There is some evidence that zinc may have an effect on cancer and further study is recommended.

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.

Global efforts to support national governments in addressing VAD are led by the Global Alliance for Vitamin A (GAVA), which is an informal partnership between A2Z, the Canadian International Development Agency, Helen Keller International, Micronutrient Initiative, UNICEF, USAID, and the World Bank. Joint GAVA activity is coordinated by the Micronutrient Initiative.

Vitamin Angels has committed itself to eradicating childhood blindness due to VAD on the planet by the year 2020. Operation 20/20 was launched in 2007 and will cover 18 countries. The program gives children two high-dose vitamin A and antiparasitic supplements (twice a year for four years), which provides children with enough of the nutrient during their most vulnerable years to prevent them from going blind and suffering from other life-threatening diseases related to VAD.

About 75% the vitamin A required for supplementation activity by developing countries is supplied by the Micronutrient Initiative with support from the Canadian International Development Agency.

An estimated 1.25 million deaths due to VAD have been averted in 40 countries since 1998.

In 2008, an estimated annual investment of US$60 million in vitamin A and zinc supplementation combined would yield benefits of more than US$1 billion per year, with every dollar spent generating benefits of more than US$17. These combined interventions were ranked by the Copenhagen Consensus 2008 as the world’s best development investment.

Treatment of VAD can be undertaken with both oral and injectable forms, generally as vitamin A palmitate.

- As an oral form, the supplementation of vitamin A is effective for lowering the risk of morbidity, especially from severe diarrhea, and reducing mortality from measles and all-cause mortality. Vitamin A supplementation of children under five who are at risk of VAD can reduce all‐cause mortality by 23%. Some countries where VAD is a public-health problem address its elimination by including vitamin A supplements available in capsule form with national immunization days (NIDs) for polio eradication or measles. Additionally, the delivery of vitamin A supplements, during integrated child health events such as child health days, have helped ensure high coverage of vitamin A supplementation in a large number of least developed countries. Child health events enable many countries in West and Central Africa to achieve over 80% coverage of vitamin A supplementation. According to UNICEF data, in 2013 worldwide, 65% of children between the ages of 6 and 59 months were fully protected with two high-dose vitamin A supplements. Vitamin A capsules cost about US$0.02. The capsules are easy to handle; they do not need to be stored in a refrigerator or vaccine carrier. When the correct dosage is given, vitamin A is safe and has no negative effect on seroconversion rates for oral polio or measles vaccines. However, because the benefit of vitamin A supplements is transient, children need them regularly every four to six months. Since NIDs provide only one dose per year, NIDs-linked vitamin A distribution must be complemented by other programs to maintain vitamin A in children Maternal high supplementation benefits both mother and breast-fed infant: high-dose vitamin A supplementation of the lactating mother in the first month postpartum can provide the breast-fed infant with an appropriate amount of vitamin A through breast milk. However, high-dose supplementation of pregnant women should be avoided because it can cause miscarriage and birth defects.

- Food fortification is also useful for improving VAD. A variety of oily and dry forms of the retinol esters, retinyl acetates, and retinyl palmitate are available for food fortification of vitamin A. Margarine and oil are the ideal food vehicles for vitamin A fortification. They protect vitamin A from oxidation during storage and prompt absorption of vitamin A. Beta-carotene and retinyl acetate or retinyl palmitate are used as a form of vitamin A for vitamin A fortification of fat-based foods. Fortification of sugar with retinyl palmitate as a form of vitamin A has been used extensively throughout Central America. Cereal flours, milk powder, and liquid milk are also used as food vehicles for vitamin A fortification. Genetic engineering is another method of food fortification, and this has been achieved with golden rice, but opposition to genetically modified foods has prevented its use as of July 2012.

- Dietary diversification can also control VAD. Nonanimal sources of vitamin A which contain preformed vitamin A account for greater than 80% of intake for most individuals in the developing world. The increase in consumption of vitamin A-rich foods of animal origin in addition to fruits and vegetables has beneficial effects on VAD. Researchers at the U. S. Agricultural Research Service have been able to identify genetic sequences in corn that are associated with higher levels of beta-carotene, the precursor to vitamin A. They found that breeders can cross certain variations of corn to produce a crop with an 18-fold increase in beta-carotene. Such advancements in nutritional plant breeding could one day aid in the illnesses related to VAD in developing countries.

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.

Adverse effects have been documented from vitamin B supplements, but never from food sources. Damage to the dorsal root ganglia is documented in human cases of overdose of pyridoxine. Although it is a water-soluble vitamin and is excreted in the urine, doses of pyridoxine in excess of the dietary upper limit (UL) over long periods cause painful and ultimately irreversible neurological problems. The primary symptoms are pain and numbness of the extremities. In severe cases, motor neuropathy may occur with "slowing of motor conduction velocities, prolonged F wave latencies, and prolonged sensory latencies in both lower extremities", causing difficulty in walking. Sensory neuropathy typically develops at doses of pyridoxine in excess of 1,000 mg per day, but adverse effects can occur with much less, so doses over 200 mg are not considered safe. Symptoms among women taking lower doses have been reported.

