Alternatively, a single-dose therapy is used for instance if there are concerns regarding the patient's compliance. The single-dose therapy can be given as an injection, but is normally given in form of an oral medication.

For treating rickets, the American Academy of Pediatrics (AAP) has recommended that pediatric patients receive an initial two- to three-month treatment of "high-dose" vitamin D therapy. In this regime, the daily dose of cholecalciferol is 1,000 IU for newborns, 1,000 to 5,000 IU for 1- to 12-months old infants, and 5,000 IU for patients over 1 year of age.

For adults, other dosages have been called for. A review of 2008/2009 recommended dosages of 1,000 IU cholecalciferol per 10 ng/ml required serum increase, to be given daily over two to three months. In another proposed cholecalciferol loading dose guideline for vitamin D-deficient adults, a weekly dosage is given, up to a total amount that is proportional to the required serum increase (up to the level of 75 nml/l) and, within certain body weight limits, to body weight.

Treatment involves a diet which includes an adequate amount of riboflavin containing foods. Multi-vitamin and mineral dietary supplements often contain 100% of the Daily Value (1.3 mg) for riboflavin, and can be used by persons concerned about an inadequate diet. Over-the-counter dietary supplements are available in the United States with doses as high as 100 mg, but there is no evidence that these high doses have any additional benefit for healthy people.

Five interventional strategies can be used:

- Adding zinc to soil, called agronomic biofortification, which both increases crop yields and provides more dietary zinc.

- Adding zinc to food, called fortification.

- Adding zinc rich foods to diet. The foods with the highest concentration of zinc are proteins, especially animal meats, the highest being oysters. Per ounce, beef, pork, and lamb contain more zinc than fish. The dark meat of a chicken has more zinc than the light meat. Other good sources of zinc are nuts, whole grains, legumes, and yeast. Although whole grains and cereals are high in zinc, they also contain chelating phytates which bind zinc and reduce its bioavailability.

- Oral repletion via tablets (e.g. zinc gluconate) or liquid (e.g. zinc acetate). Oral zinc supplementation in healthy infants more than six months old has been shown to reduce the duration of any subsequent diarrheal episodes by about 11 hours.

- Oral repletion via multivitamin/mineral supplements containing zinc gluconate, sulfate, or acetate. It is not clear whether one form is better than another. Zinc is also found in some cold lozenges, nasal sprays, and nasal gels.

If untreated, pellagra can kill within four or five years. Treatment is with nicotinamide, which has the same vitamin function as niacin and a similar chemical structure, but has lower toxicity. The frequency and amount of nicotinamide administered depends on the degree to which the condition has progressed.

As a chemical compound, riboflavin is a yellow-orange solid substance with poor solubility in water compared to other B vitamins. Visually, it imparts color to vitamin supplements (and bright yellow color to the urine of persons taking a lot of it).

Novel zinc biomarkers, such as the erythrocyte LA:DGLA ratio, have shown promise in pre-clinical and clinical trials and are being developed to more accurately detect dietary zinc deficiency.

Nutritional osteomalacia responds well to administration of 2,000-10,000 IU of vitamin D3 by mouth daily. Vitamin D3 (cholecalciferol) is typically absorbed more readily than vitmin D2 (ergocalciferol). Osteomalacia due to malabsorption may require treatment by injection or daily oral dosing of significant amounts of vitamin D3.

Iodine deficiency is treated by ingestion of iodine salts, such as found in food supplements. Mild cases may be treated by using iodized salt in daily food consumption, or drinking more milk, or eating egg yolks, and saltwater fish. For a salt and/or animal product restricted diet, sea vegetables (kelp, hijiki, dulse, nori (found in sushi)) may be incorporated regularly into a diet as a good source of iodine.

The recommended daily intake of iodine for adult women is 150–300 µg for maintenance of normal thyroid function; for men it is somewhat less at 150 µg.

However, too high iodine intake, for example due to overdosage of iodine supplements, can have toxic side effects. It can lead to hyperthyroidism and consequently high blood levels of thyroid hormones (hyperthyroxinemia). In case of extremely high single-dose iodine intake, typically a short-term suppression of thyroid function (Wolff–Chaikoff effect) occurs. Persons with pre-existing thyroid disease, elderly persons, fetuses and neonates, and patients with other risk factors are at a higher risk of experiencing iodine-induced thyroid abnormalities. In particular, in persons with goiter due to iodine deficiency or with altered thyroid function, a form of hyperthyroidism called Jod-Basedow phenomenon can be triggered even at small or single iodine dosages, for example as a side effect of administration of iodine-containing contrast agents. In some cases, excessive iodine contributes to a risk of autoimmune thyroid diseases (Hashimoto's thyroiditis and Graves' disease).

