100% vitamins and minerals in one packet.

1. The effects Vitamins and Minerals have on your body
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Soyfoods are a source of high-quality protein. In addition, consumption of soy protein provides health benefits that may help prevent or treat
certain chronic diseases. Currently, a great deal of research is being conducted to investigate possible health benefits of soy.
Childhood obesity continues to increase at alarming rates. One way to reverse this trend is to start early and start right by teaching your child
good nutrition habits that will last a lifetime. Starting right also means offering soyfoods. Soyfoods provide critical vitamins, minerals, fiber and
protein for growing children. Plus, many soyfoods contain fewer calories and fat grams, making weight loss or maintaining a healthy weight
much easier.
Weight Loss & Dietary Fiber Eating more high-fiber foods like fruits, vegetables, whole grains and soyfoods may help with weight loss efforts
when substituted for higher calorie foods. Many soyfoods are filled with fiber; ongoing medical research is showing that fiber provides a feeling of
satiety and fullness in between meals and reduces hunger cravings. Ultimately, this helps prevent unnecessary eating and excessive calories which
can lead to weight gain. Aim for 25 grams of fiber every day. A serving of green sweet soybeans contains 3 grams of fiber.
In addition, many soyfoods contain fewer calories and fat grams, making weight loss even easier.
Weight Loss & Breakfast Losing weight may be a lot easier if breakfast becomes a priority every day, and soyfoods may help with weight
loss efforts when substituted for higher caloric foods. Eating breakfast provides a feeling of fullness, or satiety, which helps curb hunger and
prevents overeating of high-calorie snacks and foods. In addition, research indicates fewer calories may be consumed at the next eating occasion or
meal. Soyfoods are perfect for breakfast, especially when trying to lose weight because they are filled with bone-building and heart-healthy soy
protein, plus they reduce overall calories and fat grams. For example, traditional sausage links contain 160 calories and 14 grams of fat; soy
breakfast links have only 70 calories and 3 grams of fat. Other soy breakfast foods include bagels made with soynuts and soy cereal with vanilla
soymilk.
Fad Diets Being on a low carb or the next fad diet when trying to lose weight should not come at the expense of having a healthy heart. Eating
unlimited amounts of high-protein foods loaded with fat and saturated fat could prove detrimental over time. Soyfoods help promote healthier
eating habits with low carb diets, because many soyfoods are naturally low in fat and saturated fat, while being high in heart-healthy protein. For
example, the average soy veggie burger provides 12 grams of soy protein with only five grams of total fat, one gram of saturated fat and just three
grams of net carbs.
Heart Health and Heart Disease Soyfoods containing soy protein can be allies in the ongoing battle against heart disease, the number one killer
of adult men and women. Over 40 scientific studies have proven the positive effect of soy protein on lowering cholesterol levels, including the
harmful LDL cholesterol, which leads to the decreased risk of heart disease. In fact, the Food & Drug Administration recommends eating
25 grams of soy protein every day as part of a diet low in saturated fat and cholesterol. A serving of soy latte provides seven grams of soy protein,
roasted salted soynuts contain 12 grams and a soy cheeseburger has nine grams of heart-healthy soy protein.
Omega-3's Certain fatty fish, like salmon and tuna, contain heart-healthy omega-3 fatty acids. But certain plant foods, like flaxseed and
soybeans, also contain these fatty acids. Soybeans are one of the best non-fish sources of essential omega-3 fatty acids, which may help
reduce the risk of coronary heart disease. Compared to other beans like pinto beans and navy beans, soybeans have a higher fat content, but
this fat contains these heart-healthy omega-3's.
Blood Pressure & Soy Soy protein may provide positive results for people with high blood pressure. According to a recently published
scientific study, researchers found that both the systolic and diastolic blood pressure were reduced in middle-aged and elderly women who ate at
least 25 grams of soy protein daily. Since supermarkets today are filled with numerous soyfoods, eating 25 grams of soy protein is easy. Start
the day with soy cereal for breakfast (eight grams soy protein). Add BBQ soy chips for lunch (seven grams soy protein). Grab a soy-protein-energy-
bar for an afternoon snack (10 grams soy protein). Total soy protein equals 25 grams.
Menopause While soy protein may or may not help reduce hot flashes for women going through menopause, soy protein has other proven
benefits extending well into post-menopausal years. Research has found that consuming soy protein before, as well as after, menopause may help
protect bones from becoming weak and brittle. And since post-menopausal women face an increased risk for osteoporosis, keeping bones
healthy with soy protein-rich foods is critical. In addition, soy protein may help reduce the risk of heart disease, another major concern after
menopause.
Pregnancy & Omega-3's The link between omega-3 fatty acids and a healthy heart is well established. But there's yet another reason - geared
toward mothers and their daughters - for eating more omega-3's.
A newly released scientific study found that mothers who eat foods rich in omega-3 fatty acids during pregnancy (and while breastfeeding),
may help to significantly reduce their daughters' risk of developing breast cancer later in life. In addition, this study found that including omega-3
rich foods throughout childhood and teenage years may continue to help provide protective benefits against breast cancer. Soybeans contain these
critical omega-3's.
Breast Cancer Including soyfoods during a teenage girl's adolescence years may provide increased protective benefits and reduce the risk of
developing breast cancer later in life. Although there is a lack of evidence that consuming soy as an adult may reduce the risk of breast cancer,
ongoing scientific research is showing that consuming soy protein as a teenager may help reduce breast cancer risk as an adult by nearly 50
percent. These impressive results were obtained by eating just 11 grams of soy protein daily. Eleven grams of soy protein is found in one serving
of honey roasted soynuts or two servings of barbecued soy chips.
In addition to reducing risk of breast cancer, soy protein-rich foods may promote a healthy heart and strong bones.
Cancer & Soy Isoflavones Medical research has determined that foods rich in fiber, low in fat and high in phytochemicals may help reduce your
risk of developing certain cancers. Consuming soyfoods may prove beneficial when eating to reduce cancer risk because many soyfoods are not only
high in fiber, they are low in total fat and high in soy protein and phytochemicals called isoflavones.
Isoflavones are naturally-occurring plant compounds that have been attributed in numerous medical and scientific studies to reducing risk of colon,
breast and prostate cancer.

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Prostate and Colon Cancer Some of the same foods that can lower risk of heart disease, like soyfoods, may also reduce the risk of the second
most common cancer in men. Medical research has shown that foods rich in soy protein may be protective against prostate cancer by helping
to promote healthier prostate tissues. And although a specific level of soy protein hasn't been recommended yet for reducing prostate cancer risk,
adding one soyfood every day could be beneficial. Plus soyfoods will provide heart-healthy and bone-building benefits at the same time.
Colon Cancer The latest medical research has found that several natural components of soy may help protect against colon cancer, which is the
second leading cause of cancer death in the United States. The components of soy that may be helping prevent colon cancer are called
isoflavones and saponins. Both are found in soyfoods such as soymilk, soynuts, and green and yellow soybeans.
Many soyfoods are not only good sources of these isoflavones and saponins, but they are high in fiber, and fiber-rich foods have also been
associated with lower cancer risk. Limiting high fat foods may also help reduce risk of developing colon cancer. Substituting soy veggie burgers or
tofu for higher fat protein foods will help cut fat considerably.
Diabetes Several benefits of soy protein exist for the management of diabetes and provide support for the importance of adding soyfoods to a
diabetic diet.
First, many soyfoods have a lower glycemic index. Foods with a low glycemic index help keep blood sugar levels more stable, making diabetes
much easier to control. Soyfoods like canned yellow soybeans and frozen green sweet soybeans have a lower glylcemic index than other soyfoods.
Secondly, many soyfoods are high in dietary fiber, and fiber also helps stabilize blood sugar levels. Everyone - including people with diabetes -
should aim for at least 25 grams of fiber daily. Roasted soynuts contain six grams of fiber and a soy veggie burger has four grams.
Plus, soyfoods can provide additional benefits for controlling one of the most prevalent complications of diabetes - heart disease.
Beta-sitosterol
β-sitosterol is one of several phytosterols with chemical structures similar to that of cholesterol. It is white in colour and waxy in nature.
It is widely distributed in the plant kingdom and found in pecans, Serenoa repens (saw palmetto), avocados, Curcurbita pepo (pumpkin seed),
Pygeum africanum, cashew fruit, rice bran, wheat germ, corn oils, soybeans, sea-buckthorn and wolfberries.
Alone and in combination with similar phytosterols, β-sitosterol reduces blood levels of cholesterol, and is sometimes used in treating
hypercholesterolemia. One small study shows a positive effect on male hair loss in combination with Saw palmetto. In Europe iβ-sitosterol plays a
major role in treatment of herbal therapy of benign prostatic hypertrophy (BPH).
