

The nutritional disease kwashiorkor was first described in the medical literature in the 1930s and a very tentative suggestion made that it might due to dietary protein deficiency.

In protein deficiency, when the diet supplies too little protein or lacks a specific essential amino acid relative to the others, the body slows it synthesis of proteins whole increasing its breakdown of body tissue protein to liberate the amino acids it needs to build other proteins of critical importance.

The first sign of protein deficiency is likely to be weak muscles – the body tissue most reliant on protein.

A protein deficiency may also show up in the blood. Red blood cells live for only 12 days. Protein is needed to produce new ones.

People who do not get enough protein may become anemic, having fewer red blood cells than they needed.
Protein deficiency symptoms

Vitamin A in general

Vitamin A is a fat soluble vitamin. It is found only in animals, although a number of plants contain carotene, from which vitamin A can be produced in the body once the plants contain carotene are eaten.

Vitamin A may be formed in the body from the yellow pigments (containing carotene) of many fruits and vegetables, especially carrots.

Vitamin A is required for vision. Epithelial cells (those cells present in the lining of body cavities and in the skin and glands) require vitamin A.

This vitamin also required for resistance to infection.

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.

Vitamin A deficient animals die much earlier and at a far higher rate than vitamin A sufficient controls.

Under experimental conditions of gradual progression deficiency, mortality begins to take its toll even before the appearance of xerophthalmia.

The situation in humans is far more complex. Vitamin A deficiency rarely occurs as an isolated disturbance; when it does, it is rarely recognized in the absence of severe xerophthalmia, a condition long associated with increased mortality.
Vitamin A in general 

Vitamin B of Riboflavin

Riboflavin – vitamin B2 is water soluble. It is one of the essential vitamins, is obtained by the human organism from the diet through small intestine absorption or alternatively, from indigenous bacteria which colonize large intestine.

This vitamin makes up a part of enzyme systems involved in the oxidation and reduction of different materials in the body.

Riboflavin is delivered in form of free vitamin or as its coenzyme, i.e. flavins mononucleotide and adenine dinucleotide, which occurs mainly as a prosthetic group of flavorproteins.

Riboflavin deficiency signs and symptoms had been observed in humans consuming nutritionally poor diet and under experimental conditions. It may result in vision impairment, sealing of the skin, and lesions on mucous tissue. Neuritis is another deficiency effect.

A primary deficiency of dietary riboflavin had wide implication for other vitamin, as flavin coenzymes are involves in the metabolism of folic acid, pyridoxine, vitamin K, niacin and vitamin D. The minimum intake of riboflavin for an adult is about 2.0mg per day.

The liver and kidney of pork, beef, and lamb are excellent sources of riboflavin, and the heart of these animals is a good source. Fair amounts of riboflavin are found in the muscular tissues of pork, beef, and lamb, while more is found in veal.
Vitamin B of Riboflavin

Copper Deficiency

The human body contains around 110 mg of copper. One of its most important functions is as a cofactor for lysyl oxidase, which is responsible for the formation of collagen cross links in connective tissue and bone. 

Copper is an antioxidant found in enzymes that deactivate free radicals and make it possible for body to use iron.

Copper deficiency has been clearly documented in infants recovering from malnutrition, in premature and low-birth-weight infants fed milk diet, and in patients receiving prolonged total parental nutritional solution without added copper.

Copper also may play a role in slowing the aging process by decreasing the incidence of protein glycation, a reaction in which sugar molecules hook up with protein molecules in the blood stream twist the protein molecules out of shape, and make them unusable.

Protein glycation may result in bone loss, high cholesterol, cardiac abnormalities, and a slew of other unpleasantries.

Most copper deficient patients are malnourished and suffer from impaired weight gain. The immune system requires copper to perform several functions. Research showed that interleukin 2 is reduced in copper deficiency and is probably the mechanisms by which T-cell proliferation is reduced.

Copper is also used for the metabolism of essential fatty acids. In people with diabetes excess protein glycation may also be one factor involved in complications such as loss of vision.

A mild copper deficiency impairs the ability of white blood cells to fight infection. If the body does not get a sufficient amount of copper, hemoglobin production decreases and copper deficiency anemia can result.

The most frequent symptoms of copper deficiency are hypopigmentation, increased incidence of infections, and abnormalities of glucose and cholesterol metabolism, electrocardiograms, inefficient utilization of iron and protein and stunted growth.

In babies, the development of nerve, bone, and lung tissue can be impaired and the structure of these body parts may altered.

Anemia has also been related to copper deficiency at three or four months of age in premature babies and babies of low birth-weight and in young babies receiving prolonged parental alimentation after bowel resection or for other reason.