The treatment for Keshan disease is selenium supplementation. The recommended amounts are fifty-five micrograms of selenium per day for adult men and women, sixty micrograms a day for women during pregnancy and seventy micrograms per day for women after pregnancy. A doctor may insist that if a man is sexually active, he may have to take up to seventy micrograms of selenium per day. A doctor may also recommend that the individual take vitamin E; selenium and vitamin E are medically linked and seem to work to together. An individual will also be advised to have a diet that includes seafood, meats such as kidney, and liver, and some grains and seeds; all of these are high in selenium. Brewer's yeast and wheat germ both contain high levels of selenium. Garlic, onions, mushroom, broccoli, tomatoes, radishes, and Swiss chard may be good sources of selenium if the soil in which they are grown contains it. An individual will have to be monitored once they begin to take the selenium supplements, due to the fact that too much of it can cause balding, intestinal distress, weakness, and slow mental functioning. Individuals in China with the disease treat it with a herb called "Astragalus", which accumulates selenium from the soil.

Prevention of osteomalacia rests on having an adequate intake of vitamin D and calcium. Vitamin D3 Supplementation is often needed due to the scarcity of Vitamin D sources in the modern diet.

In order to avoid problems, the person must be rehabilitated with small but frequent rations, given every two to four hours. During one week, the diet, hyperglucidic, is gradually enriched in protein as well as essential elements: sweet milk with mineral salts and vitamins. The diet may include lactases - so that children who have developed lactose intolerance can ingest dairy products - and antibiotics - to compensate for immunodeficiency. After two to three weeks, the milk is replaced by boiled cereals fortified with minerals and vitamins until its mass is at least 80% of normal weight. Traditional food can then be reintroduced. The child is considered healed when his mass reaches 85% of normal.

The individual should consult the doctor if their symptoms worsen to prevent any major complications of the condition.

Avoid alcohol—avoid alcohol consumption during the duration of the illness, because alcohol may increase stress on the already strained heart and can make symptoms worse.

Increase consumption of foods rich in selenium—eat foods rich in selenium to help the individual’s heart heal more quickly (in addition to any supplements they may also be taking).

Monitor side effects to medications—if the patient was prescribed with medication, it may be helpful if they can monitor any side effects they have (if they are present) and see their doctor if the side effects are more than just the mildly common ones.

Increase sleep—it is important to get an adequate rest due to poor heart condition. In the case of mild Keshan's disease caused by a viral agent, the individuals doctor will advise them to have complete rest (and adequate fluids) for a specific period to help their body's immune system fight the infection and heal.

Supplements—an individual will most likely be prescribed selenium supplements (in the form of selenomethionine) or have injections of this mineral.

Surgery—if surgery has been advised (implants, stents or full heart transplant) the individual cardiac specialist will advise you about the pre-operative and post-operative care that they will need to undergo and how to best take care of themselves during this time, to avoid complications or worsening of any symptoms or the hhealth.

With few exceptions, like some vitamins from B-complex, hypervitaminosis usually occurs more with fat-soluble vitamins (D, E, K and A or 'DEKA'), which are stored in the liver and fatty tissues of the body. These vitamins build up and remain for a longer time in the body than water-soluble vitamins.

Conditions include:

- Hypervitaminosis A

- Hypervitaminosis D

- Hypervitaminosis E

- Hypervitaminosis K, unique as the true upper limit is less clear as is its bioavailability.

According to Williams' Essentials of Diet and Nutrition Therapy it is difficult to set a DRI for vitamin K because part of the requirement can be met by intestinal bacterial synthesis.

- Reliable information is lacking as to the vitamin K content of many foods or its bioavailability. With this in mind the Expert Committee established an AI rather than an RDA.

- This RDA (AI for men age 19 and older is 120 µg/day, AI for women is 90 µg/day) is adequate to preserve blood clotting, but the correct intake needed for optimum bone health is unknown. Toxicity has not been reported.

High-dosage A; high-dosage, slow-release vitamin B; and very high-dosage vitamin B alone (i.e. without vitamin B complex) hypervitaminoses are sometimes associated with side effects that usually rapidly cease with supplement reduction or cessation.

High doses of mineral supplements can also lead to side effects and toxicity. Mineral-supplement poisoning does occur occasionally, most often due to excessive intake of iron-containing supplements.