It is also used in Europe for the treatment of prostatic carcinoma and breast cancer although the benefits are still being evaluated in the United
States.
From Wikipedia, the free encyclopedia –
Carotene is responsible for the orange colour of the carrots and many other fruits and vegetables. Carotene is an orange photosynthetic pigment
important for photosynthesis. It is responsible for the orange colour of the carrot and many other fruits and vegetables. It contributes to
photosynthesis by transmitting the light energy it absorbs to chlorophyll. Chemically, carotene is a terpene, synthesized biochemically from eight
isoprene units. It comes in two primary forms designated by characters from the Greek alphabet: alpha-carotene (α-carotene) and beta-carotene
(β-carotene). As hydrocarbons, carotenes are fat-soluble and insoluble in water. Beta-carotene is composed of two retinyl groups, and is broken
down in the mucosa of the small intestine by beta-carotene dioxygenase to retinal, a form of vitamin A. Carotene can be stored in the liver and
converted to vitamin A as needed, thus making it a provitamin.
Vitamin A, a bi-polar molecule formed with bi-polar covalent bonds between carbon and hydrogen, is linked to a family of similarly shaped
molecules, the retinoids, which complete the remainder of the vitamin sequence. Its important part is the retinyl group, which can be found in
several forms. In foods of animal origin, the major form of vitamin A is an ester, primarily retinyl palmitate, which is converted to an alcohol (retinol)
in the small intestine. Vitamin A can also exist as an aldehyde (retinal), or as an acid (retinoic acid). Precursors to the vitamin (provitamins) are
present in foods of plant origin as some of the members of the carotenoid family of compounds.
Deficiency in Vitamin A is estimated to affect millions of children around the world. Approximately 250,000-500,000 children in developing
countries become blind each year owing to vitamin A deficiency, with the highest prevalence in Southeast Asia and Africa.[17]
According to the
World Health Organization (WHO), vitamin A deficiency is under control in the United States, but in developing countries vitamin A deficiency is a
significant concern. With the high prevalence of vitamin A deficiency, the WHO has implemented several initiatives for supplementation of vitamin A
in developing countries. Some of these strategies include intake of vitamin A through a combination of breast feeding, dietary intake, food
fortification, and supplementation. Through the efforts of WHO and its partners, an estimated 1.25 million deaths since 1998 in 40 countries due to
vitamin A deficiency have been averted. Vitamin A deficiency can occur as either a primary or secondary deficiency. A primary vitamin A deficiency
occurs among children and adults who do not consume an adequate intake of yellow and green vegetables, fruits and liver. Early weaning
can also increase the risk of vitamin A deficiency. Secondary vitamin A deficiency is associated with chronic malabsorption of lipids, impaired bile
production and release, low fat diets, and chronic exposure to oxidants, such as cigarette smoke. Vitamin A is a fat soluble vitamin and depends on
micellar solubilization for dispersion into the small intestine, which results in poor utilization of vitamin A from low-fat diets. Zinc deficiency can
also impair absorption, transport, and metabolism of vitamin A because it is essential for the synthesis of the vitamin A transport proteins and
the oxidation of retinol to retinal. In malnourished populations, common low intakes of vitamin A and zinc increase the risk of vitamin A deficiency
and lead to several physiological events.[13]
A study in Burkina Faso showed major reduction of malaria morbidity with combined vitamin A and
zinc supplementation in young children.
Since the unique function of retinyl group is the light absorption in Retinylidene protein, one of the earliest and specific manifestations of vitamin A
deficiency is impaired vision, particularly in reduced light - Night blindness. Persistent deficiency gives rise to a series of changes, the most
devastating of which occur in the eyes. Some other ocular changes are referred to as xerophthalmia. First there is dryness of the conjunctiva
(xerosis) as the normal lacrimal and mucus secreting epithelium is replaced by a keratinized epithelium. This is followed by the build-up of keratin
debris in small opaque plaques (Bitot's spots) and, eventually, erosion of the roughened corneal surface with softening and destruction of the
cornea (keratomalacia) and total blindness.[20]
Other changes include impaired immunity, hypokeratosis (white lumps at hair follicles)

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, keratosis pilaris and squamous metaplasia of the epithelium lining the upper respiratory passages and urinary bladder to a keratinized epithelium.
With relations to dentistry, a deficiency in Vitamin A leads to enamel hypoplasia.
Adequate supply of Vitamin A is especially important for pregnant and breastfeeding women, since deficiencies cannot be compensated
by postnatal supplementation.
Thiamin, also known as vitamin B1 and aneurine hydrochloride, is the term for a family of molecules sharing a common structural feature
responsible for its activity as a vitamin. It is one of the B vitamins. Its most common form is a colorless chemical compound with a chemical formula
C12H17N4OS. This form of thiamin is soluble in water. Another form of thiamin known as TTFD has different solubility properties and belongs to a
family of molecules often referred to as fat-soluble thiamins. Thiamin decomposes if heated. Its chemical structure contains a pyrimidine ring and a
thiazole ring. Thiamin is one of only four nutrients associated with a pandemic human deficiency disease. It is essential for neural function and
carbohydrate metabolism.
Thiamin deficiency results in beriberi, a disease characterized by a bewildering variety of symptoms. Common symptoms often involve the
nervous system and the heart. In less severe deficiency, nonspecific signs include malaise, weight loss, irritability and confusion.[1]
Thiamin deficiency can lead to myriad problems including neurodegeneration, wasting and death. A lack of thiamin can be caused by malnutrition,
alcoholism, a diet high in thiaminase-rich foods (raw freshwater fish, raw shellfish, ferns) and/or foods high in anti-thiamin factors (tea, coffee, betel
nuts).[10]
Well-known syndromes caused by thiamin deficiency include Wernicke-Korsakoff syndrome and beriberi, diseases also common with chronic
alcoholism.
There is only one book in English devoted entirely to the clinical use of vitamin B1. It was written by Derrick Lonsdale. According to the author,
early signs of thiamin deficiency include anorexia, insomnia, sleep apnea, dementia, depression, impotence, and infertility. Extensive
published research reviewed in the book provides statistically significant data supporting this position.
An important property of thiamin that distinguishes it from the other three vitamins associated with vitamin deficiency (vitamin C, vitamin B3, and
vitamin D) is that it is extracted from food in the digestive tract in a form that requires specialized proteins for absorption into the
bloodstream. Once in the bloodstream, this form of thiamin requires specialized proteins for distribution to cells throughout the body.
Because thiamin requires specialized transport proteins, malfunctions of these proteins can cause localized deficiency even when the diet contains
more than twice the recommended daily allowance. Symptoms of PEM include a profuse, but transient diarrhea, listlessness, circling
movements, star gazing or opisthotonus (head drawn back over neck), and muscle tremors.[11]
It is thought that many people with diabetes have a deficiency of thiamin and that this may be linked to some of the complications that can
occur.[12][13]
Riboflavin (E101), also known as vitamin B2, is an easily absorbed micronutrient with a key role in maintaining health in humans and animals. It
is the central component of the cofactors FAD and FMN, and is therefore required by all flavoproteins. As such, vitamin B2 is required for a wide
variety of cellular processes. Like the other B vitamins, it plays a key role in energy metabolism, and is required for the metabolism of fats,
ketone bodies, carbohydrates, and proteins.
Legumes such as mature soybeans, are good sources of vitamin B2, but exposure to light destroys riboflavin.
Riboflavin deficiency
Riboflavin is continuously excreted in the urine of healthy individuals[1]
, making deficiency relatively common when dietary intake is insufficient.
However, riboflavin deficiency is always accompanied by deficiency of other vitamins[1]
.
A deficiency of riboflavin can be primary - poor vitamin sources in one's daily diet - or secondary, which may be a result of conditions that affect
absorption in the intestine, the body not being able to use the vitamin, or an increase in the excretion of the vitamin from the body.
In humans, signs and symptoms of riboflavin deficiency (ariboflavinosis) include cracked and red lips, inflammation of the lining of mouth and
tongue, mouth ulcers, cracks at the corners of the mouth (angular cheilitis), and a sore throat. A deficiency may also cause dry and scaling
skin, fluid in the mucous membranes, and iron-deficiency anemia. The eyes may also become bloodshot, itchy, watery and sensitive to
bright light.