Existing authorizations and valuations vary considerably worldwide. As noted, the U.S. Institute of Medicine set an adult UL at 100 mg/day. The European Community Scientific Committee on Food defined intakes of 50 mg of vitamin B per day as harmful and established a UL of 25 mg/day. The nutrient reference values in Australia and New Zealand recommend an upper limit of 50 mg/day in adults. "The same figure was set for pregnancy and lactation as there is no evidence of teratogenicity at this level. The UL was set based on metabolic body size and growth considerations for all other ages and life stages except infancy. It was not possible to set a UL for infants, so intake is recommended in the form of food, milk or formula." The ULs were set using results of studies involving long-term oral administration of pyridoxine at doses of less than 1 g/day. "A no-observed-adverse-effect level (NOAEL) of 200 mg/day was identified from the studies of Bernstein & Lobitz (1988) and Del Tredici "et al" (1985). These studies involved subjects who had generally been on the supplements for five to six months or less. The study of Dalton and Dalton (1987), however, suggested the symptoms might take substantially longer than this to appear. In this latter retrospective survey, subjects who reported symptoms had been on supplements for 2.9 years, on average. Those reporting no symptoms had taken supplements for 1.9 years."

A deficiency of vitamin B 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 B deficiency, as well as other micronutrient deficiencies. Evidence exists for decreased levels of vitamin B in women with type 1 diabetes and in patients with systemic inflammation, liver disease, rheumatoid arthritis, and those infected with HIV. Use of oral contraceptives and treatment with certain anticonvulsants, isoniazid, cycloserine, penicillamine, and hydrocortisone negatively impact vitamin B status. Hemodialysis reduces vitamin B plasma levels.

Micronutrient deficiencies affect more than two billion people of all ages in both developing and industrialized countries. They are the cause of some diseases, exacerbate others and are recognized as having an important impact on worldwide health. Important micronutrients include iodine, iron, zinc, calcium, selenium, fluorine, and vitamins A, B, B, B, B, B, and C.

Micronutrient deficiencies are associated with 10% of all children's deaths, and are therefore of special concern to those involved with child welfare. Deficiencies of essential vitamins or minerals such as Vitamin A, iron, and zinc may be caused by long-term shortages of nutritious food or by infections such as intestinal worms. They may also be caused or exacerbated when illnesses (such as diarrhoea or malaria) cause rapid loss of nutrients through feces or vomit.

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.

Mild iron deficiency can be prevented or corrected by eating iron-rich foods and by cooking in an iron skillet. Because iron is a requirement for most plants and animals, a wide range of foods provide iron. Good sources of dietary iron have heme-iron, as this is most easily absorbed and is not inhibited by medication or other dietary components. Three examples are red meat, poultry, and insects. Non-heme sources do contain iron, though it has reduced bioavailability. Examples are lentils, beans, leafy vegetables, pistachios, tofu, fortified bread, and fortified breakfast cereals.

Iron from different foods is absorbed and processed differently by the body; for instance, iron in meat (heme-iron source) is more easily absorbed than iron in grains and vegetables ("non-heme" iron sources). Minerals and chemicals in one type of food may also inhibit absorption of iron from another type of food eaten at the same time. For example, oxalates and phytic acid form insoluble complexes which bind iron in the gut before it can be absorbed.

Because iron from plant sources is less easily absorbed than the heme-bound iron of animal sources, vegetarians and vegans should have a somewhat higher total daily iron intake than those who eat meat, fish or poultry. Legumes and dark-green leafy vegetables like broccoli, kale and oriental greens are especially good sources of iron for vegetarians and vegans. However, spinach and Swiss chard contain oxalates which bind iron, making it almost entirely unavailable for absorption. Iron from non-heme sources is more readily absorbed if consumed with foods that contain either heme-bound iron or vitamin C. This is due to a hypothesised "meat factor" which enhances iron absorption.

Following are two tables showing the richest foods in heme and non-heme iron.

In both tables, food serving sizes may differ from the usual 100g quantity for relevancy reasons. Arbitrarily, the guideline is set at 18 mg, which is the USDA Recommended Dietary Allowance for women aged between 19 and 50.

Iron deficiency can have serious health consequences that diet may not be able to quickly correct; hence, an iron supplement is often necessary if the iron deficiency has become symptomatic.