Treatment of KBD is palliative. Surgical corrections have been made with success by Chinese and Russian orthopedists. By the end of 1992, Médecins Sans Frontières—Belgium started a physical therapy programme aiming at alleviating the symptoms of KBD patients with advanced joint impairment and pain (mainly adults), in Nyemo county, Lhasa prefecture. Physical therapy had significant effects on joint mobility and joint pain in KBD patients. Later on (1994–1996), the programme has been extended to several other counties and prefectures in Tibet.

Prevention of Kashin–Beck disease has a long history. Intervention strategies were mostly based on one of the three major theories of its cause.

Selenium supplementation, with or without additional antioxidant therapy (vitamin E and vitamin C) has been reported to be successful, but in other studies no significant decrease could be shown compared to a control group. Major drawbacks of selenium supplementation are logistic difficulties (daily or weekly intake, drug supply), potential toxicity (in case of less controlled supplementation strategies), associated iodine deficiency (that should be corrected before selenium supplementation to prevent further deterioration of thyroid status) and low compliance. The latter was certainly the case in Tibet, where a selenium supplementation has been implemented from 1987 to 1994 in areas of high endemicity.

With the mycotoxin theory in mind, backing of grains before storage was proposed in Guangxi province, but results are not reported in international literature. Changing from grain source has been reported to be effective in Heilongjiang province and North Korea.

With respect to the role of drinking water, changing of water sources to deep well water has been reported to decrease the X-ray metaphyseal detection rate in different settings.

In general, the effect of preventive measures however remains controversial, due to methodological problems (no randomised controlled trials), lack of documentation or, as discussed above, due to inconsistency of results.

In cases of suspected copper poisoning, penicillamine is the drug of choice, and dimercaprol, a heavy metal chelating agent, is often administered. Vinegar is not recommended to be given, as it assists in solubilizing insoluble copper salts. The inflammatory symptoms are to be treated on general principles, as are the nervous ones.

There is some evidence that alpha-lipoic acid (ALA) may work as a milder chelator of tissue-bound copper. Alpha lipoic acid is also being researched for chelating other heavy metals, such as mercury.

The European Food Safety Authority concluded that chromium is not an essential nutrient, making this the only mineral for which the United States and the European Union disagree. The proposed mechanism for cellular uptake of Cr via transferrin has been called into question. There is no proof that chromium supplementation has physiological effects on body mass or composition, and its use as a supplement may be unsafe. A 2014 systematic review concluded that chromium supplementation had no effect on glycemic control, fasting plasma glucose levels, or body weight in people with or without diabetes.

Chromium may be needed as an ingredient in total parenteral nutrition (TPN), since deficiency may occur after months of intravenous feeding with chromium-free TPN. For this reason, chromium is added to normal TPN solutions for people with diabetes, and in nutritional products for preterm infants.

In plants a micronutrient deficiency (or trace mineral deficiency) is a physiological plant disorder which occurs when a micronutrient is deficient in the soil in which a plant grows. Micronutrients are distinguished from macronutrients (nitrogen, phosphorus, sulfur, potassium, calcium and magnesium) by the relatively low quantities needed by the plant.

A number of elements are known to be needed in these small amounts for proper plant growth and development. Nutrient deficiencies in these areas can adversely affect plant growth and development. Some of the best known trace mineral deficiencies include: zinc deficiency, boron deficiency, iron deficiency, and manganese deficiency.

Micronutrient deficiency or dietary deficiency is a lack of one or more of the micronutrients required for plant or animal health. In humans and other animals they include both vitamin deficiencies and mineral deficiencies, whereas in plants the term refers to deficiencies of essential trace minerals.

Pellagra can develop according to several mechanisms, classically as a result of niacin (vitamin B3) deficiency, which results in decreased NAD production leading to most of the pathology (since NAD and its phosphorylated NADP form are cofactors required in many body processes, the pathological impact of pellagra is broad and results in death if not treated).

The first mechanism is simple dietary lack of niacin. Second, it may result from deficiency of tryptophan, an essential amino acid found in meat, poultry, fish, eggs, and peanuts that the body converts into niacin. Third, it may be caused by excess leucine, as it inhibits quinolinate phosphoribosyl transferase (QPRT) and inhibits the formation of Niacin or Nicotinic acid to Nicotinamide mononucleotide (NMN) causing pellegra like symptoms to occur.