Riboflavin deficiency is classically associated with the oral-ocular-genital syndrome. Angular cheilitis, photophobia, and scrotal dermatitis are the
classic remembered signs. In animals, riboflavin deficiency results in lack of growth, 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 mucus membrane of the gastrointestinal tract. Post-mortem studies
in rhesus monkeys fed a riboflavin-deficient diet revealed that about one-third the normal amount of riboflavin was present in the liver, which is the
main storage organ for riboflavin in mammals. These overt clinical signs of riboflavin deficiency are rarely seen among inhabitants of the developed
countries. However, about 28 million Americans exhibit a common ‘sub-clinical’ stage, characterized by a change in biochemical indices (e.g.
reduced plasma erythrocyte glutathione reductase levels). Although the effects of long-term sub-clinical riboflavin deficiency are unknown, in
children this deficiency results in reduced growth. Subclinical riboflavin deficiency has also been observed in women taking oral
contraceptives, in the elderly, in people with eating disorders, and in disease states such as HIV, inflammatory bowel disease,
diabetes and chronic heart disease. The fact that riboflavin deficiency does not immediately lead to gross clinical manifestations indicates that
the systemic levels of this essential vitamin are tightly regulated.
Niacin, also known as vitamin B3, is a water-soluble vitamin which prevents the deficiency disease pellagra. It is an organic compound. It is a
derivative of pyridine, with a carboxyl group (COOH) at the 3-position. Other forms of vitamin B3 include the corresponding amide, nicotinamide
("niacinamide"), where the carboxyl group has been replaced by an amide group (CONH2), as well as more complex amides and a variety of esters.
The terms niacin, nicotinamide, and vitamin B3 are often used interchangeably to refer to any one of this family of molecules, since they have a
common biochemical activity.
Niacin is converted to nicotinamide and then to NAD and NADP in vivo. Although the two are identical in their vitamin activity, nicotinamide does not
have the same pharmacological effects of niacin, which occur as side-effects of niacin's conversion. Thus nicotinamide does not reduce
cholesterol or cause flushing,[1]
although nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults. Niacin is a precursor to
NADH, NAD, NAD+
, NADP and NADPH, which play essential metabolic roles in living cells.[3]
DNA repair, and the production of steroid hormones in
the adrenal gland. Niacin is one of five vitamins associated with a pandemic deficiency disease: these are niacin (pellagra), vitamin C (scurvy),
thiamin (beriberi), vitamin D (rickets), and vitamin A (no common name, but one of the most common symptomatic deficiences worldwide).

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Pantothenic acid, also called vitamin B5 (a B vitamin), is a water-soluble vitamin required to sustain life (essential nutrient). Pantothenic acid is
needed to form coenzyme-A (CoA), and is critical in the metabolism and synthesis of carbohydrates, proteins, and fats. In chemical structure, it is
the amide between D-pantoate and beta-alanine. Its name is derived from the Greek pantothen (παντόθεν) meaning "from everywhere" and small
quantities of pantothenic acid are found in nearly every food, with high amounts in whole-grain cereals, legumes, eggs, meat, and royal jelly. It is
commonly found as its alcohol analog, the provitamin panthenol, and as calcium pantothenate.
Pantothenic acid deficiency is exceptionally rare and has not been thoroughly studied. In the few cases where deficiency has been seen (victims
of starvation and limited volunteer trials), nearly all symptoms can be reversed with the return of pantothenic acid.
Symptoms of deficiency are similar to other vitamin B deficiencies. Most are minor, including fatigue, allergies, nausea, and abdominal pain.
In a few rare circumstances more serious (but reversible) conditions have been seen, such as adrenal insufficiency and hepatic encephalopathy.
It has been noted that painful burning sensations of the feet were reported in tests conducted on volunteers. Deficiency of pantothenic acid may
explain similar sensations reported in malnourished prisoners of war.
Deficiency symptoms in other non-ruminant animals include disorders of the nervous, gastrointestinal, and immune systems, reduced
growth rate, decreased food intake, skin lesions and changes in hair coat, alterations in lipid and carbohydrate metabolism.[11]
Vitamin B6 is a water-soluble vitamin. Pyridoxal phosphate (PLP) is the active form and is a cofactor in many reactions of amino acid metabolism,
including transamination, deamination, and decarboxylation. PLP also is necessary for the enzymatic reaction governing the release of glucose from
glycogen.
Deficiencies
The classic clinical syndrome for B6 deficiency is a seborrheic dermatitis-like eruption, atrophic glossitis with ulceration, angular
cheilitis, conjunctivitis, intertrigo, and neurologic symptoms of somnolence, confusion, and neuropathy. Pyroluria is one cause of
vitamin B6 deficiency.
While severe vitamin B6 deficiency results in dermatologic and neurologic changes, less severe cases present with metabolic lesions associated
with insufficient acitivities of the coenzyme pyridoxal phosphate. The most prominent of the lesions is due to impaired tryptophan-niacin conversion.
This can be detected based on urinary excretion of xanthurenic acid after an oral tryptophan load. Vitamin B6 deficiency can also result from
impaired transsulfuration of methionine to cysteine. The pyridoxal phosphate-dependent transaminases and glycogen phosphorylase provide the
vitamin with its role in gluconeogenesis, so deprivation of vitamin B6 results in impaired glucose tolerance.
A deficiency of vitamin B6 alone is relatively uncommon and often occurs in association with other vitamins of the B complex. The elderly and
alcoholics have an increased risk of vitamin B6 deficiency, as well as other micronutrient deficiencies.
Vitamin B-12 is a vitamin, one of eight B vitamins which is important for the normal functioning of the brain and nervous system, and for the
formation of blood. It is normally involved in the metabolism of every cell of the body, especially affecting DNA synthesis and regulation, but
also fatty acid synthesis and energy production.
Vitamin B-12 is the name for a class of chemically-related compounds, all of which have vitamin activity. It is structurally the most complicated
vitamin. Biosynthesis of the basic structure of the vitamin can only be accomplished by bacteria, but conversion between different forms of the
vitamin can be accomplished in the human body. A common synthetic form of the vitamin, cyanocobalamin, does not occur in nature, but is used in
many pharmaceuticals, supplements and as food additive, due to its stability and lower cost. In the body it is converted to the physiological forms,
methylcobalamin and adenosylcobalamin, leaving behind the toxic cyanid, albeit in minimal concentration. More recently methylcobalamin and
adenosylcobalamin can also be found in high quality supplements.
Historically, vitamin B-12 was discovered from its relationship to the disease pernicious anemia, which was eventually discovered to result from an
effective lack of this vitamin due to problems with the mechanisms in the body which normally absorb it. Many other subtler kinds of vitamin B12
deficiency, and their biochemical effects, have since been elucidated.
Vitamin B-12 deficiency can potentially cause severe and irreversible damage, especially to the brain and nervous system. At levels only
slightly lower than normal, a range of symptoms such as fatigue, depression, and poor memory may be experienced. However, these
symptoms by themselves are too nonspecific to diagnose deficiency of the vitamin. Vitamin B-12 deficiency can also cause symptoms of mania and
psychosis.
Vitamin B-12 deficiency has the following pathomorphology and symptoms:
Pathomorphology includes: A spongiform state of neural tissue along with edema of fibers and deficiency of tissue. The myelin decays, along with
axial fiber. In later phases, fibric sclerosis of nervous tissues occurs. Those changes apply to dorsal parts of the spinal cord, and to pyramidal tracts
in lateral cords.
In the brain itself, changes are less severe: they occur as small sources of nervous fibers decay and accumulation of astrocytes, usually
subcortically located, an also round hemorrhages with a torus of glial cells. Pathological changes can be noticed as well in the posterior roots of
the cord and, to lesser extent, in peripheral nerves.
Clinical symptoms : The main syndrome of vitamin B-12 deficiency is Biermer's disease (pernicious anemia). It is characterized by a triad of
symptoms: Anemia with bone marrow promegaloblastosis (megaloblastic anemia)
Gastrointestinal symptoms, Neurological symptoms.
Each of those symptoms can occur either alone or along with others. The neurological complex, defined as myelosis funicularis, consists of the
following symptoms:
Impaired perception of deep touch, pressure and vibration, abolishment of sense of touch, very annoying and persistent paresthesias. Ataxia of
dorsal cord type Decrease or abolishment of deep muscle-tendon reflexes; Pathological reflexes - Babinski, Rossolimo and others, also severe
paresis.
During the course of disease, mental disorders can occur which include: irritability, focus/concentration problems, depressive state with
suicidal tendencies, paraphrenia complex. These symptoms may not reverse after correction of hematological abnormalities, and the chance of
complete reversal decreases with the length of time the neurological symptoms have been present.