Since the body does not manufacture copper, it must be taken in through the diet.
Copper Deficiency

Symptoms of manganese deficiency

The total amount of manganese in the adult human is approximately 15 mg. Up to 25% of the total body stores of manganese may be located in the skeleton.

Manganese deficiency is associated with diverse physiological malfunction. Manganese deficiency generally does not developed unless the mineral is deliberately eliminated from the diet.

A deficiency of manganese 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. 

Other problems associated with deficiency include the occurrence of ataxia, loss of equilibrium, cell ultrastructure abnormalities, compromised reproductive function, abnormal glucose tolerance, and impaired lipid metabolism.

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 may be more frequent in infants owing to the low concentration of manganese in human breast milk and varying levels in infant formulae.

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.
Symptoms of manganese deficiency

The effect of magnesium deficiency to human health

Human body loses magnesium from diarrhea, diet and stress. Diarrhea causes much of the magnesium in intestines to be excreted.

Gastric juice contains a fair amount of magnesium and excessive vomiting could result in substantial losses of the mineral in addition to the loss resulting from the failure to retain ingested food.

In 1900, the average American diet provided about 450 mgs of magnesium a day.In 2000, the average diet provided only 200 to 225 mgs per day.

A deficiency of magnesium is responsible for the majority of the ill-health and attendant pain and suffering in the US including heart disease, diabetes, obesity and related diseases.

Magnesium deficiency has been reported in children with protein-calorie malnutrition due to primarily to diarrhea which increases fecal loss of the mineral.

Hypomagnesaemia is associated with chronic alcoholism and with the neuromuscular symptoms of alcoholic withdrawal. It is important to know that magnesium excretion is promoted by drinking too much alcohol or caffeine and by eating high amounts of animal protein or sugar.

When pancreatitis is also present, magnesium replacement therapy becomes an important part of treatment because magnesium (and calcium) in blood may be decreased due to presumably to deposition in areas of adipose tissue.

Magnesium content of adipose tissue has been shown to be markedly increased in humans dying from acute pancreatitis and in animals in whom pancreatitis was induce experimentally.

The classical manifestations of magnesium deficiency are neuromuscular. They may occur at the level of the skeletal muscles, resulting in spasmophilia under all its form, at the level of the myocardium, resulting in various cardiac disturbances and also at the level of the smooth muscles.

Cellular loss of magnesium may be a primarily biochemical mechanism in the etiology of various types of myocardial lesions. Most modern heart disease is caused by magnesium deficiency. The diet of the industrial world is short on magnesium, and this causing an epidemic of heart disease in the modern world.

Heart is a muscle that pumps by constantly contracting and relaxing. Calcium helps heart and other muscle to contract. Magnesium helps them to relax. The researchers found that a magnesium deficiency cause of death from sudden heart attacks in 8 million people in US between 1940 and 1994.
The effect of magnesium deficiency to human health

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

Human Deficiency of Vitamin E

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.
Human Deficiency of Vitamin E

Potassium deficiency symptom

The adult human body contains about 250g of potassium. It is entirely present in the cell, while normal human plasma contains only about 5 milliequivalent of potassium of potassium per liter.

Physical symptoms of potassium deficiency can include muscular cramps and twitching, muscular weakness, even actual muscle damage, reduced or absent reflexes, fatigue, fragile bones, irregular heartbeat and other cardiovascular irregularities, kidney failure, lung failure, and disturbances in conductivity and contractibility of heart muscle.

The skin and muscle tone will be bad. The flesh does not cling firmly to the body’s bony framework. Lines and wrinkles fill the face and neck.

Potassium depletion results in muscular weakness and mental confusion and is reflected in electrocardiographic changes and loss of smooth muscle motility e.g. in the intestine.

Mental symptoms can include nervous disorders of various types, anorexia, insomnia, a slowdown of cognitive processes, and depression.

Death in potassium deficiency may result from cardiac or respiratory failure or from paralytic ileus.

There are certain health situations that can make a person more susceptible to suffering from a deficiency of potassium.

These include alcoholism, health conditions requiring the use of certain types of diuretics, periods of high stress and illnesses or conditions that result in extended periods of diarrhea and vomiting.

Some situations of people own making can contribute to potassium deficiency. These include excessive caffeine intake and a diet made up of mostly processed foods. Millions living in today’s civilization and eating its commercialized, processed foods have a potassium deficiency. C

onsuming excessive amount of salt daily can also attribute to the decrease of potassium in the human body.

Deficiency can occur as a result of vomiting, diarrhea and chronic usage of purgatives. It may also occurs as a result of urine loss in wasting disease and starvation, overdosage with drugs. Prevention is always better than trying to cure illness or repair damage.

Potassium deficiency symptom

Deficiency of vitamin B complex

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.

Deficiency of vitamin B complex