Iron is needed for bacterial growth making its bioavailability an important factor in controlling infection. Blood plasma as a result carries iron tightly bound to transferrin, which is taken up by cells by endocytosing transferrin, thus preventing its access to bacteria. Between 15 and 20 percent of the protein content in human milk consists of lactoferrin that binds iron. As a comparison, in cow's milk, this is only 2 percent. As a result, breast fed babies have fewer infections. Lactoferrin is also concentrated in tears, saliva and at wounds to bind iron to limit bacterial growth. Egg white contains 12% conalbumin to withhold it from bacteria that get through the egg shell (for this reason, prior to antibiotics, egg white was used to treat infections).

To reduce bacterial growth, plasma concentrations of iron are lowered in a variety of systemic inflammatory states due to increased production of hepcidin which is mainly released by the liver in response to increased production of pro-inflammatory cytokines such as Interleukin-6. This functional iron deficiency will resolve once the source of inflammation is rectified; however, if not resolved, it can progress to Anaemia of Chronic Inflammation. The underlying inflammation can be caused by fever, inflammatory bowel disease, infections, Chronic Heart Failure (CHF), carcinomas, or following surgery.

Reflecting this link between iron bioavailability and bacterial growth, the taking of oral iron supplements in excess of 200 mg/day causes a relative overabundance of iron that can alter the types of bacteria that are present within the gut. There have been concerns regarding parenteral iron being administered whilst bacteremia is present, although this has not been borne out in clinical practice. A moderate iron deficiency, in contrast, can provide protection against acute infection, especially against organisms that reside within hepatocytes and macrophages, such as malaria and tuberculosis. This is mainly beneficial in regions with a high prevalence of these diseases and where standard treatment is unavailable.

Measures have been taken to reduce child malnutrition. Studies for the World Bank found that, from 1970 to 2000, the number of malnourished children decreased by 20 percent in developing countries. Iodine supplement trials in pregnant women have been shown to reduce offspring deaths during infancy and early childhood by 29 percent. However, universal salt iodization has largely replaced this intervention.

The Progresa program in Mexico combined conditional cash transfers with nutritional education and micronutrient-fortified food supplements; this resulted in a 10 percent reduction the prevalence of stunting in children 12–36 months old. Milk fortified with zinc and iron reduced the incidence of diarrhea by 18 percent in a study in India.

Manufacturers are trying to fortify everyday foods with micronutrients that can be sold to consumers such as wheat flour for Beladi bread in Egypt or fish sauce in Vietnam and the iodization of salt.

For example, flour has been fortified with iron, zinc, folic acid and other B vitamins such as thiamine, riboflavin, niacin and vitamin B12.

The figures provided in this section on epidemiology all refer to "undernutrition" even if the term malnutrition is used which, by definition, could also apply to too much nutrition.

Breastfeeding can reduce rates of malnutrition and dehydration caused by diarrhea, but mothers are sometimes wrongly advised to not breastfeed their children. Breastfeeding has been shown to reduce mortality in infants and young children. Since only 38 percent of children worldwide under 6 months are exclusively breastfed, education programs could have large impacts on children malnutrition rates. However, breastfeeding cannot fully prevent PEM if not enough nutrients are consumed.

Iron deficiency can be avoided by choosing appropriate soil for the growing conditions (e.g., avoid growing acid loving plants on lime soils), or by adding well-rotted manure or compost. If iron deficit chlorosis is suspected then check the pH of the soil with an appropriate test kit or instrument. Take a soil sample at surface and at depth. If the pH is over seven then consider soil remediation that will lower the pH toward the 6.5 - 7 range. Remediation includes: i) adding compost, manure, peat or similar organic matter (warning. Some retail blends of manure and compost have pH in the range 7 - 8 because of added lime. Read the MSDS if available. Beware of herbicide residues in manure. Source manure from a certified organic source.) ii) applying Ammonium Sulphate as a Nitrogen fertilizer (acidifying fertilizer due to decomposition of ammonium ion to nitrate in the soil and root zone) iii) applying elemental Sulphur to the soil (oxidizes over the course of months to produce sulphate/sulphite and lower pH). Note: adding acid directly e.g. sulphuric/hydrochloric/citric acid is dangerous as you may mobilize metal ions in the soil that are toxic and otherwise bound. Iron can be made available immediately to the plant by the use of iron sulphate or iron chelate compounds. Two common iron chelates are Fe EDTA and Fe EDDHA. Iron sulphate (Iron(II)_sulfate) and iron EDTA are only useful in soil up to PH 7.1 but they can be used as a foliar spray (Foliar_feeding). Iron EDDHA is useful up to PH 9 (highly alkaline) but must be applied to the soil and in the evening to avoid photodegradation. EDTA in the soil may mobilize Lead, EDDHA does not appear to.

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).

In view of large-scale epidemiological studies of iodine levels in populations, a method of capillary electrophoresis with UV detection of iodine has been proposed.