Vitamin C is an essential nutrient for a large number of higher primate species. The presence of ascorbate is required for a range of essential
metabolic reactions in all animals and plants. It is made internally by almost all organisms, humans being the most well-known exception. It is
widely known as the vitamin whose deficiency causes scurvy in humans. The pharmacophore of vitamin C is the ascorbate ion. In living organisms,
ascorbate is an antioxidant, since it protects the body against oxidative stress,[5]
and is a cofactor in several vital enzymatic reactions.[6]
The uses and the daily requirement amounts of vitamin C are matters of on-going debate. People consuming diets rich in ascorbate from natural
foods, such as fruits and vegetables, are healthier and have lower mortality from a number of chronic illnesses. However, a recent meta-analysis of
68 reliable antioxidant supplementation experiments involving a total of 232,606 individuals concluded that consuming additional ascorbate from
supplements may not be as beneficial as thought.
Deficiency

5. The effects Vitamins and Minerals have on your body
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Scurvy is an avitaminosis resulting from lack of vitamin C, since without this vitamin, the synthesised collagen is too unstable to perform its function.
Scurvy leads to the formation of liver spots on the skin, spongy gums, and bleeding from all mucous membranes. The spots are most
abundant on the thighs and legs, and a person with the ailment looks pale, feels depressed, and is partially immobilized. In advanced scurvy there
are open, suppurating wounds and loss of teeth and, eventually, death. The human body can store only a certain amount of vitamin C, and so the
body soon depletes itself if fresh supplies are not consumed.
It has been shown that smokers who have diets poor in vitamin C are at a higher risk of lung-borne diseases than those smokers who have higher
concentrations of Vitamin C in the blood.
Cholecalciferol is called vitamin D3. It is structurally similar to steroids such as testosterone, cholesterol, and cortisol (though vitamin D3 itself is
a secosteroid).
Vitamin D is a group of fat-soluble prohormones, the two major forms of which are vitamin D2 (or ergocalciferol) and vitamin D3 (or
cholecalciferol).[1]
The term vitamin D also refers to metabolites and other analogues of these substances. Vitamin D3 is produced in skin exposed to
sunlight, specifically ultraviolet B radiation.
Vitamin D plays an important role in the maintenance of organ systems. Vitamin D regulates the calcium and phosphorus levels in the blood by
promoting their absorption from food in the intestines, and by promoting re-absorption of calcium in the kidneys, which enables normal
mineralization of bone and prevents hypocalcemic tetany. It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts.
Absent vitamin K or with drugs (particularly blood thinners) which interfere with Vitamin K metabolism, Vitamin D can promote soft tissue
calcification.
It inhibits parathyroid hormone secretion from the parathyroid gland. Vitamin D affects the immune system by promoting phagocytosis, anti-
tumor activity, and immunomodulatory functions.
Vitamin D deficiency can result from inadequate intake coupled with inadequate sunlight exposure, disorders that limit its absorption, conditions
that impair conversion of vitamin D into active metabolites, such as liver or kidney disorders, or, rarely, by a number of hereditary disorders.
Deficiency results in impaired bone mineralization, and leads to bone softening diseases, rickets in children and osteomalacia in adults, and
possibly contributes to osteoporosis. Vitamin D regulates the expression of genes associated with cancers and autoimmune disease by
controlling the activation of the vitamin D receptor (VDR), a type 1 nuclear receptor and DNA transcription factor. Research has indicated that
vitamin D deficiency is linked to colon cancer and more recently, to breast cancer. Conflicting evidence links vitamin D deficiency to other
forms of cancer.
Vitamin E is the collective name for a set of 8 related tocopherols and tocotrienols, which are fat-soluble vitamins with antioxidant properties. Of
these, α-tocopherol (also written as alpha-tocopherol) has been most studied as it has the highest bioavailability, with the body preferentially
absorbing and using this form. It has been claimed that α-tocopherol is the most important lipid-soluble antioxidant, and that it protects cell
membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction. This would remove the free radical
intermediates and prevent the oxidation reaction from continuing. The oxidised α-tocopheroxyl radicals produced in this process may be recycled
back to the active reduced form through reduction by other antioxidants, such as ascorbate, retinol or ubiquinol. The functions of the other forms of
vitamin E are less well-studied, although γ-tocopherol is a nucleophile that may react with electrophilic mutagens, and tocotrienols may have a
specialized role in protecting neurons from damage. Most studies about Vitamin E have supplemented only alpha-tocopherol, but doing so leads to
reduced serum gamma- and delta-tocopherol concentrations.
Biotin, also known as vitamin H or B7, is a water-soluble B-complex vitamin which is composed of an ureido (tetrahydroimidizalone) ring fused
with a tetrahydrothiophene ring. A valeric acid substituent is attached to one of the carbon atoms of the tetrahydrothiophene ring. Biotin is a
cofactor in the metabolism of fatty acids and leucine, and in gluconeogenesis.
Biotin is necessary for cell growth, the production of fatty acids, and the metabolism of fats and amino acids. It plays a role in the Citric acid
cycle, which is the process by which biochemical energy is generated during aerobic respiration. Biotin not only assists in various metabolic
reactions, but also helps to transfer carbon dioxide. Biotin is also helpful in maintaining a steady blood sugar level. Biotin is often
recommended for strengthening hair and nails. Consequently, it is found in many cosmetic and health products for the hair and skin.
Biotin deficiency is relatively rare and mild, and can be addressed with supplementation. Such deficiency can be caused by the excessive
consumption of raw egg whites, which contain high levels of the protein avidin, which binds biotin strongly. Avidin is deactivated by cooking, while
the biotin remains intact.
Biotinidase deficiency is not due to inadequate biotin, but rather to a deficiency in the enzymes which process it. Signs of Biotin Deficiency: In
general, appetite and growth are decreased. Dermatologic symptoms include dermatitis, alopecia, and achromotrichia (absence or loss of
pigment in the hair). Perosis (a shortening and thickening of bones) is seen in the skeleton. FLKS (fatty liver and kidney syndrome) and hepatic
steatosis also can occur.
Folic acid (also known as Vitamin M and Folacin) and Folate (the anionic form) are forms of the water-soluble Vitamin B9. These occur naturally
in food and can also be taken as supplements. Folate is necessary for the production and maintenance of new cells.This is especially important
during periods of rapid cell division and growth such as infancy and pregnancy. Folate is needed to synthesize DNA bases (most notably
thymine, but also purine bases) needed for DNA replication. Thus folate deficiency hinders DNA synthesis and cell division, affecting most notably
bone marrow and cancer, both of which participate in rapid cell division. RNA transcription, and subsequent protein synthesis, are less affected by
folate deficiency as the mRNA can be recycled and used again (as opposed to DNA synthesis where a new genomic copy must be created). Since
folate deficiency limits cell division, erythropoiesis, production of red blood cells (RBCs) is hindered and leads to megaloblastic anemia which is
characterized by large immature RBCs. This pathology results from persistently thwarted attempts at normal DNA replication, DNA repair, and cell
division and produces abnormally large cells (megaloblasts) with abundant cytoplasm capable of RNA and protein synthesis but with clumping and
fragmentation of nuclear chromatin. Some of these large cells, although immature, are released early from the marrow in an attempt to compensate
for the anemia caused by lack of RBCs. Both adults and children need folate to make normal RBCs and prevent anemia. Deficiency of folate in
pregnant women has been implicated in neural tube defects and so many cereals sold in developed countries are enriched with folate to avoid such
complications.
The pathway leading to the formation of tetrahydrofolate (FH4) begins when folate (F) is reduced to dihydrofolate (DHF) (FH2), which is then
reduced to THF. Dihydrofolate reductase catalyses the last step.[4]
Vitamin B3 in the form of NADPH is a necessary cofactor for both steps of the
synthesis.
Methylene-THF (CH2FH4) is formed from THF by the addition of methylene groups from one of three carbon donors: formaldehyde, serine, or
glycine. Methyl tetrahydrofolate (CH3-THF) can be made from methylene-THF by reduction of the methylene group with NADPH. It is important to
note that Vitamin B12 is the only acceptor of methyl-THF. There is also only one acceptor for methyl-B12 which is homocysteine in a reaction
catalyzed by homocysteine methyltransferase. This is important because a defect in homocysteine methyltransferase or a defeciency of B12 can lead

6. The effects Vitamins and Minerals have on your body
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to a methyl-trap of THF and a subsequent deficiency. Thus, a deficiency in B12 can generate a large pool of methyl-THF that is unable to undergo
reactions and will mimic folate deficiency. Another form of THF, formyl-THF or folinic acid) results from oxidation of methylene-THF or is formed
from formate donating formyl group to THF. Finally, histidine can donate a single carbon to THF to form methenyl-THF.