Some conditions can prevent the absorption of dietary niacin or tryptophan and lead to pellagra. Inflammation of the jejunum or ileum can prevent nutrient absorption, leading to pellagra, and this can in turn be caused by Crohn's disease. Gastroenterostomy can also cause pellagra. Chronic alcoholism can also cause poor absorption which combines with a diet already low in niacin and tryptophan to produce pellagra. Hartnup disease is a genetic disorder that reduces tryptophan absorption, leading to pellagra.

Alterations in protein metabolism may also produce pellagra-like symptoms. An example is carcinoid syndrome, a disease in which neuroendocrine tumors along the GI tract use tryptophan as the source for serotonin production, which limits the available tryptophan for niacin synthesis. In normal patients, only one percent of dietary tryptophan is converted to serotonin; however, in patients with carcinoid syndrome, this value may increase to 70%. Carcinoid syndrome thus may produce niacin deficiency and clinical manifestations of pellagra. Anti-tuberculosis medication tends to bind to vitamin B and reduce niacin synthesis, since B (aka pyridoxine) is a required cofactor in the tryptophan-to-niacin reaction.

Several therapeutic drugs can provoke pellagra. These include the antibiotics isoniazid, which decreases available B by binding to it and making it inactive, so it cannot be used in niacin synthesis, and chloramphenicol; the anti-cancer agent fluorouracil; and the immunosuppressant mercaptopurine.

In the United States, overdose exposure to all formulations of "vitamins" was reported by 62,562 individuals in 2004 (nearly 80% [~78%, n=48,989] of these exposures were in children under the age of 6), leading to 53 "major" life-threatening outcomes and 3 deaths (2 from vitamins D and E; 1 from polyvitaminic type formula, with iron and no fluoride). This may be compared to the 19,250 people who died of unintentional poisoning of all kinds in the U.S. in the same year (2004). In 2010, 71,000 exposures to various vitamins and multivitamin-mineral formulations were reported to poison control centers, which resulted in 15 major reactions but no deaths.

Before 1998, several deaths per year were associated with pharmaceutical iron-containing supplements, especially brightly colored, sugar-coated, high-potency iron supplements, and most deaths were children. Unit packaging restrictions on supplements with more than 30 mg of iron have since reduced deaths to 0 or 1 per year. These statistics compare with 59 confirmed deaths due to aspirin poisoning in 2003 and 147 deaths known to be associated with acetaminophen-containing products in 2003.

When treating iron-deficiency anemia, considerations of the proper treatment methods are done in light of the "cause and severity" of the condition. If the iron-deficiency anemia is a downstream effect of blood loss or another underlying cause, treatment is geared toward addressing the underlying cause when possible. In severe acute cases, treatment measures are taken for immediate management in the interim, such as blood transfusions or even intravenous iron.

Iron-deficiency anemia treatment for less severe cases includes dietary changes to incorporate iron-rich foods into regular oral intake. Foods rich in ascorbic acid (vitamin C) can also be beneficial, since ascorbic acid enhances iron absorption. Other oral options are iron supplements in the form of pills or drops for children.

As iron-deficiency anemia becomes more severe, or if the anemia does not respond to oral treatments, other measures may become necessary. In addition to the previously mentioned indication for intravenous iron or blood transfusions, intravenous iron may also be used when oral intake is not tolerated, as well as for other indications. Specifically, for those on dialysis, parenteral iron is commonly used. Individuals on dialysis who are taking forms of erythropoietin or some "erythropoiesis-stimulating agent" are given parenteral iron, which helps the body respond to the erythropoietin agents and produce red blood cells.

The various forms of treatment are not without possible adverse effects. Iron supplementation by mouth commonly causes negative gastrointestinal effects, including constipation. Intravenous iron can induce an allergic response that can be as serious as anaphylaxis, although different formulations have decreased the likelihood of this adverse effect.

Disorders usually resolve after early treatment. If the treatment is delayed, the overall health of the child is improved but physical (reduced) and intellectual (mental disabilities) sequelae are feared. Without treatment or if treatment occurs too late, death is inevitable.

A high risk of death is identified by a brachial perimeter < 11 cm or by a weight-to-height threshold < -3 SD. In practice, malnourished children with edema are suffering from potentially life-threatening severe malnutrition.

Mineral deficiency is a lack of dietary minerals, the micronutrients that are needed for an organism's proper health. The cause may be a poor diet, impaired uptake of the minerals that are consumed or a dysfunction in the organism's use of the mineral after it is absorbed. These deficiencies can result in many disorders including anemia and goitre. Examples of mineral deficiency include, zinc deficiency, iron deficiency, and magnesium deficiency.