Scurvy can be prevented by a diet that includes vitamin C-rich foods such as bell peppers (sweet peppers), blackcurrants, broccoli, chili peppers, guava, kiwifruit, and parsley. Other sources rich in vitamin C are fruits such as lemons, oranges, papaya, and strawberries. It is also found in vegetables, such as brussels sprouts, cabbage, potatoes, and spinach. Some fruits and vegetables not high in vitamin C may be pickled in lemon juice, which is high in vitamin C. Though redundant in the presence of a balanced diet, various nutritional supplements are available that provide ascorbic acid well in excess of that required to prevent scurvy.

Some animal products, including liver, Muktuk (whale skin), oysters, and parts of the central nervous system, including the adrenal medulla, brain, and spinal cord, contain large amounts of vitamin C, and can even be used to treat scurvy. Fresh meat from animals which make their own vitamin C (which most animals do) contains enough vitamin C to prevent scurvy, and even partly treat it. In some cases (notably French soldiers eating fresh horse meat), it was discovered that meat alone, even partly cooked meat, could alleviate scurvy. Conversely, in other cases, a meat-only diet could cause scurvy.

Scott's 1902 Antarctic expedition used lightly fried seal meat and liver, whereby complete recovery from incipient scurvy was reported to have taken less than two weeks.

Manganese deficiency is easy to cure and homeowners have several options when treating these symptoms. The first is to adjust the soil pH. Two materials commonly used for lowering the soil pH are aluminum sulfate and sulfur. Aluminum sulfate will change the soil pH instantly because the aluminum produces the acidity as soon as it dissolves in the soil. Sulfur, however, requires some time for the conversion to sulfuric acid with the aid of soil bacteria. If the soil pH is not a problem and there is no manganese actually in the soil then Foliar feeding for small plants and medicaps for large trees are both common ways for homeowners to get manganese into the plant.

Almost all plant and animal species synthesize vitamin C. Notable mammalian exceptions include most or all of the order Chiroptera (bats), and one of the two major primate suborders, the "Anthropoidea" (Haplorrhini) which include tarsiers, monkeys, and apes, including human beings. The Strepsirrhini (non-tarsier prosimians) can make their own vitamin C, and these include lemurs, lorises, pottos, and galagos. Ascorbic acid is also not synthesized by at least two species of Caviidae, the capybara and the guinea pig. There are known species of birds and fish that do not synthesize their own Vitamin C. All species that do not synthesize ascorbate require it in the diet. Deficiency causes scurvy in humans, and somewhat similar symptoms in other animals.

Symptoms include leaves turning yellow or brown in the margins between the veins which may remain green, while young leaves may appear to be bleached. Fruit would be of poor quality and quantity. Any plant may be affected, but raspberries and pears are particularly susceptible, as well as most acid-loving plants such as azaleas and camellias.

Correction and prevention of phosphorus deficiency typically involves increasing the levels of available phosphorus into the soil. Planters introduce more phosphorus into the soil with bone meal, rock phosphate,manure, and phosphate-fertilizers. The introduction of these compounds into the soil however does not ensure the alleviation of phosphorus deficiency. There must be phosphorus in the soil, but the phosphorus must also be absorbed by the plant. The uptake of phosphorus is limited by the chemical form in which the phosphorus is available in the soil. A large percentage of phosphorus in soil is present in chemical compounds that plants are incapable of absorbing. Phosphorus must be present in soil in specific chemical arrangements to be usable as plant nutrients. Facilitation of usable phosphorus in soil can be optimized by maintaining soil within a specified pH range. Soil acidity, measured on the pH scale, partially dictates what chemical arrangements that phosphorus forms. Between pH 6 and 7, phosphorus makes the fewest number of bonds which render the nutrient unusable to plants. At this range of acidity the likeliness of phosphorus uptake is increased and the likeliness of phosphorus deficiency is decreased. Another component in the prevention and treatment of phosphorus is the plant’s disposition to absorb nutrients. Plant species and different plants within in the same species react differently to low levels of phosphorus in soil. Greater expansion of root systems generally correlate to greater nutrient uptake. Plants within a species that have larger roots are genetically advantaged and less prone to phosphorus deficiency. These plants can be cultivated and bred as a long term phosphorus deficiency prevention method. In conjunction to root size, other genetic root adaptations to low phosphorus conditions such as mycorrhizal symbioses have been found to increase nutrient intake. These biological adaptations to roots work to maintain the levels of vital nutrients. In larger commercial agriculture settings, variation of plants to adopt these desirable phosphorus intake adaptations may be a long-term phosphorus deficiency correction method.

Manganese deficiency can be easy to spot in plants because, much like magnesium deficiency, the leaves start to turn yellow and undergo interveinal chlorosis. The difference between these two is that the younger leaves near the top of the plant show symptoms first because manganese is not mobile while in magnesium deficiency show symptoms in older leaves near the bottom of the plant.