Heart disease
Adequate concentrations of folate, vitamin B12, or vitamin B6 may decrease the circulating level of homocysteine, an amino acid normally found in
blood. There is evidence that an elevated homocysteine level is an independent risk factor for heart disease and stroke. The evidence suggests that
high levels of homocysteine may damage coronary arteries or make it easier for blood clotting cells called platelets to clump together and form a
clot. However, there is currently no evidence available to suggest that lowering homocysteine with vitamins will reduce risk of heart disease. Clinical
intervention trials are needed to determine whether supplementation with folic acid, vitamin B12 or vitamin B6 can lower the risk of developing
coronary heart disease. A 2005 study found that 5 mg. of folate daily over a three-week period reduced pulse pressure by 4.7 mmHg. compared
with a placebo, and concluded that Folic acid is a safe and effective supplement that targets large artery stiffness and may prevent isolated systolic
hypertension.
Also, as a result of new research, "heart experts" at Johns Hopkins Medical Center reported in March 2008 in favour of therapeutic folate, although
they cautioned that it is premature for people to begin to self-medicate by taking high doses of folic acid."
Stroke
Folic acid appears to reduce the risk of stroke. The reviews indicate only that in some individuals the risk of stroke appears to be reduced, but a
definite recommendation regarding supplementation beyond the current recommended daily allowance has not been established for stroke
prevention. Observed stroke reduction is consistent with the reduction in pulse pressure produced by folate supplementation of 5 mg per day, since
hypertension is a key risk factor for stroke.
Cancer
The association between folate and cancer appears to be complex. It has been suggested that folate may help prevent cancer, as it is involved in
the synthesis, repair, and functioning of DNA, and a deficiency of folate may result in damage to DNA that may lead to cancer. Some investigations
have proposed that good levels of folic acid may be related to lower risk of esophageal, stomach and ovarian cancer, but benefices of folic acid
against cancer may depend on when it is taken and on individual conditions. In addition folic acid may not be helpful, and could even be damaging,
in people who already are suffering from cancer or from a precancerous condition. Conversely, it has been suggested that excess folate may
promote tumor initiation. Diets high in folate are associated with decreased risk of colorectal cancer; some studies show an association which is
stronger for folate from foods alone than for folate from foods and supplements, while other studies find that folate from supplements is more
effective due to greater bioavailability. A 2006 prospective study of 81,922 Swedish adults found that diets high in folate from foods, but not from
supplements, were associated with a reduced risk of pancreatic cancer. Most epidemiologic studies suggest that diets high in folate are associated
with decreased risk of breast cancer, but results are not uniformly consistent: one large cancer screening trial reported a potential harmful effect
of high folate intake on breast cancer risk, suggesting that routine folate supplementation should not be recommended as a breast cancer
preventive, but a 2007 Swedish prospective study found that a high folate intake was associated with a lower incidence of postmenopausal breast
cancer. It is very difficult to affirm how each nutrient or nutrient combination affects a person’s risk of cancer. People whose diets are rich in
vegetables and low in animal fat and meat have lower risks for some of the most frequent types of cancer. Taking a variety of healthful foods,
with most of them coming from plant sources, is a better solution than taking vitaminic supplements. So the authorities are not really
sure if this will work for cancer or not, (or the age at which it is safe to start taking folate supplements) but hopefully this will all become clear in the
light of research now underway.
Antifolates
Folate is important for cells and tissues that rapidly divide. Cancer cells divide rapidly, and drugs that interfere with folate metabolism are used to
treat cancer. The antifolate methotrexate is a drug often used to treat cancer because it inhibits the production of the active form of THF from the
inactive dihydrofolate (DHF). Unfortunately, methotrexate can be toxic, producing side effects such as inflammation in the digestive tract that make
it difficult to eat normally.
Folinic acid, under the drug name leucovorin, is a form of folate (formyl-THF) that can help "rescue" or reverse the toxic effects of methotrexate.
Folinic acid is not the same as folic acid. Folic acid supplements have little established role in cancer chemotherapy. There have been cases of
severe adverse effects of accidental substitution of folic acid for folinic acid in patients receiving methotrexate cancer chemotherapy. It is important
for anyone receiving methotrexate to follow medical advice on the use of folic or folinic acid supplements. The supplement of folinic acid in patients
undergoing methotrexate treatment is to give non rapidly dividing cells enough folate to maintain normal cell functions. The amount of folate given
will be depleted by rapidly dividing cells (cancer) very fast and so will not negate the effects of methotrexate. Low dose methotrexate is used to
treat a wide variety of non-cancerous diseases such as rheumatoid arthritis, lupus, scleroderma, psoriasis, asthma, sarcoidoisis,
primary biliary cirrhosis, and inflammatory bowel disease. Low doses of methotrexate can deplete folate stores and cause side effects that
are similar to folate deficiency. Both high folate diets and supplemental folic acid may help reduce the toxic side effects of low dose methotrexate
without decreasing its effectiveness. Anyone taking low dose methotrexate for the health problems listed above should consult with a physician
about the need for a folic acid supplement. While the role in folate as a cancer treatment is well established its long term effectiveness is diminished
by cellular response. In response to decreased THF the cell begins to transcribe more DHF reductase, the enzyme that reduces DHF to THF.
Because methotrexate is a competitive inhibitor of DHF reductase increased concentrations of DHF reductase can overcome the drugs inhibition.
Depression
Some evidence links low levels of folate with depression. There is some limited evidence from randomised controlled trials that using folic acid in
addition to antidepressant medication may have benefits. Researchers at the University of York and Hull York Medical School have confirmed a
link between depression and low levels of folate in a research study involving 15,315. However, the evidence is probably too limited at present for
this to be a routine treatment recommendation.
Memory and mental agility
In a 3-year trial on 818 people over the age of 50, short-term memory, mental agility and verbal fluency were all found to be better among people
who took 800 micrograms of folic acid daily—twice the current RDA—than those who took placebo. The study was reported in The Lancet on 19
January 2007.
Phosphatidylcholine is a class of phospholipids which incorporate choline as a headgroup. They are a major component of biological membranes
and can be isolated from either egg yolk or soy beans from which they are mechanically extracted or chemically extracted using hexane.
Phosphatidylcholines are such a major component of lecithin, that, in some contexts, the terms are sometime used as synonyms. However, lecithin
extract consists of a mixture of phosphatidylcholine and other compounds. It is also used along with Sodium taurocholate for simulating fed- and
fasted-state biorelevant media in dissolution studies of highly-lipophilic drugs. Phosphatidylcholine is a major constituent of cell membranes, and
also plays a role in membrane-mediated cell signalling.

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Phospholipase D catalyzes the hydrolysis of phosphatidylcholine to form phosphatidic acid (PA), releasing the soluble choline headgroup into the
cytosol. Some medical researchers are experimenting with using Phosphatidylcholine in a type of injection that will break down fat cells; to be
used as an alternative to liposuction.
Calcium is a soft grey alkaline earth metal, and is the fifth most abundant element by mass in the Earth's crust. Calcium is also the fifth most
abundant dissolved ion in seawater by both molarity and mass, after sodium, chloride, magnesium, and sulfate.
Calcium is essential for living organisms, particularly in cell physiology, where movement of the calcium ion Ca2+
into and out of the cytoplasm
functions as a signal for many cellular processes. As a major material used in mineralization of bones and shells, calcium is the most abundant metal
by mass in many animals. Calcium is an important component of a healthy diet. Calcium is essential for the normal growth and maintenance of
bones and teeth, and calcium requirements must be met throughout life. Long-term calcium deficiency can lead to rickets and poor blood
clotting and in case of a menopausal woman, it can lead to osteoporosis, in which the bone deteriorates and there is an increased risk of
fractures. While a lifelong deficit can affect bone and tooth formation, over-retention can cause hypercalcemia (elevated levels of calcium in the
blood), impaired kidney function and decreased absorption of other minerals. High calcium intakes or high calcium absorption were previously
thought to contribute to the development of kidney stones. However, more recent studies show that high dietary calcium intakes actually decrease
the risk for kidney stones. Vitamin D is needed to absorb calcium.
Dairy products, such as milk and cheese, are a well-known source of calcium. However, some individuals are allergic to dairy products and even
more people, particularly those of non Indo-European descent, are lactose-intolerant, leaving them unable to consume non-fermented dairy
products in quantities larger than about half a liter per serving. Others, such as vegans, avoid dairy products for ethical and health reasons.
Fortunately, many good sources of calcium exist. These include seaweeds such as kelp, wakame and hijiki; nuts and seeds (like almonds and
sesame); blackstrap molasses; beans; oranges; figs; quinoa; amaranth; collard greens; okra; rutabaga; broccoli; dandelion leaves; kale; and
fortified products such as orange juice and soy milk. (However, calcium fortified orange juice often contains vitamin D3 derived from lanolin, and is
thus unacceptable for vegans.) An overlooked source of calcium is eggshell, which can be ground into a powder and mixed into food or a glass of
water. Cultivated vegetables generally have less calcium than wild plants.
Chromium is a steely-gray, lustrous, hard metal that takes a high polish and has a high melting point. It is also odourless, tasteless, and malleable.
Chromium was named after the Greek word "Chrōma" (χρωµα) meaning color, because of the many colorful compounds made from it.
Trivalent chromium (Cr(III) or Cr3+
) is required in trace amounts for sugar metabolism in humans (Glucose Tolerance Factor) and its deficiency
may cause a disease called chromium deficiency.
Copper is an essential trace nutrient to all high plants and animals. In animals, including humans, it is found primarily in the bloodstream, as a
co-factor in various enzymes and in copper-based pigments. However, in sufficient amounts, copper can be poisonous and even fatal to
organisms.
Copper is essential in all plants and animals. Copper is carried mostly in the bloodstream on a plasma protein called ceruloplasmin. When copper
is first absorbed in the gut it is transported to the liver bound to albumin. Copper is found in a variety of enzymes, including the copper centers of
cytochrome c oxidase and the enzyme superoxide dismutase (containing copper and zinc). In addition to its enzymatic roles, copper is used for
biological electron transport. The blue copper proteins that participate in electron transport include azurin and plastocyanin. The name "blue copper"
comes from their intense blue color arising from a ligand-to-metal charge transfer (LMCT) absorption band. Most molluscs and some arthropods
such as the horseshoe crab use the copper-containing pigment hemocyanin rather than iron-containing hemoglobin for oxygen transport, so their
blood is blue when oxygenated rather than red.
Chronic copper depletion leads to abnormalities in metabolism of fats, high triglycerides, non-alcoholic steatohepatitis (NASH), fatty liver disease
and poor melanin and dopamine synthesis causing depression and sunburn. Food rich in copper should be eaten away from any milk or egg
proteins as they block absorption.
Iodine and its compounds are primarily used in medicine, photography, and dyes. Although it is rare in the solar system and Earth's crust, the
iodides are very soluble in water, and the element is concentrated in seawater. This mechanism helps to explain how the element came to be
required in trace amounts by all animals and some plants, being by far the heaviest element known to be necessary to living organisms.
Human dietary intake Recommended Daily Allowance (RDA) is 150 micrograms per day (µg/day) for both men and women, with a Tolerable Upper
Intake Level (UL) for adults is 1,100 µg/day (1.1 mg/day). The tolerable upper limit was assessed by analyzing the effect of supplementation on
thyroid-stimulating hormone.
Natural sources of iodine include sea life, such as kelp and certain seafood, as well as plants grown on iodine-rich soil. Iodized salt is fortified with
iodine.
As of 2000, the median intake of iodine from food in the United States was 240 to 300 µg/day for men and 190 to 210 µg/day for women. In Japan,
consumption is much higher due to the frequent consumption of seaweed or kombu kelp. Although some Chinese data associates excess iodine with
autoimmune thyroiditis and hypothyroidism, these effects have not been observed in Japanese populations, and a protective effect on breast cancer
has been hypothesized.
Deficiency
In areas where there is little iodine in the diet, typically remote inland areas and semi-arid equatorial climates where no marine foods are eaten,
iodine deficiency gives rise to hypothyroidism, symptoms of which are extreme fatigue, goitre, mental slowing, depression, weight gain,
and low basal body temperatures.
Iodine deficiency is the leading cause of preventable mental retardation, a result which occurs primarily when babies or small children are
rendered hypothyroidic by a lack of the element. The addition of iodine to table salt has largely eliminated this problem in the wealthier nations, but
as of March 2006, iodine deficiency remained a serious public health problem in the developing world. Iodine deficiency is also a problem in certain
areas of Europe. In Germany it has been estimated to cause a billion dollars in healthcare costs per year.
Taking large amounts of regular iodine will saturate the thyroid and prevent uptake. Iodine pills are sometimes distributed to persons living close to
nuclear establishments, for use in case of accidents that could lead to releases of radioactive iodine.
Iron
Good sources of dietary iron include red meat, fish, poultry, lentils, beans, leaf vegetables, tofu, chickpeas, black-eyed peas, fortified bread, and
fortified breakfast cereals. Iron in low amounts is found in molasses, teff and farina. Iron in meat is more easily absorbed than iron in vegetables
(haem iron), but heme/hemoglobin from red meat has effects which may increase the likelihood of colorectal cancer.
Iron provided by dietary supplements is often found as iron (II) fumarate, although iron sulfate is cheaper and is absorbed equally well. Elemental
iron, despite being absorbed to a much smaller extent (stomach acid is sufficient to convert some of it to ferrous iron), is often added to foods such

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as breakfast cereals or "enriched" wheat flour (where it is listed as "reduced iron" in the list of ingredients). Iron is most available to the body when
chelated to amino acids - iron in this form is ten to fifteen times more bioavailable than any other, and is also available for use as a common iron
supplement. Often the amino acid chosen for this purpose is the cheapest and most common amino acid, glycine, leading to "iron glycinate"
supplements. Infants may require iron supplements if they are not breast-fed. Blood donors and pregnant women are at special risk of low iron
levels and are often advised to supplement their iron intake.
Magnesium ions are essential to all living cells, and is the 11th most abundant element by mass in the human body. The free element (metal) is
not found in nature. Once produced from magnesium salts, this alkaline earth metal is now mainly obtained by electrolysis of brine and is used as
an alloying agent to make aluminium-magnesium alloys, sometimes called "magnalium" or "magnelium".
Magnesium ions are essential to the basic nucleic acid chemistry of life, and thus are essential to all cells of all known living organisms. Plants have
an additional use for magnesium in that chlorophylls are magnesium-centered porphyrins. Many enzymes require the presence of magnesium ions
for their catalytic action, especially enzymes utilizing ATP, or those which use other nucleotides to synthesize DNA and RNA. Magnesium deficiency
in plants causes late-season yellowing between leaf veins, especially in older leaves, and can be corrected by applying epsom salts
Magnesium is a vital component of a healthy human diet.
Deficiency is relatively common, with only 32% of the United States meeting the RDA-DRI, and has been implicated in a number of human
diseases. In certain limited situations, magnesium oxide has been reported to be effective in maintenance treatment of the manic phase of bipolar
disease. There are a number of magnesium supplements available. Magnesium oxide, one of the most common, has been reported as the least
bioavailable. Magnesium citrate is more bioavailable than oxide or amino-acid chelate forms.
Excess magnesium in the blood is freely filtered at the kidneys, and for this reason it is difficult to overdose on magnesium from dietary sources
alone. With supplements overdose is possible, however, particularly in people with poor renal function, but severe hypermagnesemia can also occur
without renal dysfunction. Alcoholism can produce a magnesium deficiency which is easily reversed by oral or parenteral administration,
depending on the degree of deficiency. [12]
Manganese is an essential trace nutrient in all forms of life.
The classes of enzymes that have manganese cofactors are very broad and include such classes as oxidoreductases, transferases, hydrolases,
lyases, isomerases, ligases, lectins, and integrins. The reverse transcriptases of many retroviruses (though not lentiviruses such as HIV) contain
manganese. The best known manganese-containing polypeptides may be arginase, the diphtheria toxin, and Mn-containing superoxide dismutase
(Mn-SOD).
Mn-SOD is the type of SOD present in eukaryotic mitochondria, and also in most bacteria (this fact is in keeping with the bacterial-origin theory of
mitochondria). The Mn-SOD enzyme is probably one of the most ancient, for nearly all organisms living in the presence of oxygen use it to deal with
the toxic effects of superoxide, formed from the 1-electron reduction of dioxygen. Exceptions include a few kinds of bacteria such as Lactobacillus
plantarum and related lactobacilli, which use a different non-enzymatic mechanism, involving manganese (Mn2+
) ions complexed with polyphosphate
directly for this task, indicating how this function possibly evolved in aerobic life.
The human body contains about 10 mg of manganese, which is stored mainly in liver and kidneys.
Manganese is also important in photosynthetic oxygen evolution in chloroplasts in plants, which are also evolutionarily of bacterial origin.
Molybdenum has the sixth-highest melting point of any element, and for this reason it is often used in high-strength steel alloys. Molybdenum is
found in trace amounts in plants and animals, although excess molybdenum can be toxic in some animals. Molybdenum was discovered in 1778 by
Carl Wilhelm Scheele and first isolated in 1781 by Peter Jacob Hjelm.
The most important use of the molybdenum atom in living organisms is as a metal hetero-atom at the active site in certain enzymes. In nitrogen
fixation in certain bacteria, the nitrogenase enzyme which is involved in the terminal step of reducing molecular nitrogen, usually contains
molybdenum in the active site (though replacement of Mo with iron or vanadium is known). In March 2008, researchers reported that they had
found strong evidence for the hypothesis that a scarcity of molybdenum in the earth's early oceans was a limiting factor in the further evolution of
eukaryotic life (which includes all plants and animals) as eukaryotes cannot fix nitrogen and must acquire it from prokaryotic bacteria. The scarcity
of molybdenum resulted from the relative lack of oxygen in the early ocean. Oxygen dissolved in seawater is the primary mechanism for dissolving
molybdenum from minerals on the sea bottom.
Though molybdenum forms compounds with various organic molecules, including carbohydrates and amino acids, it is transported throughout the
human body as MoO4
2-
. Molybdenum is present in approximately 20 enzymes in animals, including aldehyde oxidase, sulfite oxidase, xanthine
oxidase. In some animals, the oxidation of xanthine to uric acid, a process of purine catabolism, is catalyzed by xanthine oxidase, a molybdenum-
containing enzyme. The activity of xanthine oxidase is directly proportional to the amount of molybdenum in the body. However, an extremely high
concentration of molybdenum reverses the trend, and can act as an inhibitor in both purine catabolism and other processes. Molybdenum
concentrations also affect protein synthesis, metabolism, and growth. These enzymes in plants and animals catalyse the reaction of oxygen in
small molecules, as part of the regulation of nitrogen-, sulfur- and carbon cycles.
In a 70 kg (150 lb) human body, there is approximately 9.3 mg molybdenum, comprising .00001% of the total body mass. It occurs in higher
concentrations in the liver and kidneys, and in lower concentrations in the vertebrae. Molybdenum is also present within human tooth enamel and
may help prevent the decaying thereof. Pork, lamb, and beef liver each have approximately 1.5 parts molybdenum per million. Other significant
dietary sources include green beans, eggs, sunflower seeds, wheat flour, lentils, and cereal grain.
Molybdenum deficiency is not usually seen in healthy people. Sodium tungstate is a competitive inhibitor of molybdenum. Dietary tungsten reduces
the concentration of molybdenum in tissues.
Phosphorus is an essential element for all living cells. Inorganic phosphorus in the form of the phosphate PO4
3-
plays a major role in biological
molecules such as DNA and RNA where it forms part of the structural framework of these molecules. Living cells also use phosphate to transport
cellular energy via adenosine triphosphate (ATP). Nearly every cellular process that uses energy obtains it in the form of ATP. ATP is also important
for phosphorylation, a key regulatory event in cells. Phospholipids are the main structural components of all cellular membranes. Calcium phosphate
salts assist in stiffening bones.
An average adult human contains a little less than 1 kg of phosphorus, about 85% of which is present in bones and teeth in the form of apatite, and
the remainder inside cells in soft tissues. A well-fed adult in the industrialized world consumes and excretes about 1-3 g of phosphorus per day in
the form of phosphate. Only about 0.1% of body phosphate circulates in the blood, but this amount reflects the amount of phosphate available to
soft tissue cells.
In medicine, low phosphate syndromes are caused by malnutrition, by failure to absorb phosphate, and by metabolic syndromes which draw
phosphate from the blood or pass too much of it into the urine. All are characterized by hypophosphatemia. Symptoms of low phosphate include
muscle and neurological dysfunction, and disruption of muscle and blood cells due to lack of ATP.

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Potassium cations are important in neuron (brain and nerve) function, and in influencing osmotic balance between cells and the interstitial fluid.
Potassium may be detected by taste because it triggers three of the five types of taste sensations, according to concentration. Dilute solutions of
potassium ion taste sweet (allowing moderate concentrations in milk and juices), while higher concentrations become increasingly bitter/alkaline,
and finally also salty to the taste. The combined bitterness and saltiness of high potassium content solutions makes high-dose potassium
supplementation by liquid drinks a palatability challenge.
Potassium is also important in allowing muscle contraction and the sending of all nerve impulses in animals through action potentials. By
nature of their electrostatic and chemical properties, K+
ions are larger than Na+
ions, and ion channels and pumps in cell membranes can
distinguish between the two types of ions, actively pumping or passively allowing one of the two ions to pass, while blocking the other.
A shortage of potassium in body fluids may cause a potentially fatal condition known as hypokalemia, typically resulting from diarrhea, increased
diuresis and vomiting. Deficiency symptoms include muscle weakness, paralytic ileus, ECG abnormalities, decreased reflex response and
in severe cases respiratory paralysis, alkalosis and cardiac arrhythmia.
Potassium is an essential mineral micronutrient in human nutrition; it is the major cation (positive ion) inside animal cells, and it is thus important in
maintaining fluid and electrolyte balance in the body. Sodium makes up most of the cations of blood plasma at about 145 milliequivalents per liter
(3345 milligrams) and potassium makes up most of the cell fluid cations at about 150 milliequivalents per liter (4800 milligrams). Plasma is filtered
through the glomerulus of the kidneys in enormous amounts, about 180 liters per day. All but the 1000-10,000 milligrams of sodium and the 1000-
4000 milligrams of potassium likely to be in the diet must be reabsorbed. Sodium must be reabsorbed in such a way as to keep the blood volume
exactly right and the osmotic pressure correct; potassium must be reabsorbed in such a way as to keep serum concentration as close as possible to
4.8 milliequivalents (about 190 milligrams) per liter. Potassium must sometimes be conserved also, but since the amount of potassium in the blood
plasma is very small and the pool of potassium in the cells is about thirty times as large, the situation is not so critical for potassium. Since
potassium is moved passively in counter flow to sodium in response to an apparent (but not actual) Donnan equilibrium, the urine can never sink
below the concentration of potassium in serum except sometimes by actively excreting water at the end of the processing. At the end of the
processing, potassium is secreted one more time if the serum levels are too high.
The potassium moves passively through pores in the cell wall. When ions move through pumps there is a gate in the pumps on either side of the
cell wall and only one gate can be open at once. As a result 100 ions are forced through per second. Pores have only one gate and there one kind
of ion only can stream through at 10 million to 100 million ions per second. The pores require calcium in order to open although it is thought that
the calcium works in reverse by blocking at least one of the pores.
Potassium in the diet can generally be guaranteed by eating a variety of foods containing potassium and deficiency is rare in healthy individuals
eating a balanced diet. Foods with high sources of potassium include orange juice, potatoes, bananas, avocados, tomatoes, broccoli, soybeans
and apricots, although it is also common in most fruits, vegetables and meats. Diets high in potassium can reduce the risk of hypertension and a
potassium deficiency combined with an inadequate thiamine intake has produced heart disease in rats. If potassium supplements are used, such as
sodium free baking powder and sodium free table salt, inadequate thiamine can cause beriberi.
Individuals suffering from kidney diseases may suffer adverse health effects from consuming large quantities of dietary potassium. Potassium ion is
a nutrient necessary for human life and health. Potassium chloride is used as a substitute for table salt by those seeking to reduce sodium intake so
as to control hypertension. Good dietary sources of potassium include celery juice. The USDA lists tomato paste, orange juice, beet greens, white
beans, bananas, and many other good dietary sources of potassium, ranked according to potassium content per measure shown.
Selenium is an essential micronutrient for animals. In plants, it occurs as a bystander mineral, sometimes in toxic proportions in forage (some
plants may accumulate selenium as a defense against being eaten by animals, but other plants such as locoweed require selenium, and their growth
indicates the presence of selenium in soil). It is a component of the unusual amino acids selenocysteine and selenomethionine. In humans, selenium
is a trace element nutrient which functions as cofactor for reduction of antioxidant enzymes such as glutathione peroxidases and certain forms of
thioredoxin reductase found in animals and some plants (this enzyme occurs in all living organisms, but not all forms of it in plants require
selenium). Selenium also plays a role in the functioning of the thyroid gland by participating as a cofactor for the three known thyroid hormone
deiodinases.
Dietary selenium comes from nuts, cereals, meat, fish, and eggs. Brazil nuts are the richest ordinary dietary source (though this is soil-dependent,
since the Brazil nut does not require high levels of the element for its own needs). High levels are found in kidney, tuna, crab and lobster, in that
order.
Deficiency is relatively rare in healthy well-nourished individuals. It can occur in patients with severely compromised intestinal function, those
undergoing total parenteral nutrition, and also on advanced aged people (over 90). Alternatively, people dependent on food grown from selenium-
deficient soil are also at risk.
Controversial health effects
Cancer
Several studies have suggested a link between cancer and selenium deficiency. A study conducted on the effect of selenium supplementation on the
recurrence of skin cancers did not demonstrate a reduced rate of recurrence of skin cancers, but did show a significantly reduced occurrence of total
cancers. Dietary selenium prevents chemically induced carcinogenesis in many rodent studies. In these studies, organic seleno-compounds are more
potent and less toxic than selenium salts (e.g., selenocyanates, selenomethionine, selenium-rich Brazil nuts, or selenium-enriched garlic or broccoli).
Selenium may help prevent cancer by acting as an antioxidant or by enhancing immune activity. Not all studies agree on the cancer-fighting
effects of selenium. One study of naturally occurring levels of selenium in over 60,000 participants did not show a significant correlation between
those levels and cancer. The SU.VI.MAX study concluded that low-dose supplementation (with 120 mg of ascorbic acid, 30 mg of vitamin E, 6 mg of
beta carotene, 100 µg of selenium, and 20 mg of zinc) resulted in a 30% reduction in the incidence of cancer and a 37% reduction in all cause
mortality in males, but did not get a significant result for females. The SELECT study is currently investigating the effect of selenium and vitamin E
supplementation on incidence of prostate cancer. However, selenium has been proven to help chemotherapy treatment by enhancing the efficacy of
the treatment, reducing the toxicity of chemotherapeutic drugs, and preventing the body's resistance to the drugs. Studies of cancer cells in vitro
showed that chemotherapeutic drugs, such as Taxol and Adriamycin, were more toxic to strains of cancer cells grown in culture when selenium was
added.
HIV/AIDS
Some research has indicated a geographical link between regions of selenium deficient soils and peak incidences of HIV/AIDS infection. For
example, much of sub-Saharan Africa is low in selenium. However, Senegal is not, and also has a significantly lower level of AIDS infection than the
rest of the continent. AIDS appears to involve a slow and progressive decline in levels of selenium in the body. Whether this decline in selenium
levels is a direct result of the replication of HIV or related more generally to the overall malabsorption of nutrients by AIDS patients remains
debated. Low selenium levels in AIDS patients have been directly correlated with decreased immune cell count and increased disease progression
and risk of death. Selenium normally acts as an antioxidant, so low levels of it may increase oxidative stress on the immune system leading to more

10. The effects Vitamins and Minerals have on your body
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rapid decline of the immune system. Others have argued that HIV encodes for the human selenoenzyme glutathione peroxidase, which depletes the
victim's selenium levels. Depleted selenium levels in turn lead to a decline in CD4 helper T-cells, further weakening the immune system.
Regardless of the cause of depleted selenium levels in AIDS patients, studies have shown that selenium deficiency does strongly correlate with the
progression of the disease and the risk of death.
Tuberculosis
Some research has suggested that selenium supplementation, along with other nutrients, can help prevent the recurrence of tuberculosis.
Diabetes
A well-controlled study showed that selenium intake is positively correlated with the risk of developing type II diabetes. Because high serum
selenium levels are positively associated with the prevalence of diabetes, and because selenium deficiency is rare, supplementation is not
recommended in well-nourished populations such as the U.S.
Mercury
Experimental findings have demonstrated an interaction between selenium and methylmercury, but epidemiological studies have found little
evidence that selenium helps to protect against the adverse effects of methylmercury
Sodium is an essential element for animal life. As such, it is classified as a “dietary inorganic macro-mineral.”
Sodium ions (often referred to as just "sodium") are necessary for regulation of blood and body fluids, transmission of nerve impulses, heart
activity, and certain metabolic functions. Interestingly, although sodium is needed by animals, which maintain high concentrations in their
blood and extracellular fluids, the ion is not needed by plants, and is generally phytotoxic. A completely plant-based diet, therefore, will be very low
in sodium. This requires some herbivores to obtain their sodium from salt licks and other mineral sources.
Sodium is the primary cation (positive ion) in extracellular fluids in animals and humans. These fluids, such as blood plasma and extracellular fluids
in other tissues, bathe cells and carry out transport functions for nutrients and wastes. Sodium is also the principal cation in seawater, although the
concentration there is about 3.8 times what it is normally in extracellular body fluids.
Although the system for maintaining optimal salt and water balance in the body is a complex one, one of the primary ways in which the human
body keeps track of loss of body water is that osmoreceptors in the hypothalamus sense a balance of sodium and water concentration in
extracellular fluids. Relative loss of body water will cause sodium concentration to rise higher than normal, a condition known as hypernatremia.
This ordinarily results in thirst. Conversely, an excess of body water caused by drinking will result in too little sodium in the blood (hyponatremia), a
condition which is again sensed by the hypothalamus, causing a decrease in vasopressin hormone secretion from the posterior pituitary, and a
consequent loss of water in the urine, which acts to restore blood sodium concentrations to normal.
Severely dehydrated persons, such as people rescued from ocean or desert survival situations, usually have very high blood sodium concentrations.
These must be very carefully and slowly returned to normal, since too-rapid correction of hypernatremia may result in brain damage from cellular
swelling, as water moves suddenly into cells with high osmolar content. Because the hypothalamus/osmoreceptor system ordinarily works well to
cause drinking or urination to restore the body's sodium concentrations to normal, this system can be used in medical treatment to regulate the
body's total fluid content, by first controlling the body's sodium content. Thus, when a powerful diuretic drug is given which causes the kidneys to
excrete sodium, the effect is accompanied by an excretion of body water (water loss accompanies sodium loss). This happens because the kidney is
unable to efficiently retain water while excreting large amounts of sodium. In addition, after sodium excretion, the osmoreceptor system may sense
lowered sodium concentration in the blood and then direct compensatory urinary water loss in order to correct the hyponatremic (low blood sodium)
state.
In humans, a high-salt intake was demonstrated to attenuate nitric oxide production. Nitric oxide (NO) contributes to vessel homeostasis by
inhibiting vascular smooth muscle contraction and growth, platelet aggregation, and leukocyte adhesion to the endothelium
Dietary uses
The most common sodium salt, sodium chloride (table salt), is used for seasoning and warm-climate food preservation, such as pickling and making
jerky (the high osmotic content of salt inhibits bacterial and fungal growth). The human requirement for sodium in the diet is about 500 mg per day,
which is typically less than a tenth as much as many diets "seasoned to taste." Most people consume far more sodium than is physiologically
needed. For certain people with salt-sensitive blood pressure, this extra intake may cause a negative effect on health.
Zinc is an essential mineral, necessary for sustaining all life. It is a key factor in prostate gland function and reproductive organ growth. It is
estimated that 3,000 of the hundreds of thousands of proteins in the human body contain zinc prosthetic groups, one type of which is the so-called
zinc finger. In addition, there are over a dozen types of cells in the human body that secrete zinc ions, and the roles of these secreted zinc signals in
medicine and health are now being actively studied. Zinc ions are now considered to be neurotransmitters. Cells in the salivary gland, prostate,
immune system and intestine use zinc signalling.
Zinc is also involved in olfaction: the olfactory receptors contain zinc binding sites and a deficiency in zinc causes anosmia. Zinc is an activator of
certain enzymes, such as carbonic anhydrase. Carbonic anhydrase is important in the transport of carbon dioxide in vertebrate blood. It is also
required in plants for leaf formation, the synthesis of indole acetic acid (auxin) and anaerobic respiration (alcoholic fermentation).
Zinc is a good lewis acid, making it a useful catalytic agent in hydroxylation and other enzymatic reactions. Also Zinc has a flexible coordination
geometry, allowing enzymes using Zinc to rapidly shift conformations and perform biological reactions. Clinical studies have found that zinc,
combined with antioxidants, may delay progression of age-related macular degeneration. Significant dietary intake of zinc has also recently been
shown to impede the onset of flu. Soil conservation analyzes the vegetative uptake of naturally occurring zinc in many soil types.
Deficiency
Zinc deficiency occurs where insufficient zinc is available for metabolic needs. It is usually nutritional, but can also be associated with malabsorption,
acrodermatitis enteropathica, chronic liver disease, chronic renal disease, sickle cell disease, diabetes, malignancy, and other chronic
illnesses.
Immune system
In clinical trials, both zinc gluconate and zinc gluconate glycine (the formulation used in lozenges) have been shown to shorten the duration of
symptoms of the common cold. The amount of glycine can vary from two to twenty moles per mole of zinc gluconate. It should be known that there
have been clinical trials that both support the use of zinc for the common cold, and are inconclusive of its effectiveness. All clinical trials have their
critics, including the dosage amount used, and the highly subjective format of patient self-reporting the results of their trials.