Severe zinc deficiency may disturb the sense of smell and taste. Night blindness may be a feature of severe zinc deficiency, however most reports of night blindness and abnormal dark adaptation in humans with zinc deficiency have occurred in combination with other nutritional deficiencies (e.g. vitamin A).

Zinc deficiency may manifest as acne, eczema, xerosis (dry, scaling skin), seborrheic dermatitis, or alopecia (thin and sparse hair). There may also be impaired wound healing.

Vitamin D deficiency can be asymptomatic, but may also cause several problems including:

- Osteomalacia, a bone-thinning disorder that occurs exclusively in adults and is characterized by proximal muscle weakness and bone fragility.

- Osteoporosis, a condition characterized by reduced bone mineral density and increased bone fragility.

- Increased risk of fracture

- Rickets, a childhood disease characterized by impeded growth and deformity of the long bones. The earliest sign of subclinical vitamin D deficiency is craniotabes, abnormal softening or thinning of the skull.

- Muscle aches and weakness

- Muscle twitching (fasciculations) is commonly seen due to reduced ionised calcium, arising from a low vitamin D.

- Light-headedness

- Periodontitis, local inflammatory bone loss that can result in tooth loss.

- Pre-eclampsia: There has been an association of vitamin D deficiency and women who develop pre-eclampsia in pregnancy. The exact relationship of these conditions is not well understood. Maternal vitamin D deficiency may affect the baby, causing overt bone disease from before birth and impairment of bone quality after birth.

- Depression: Hypovitaminosis D is a risk factor for depression. Some studies have found that low levels of vitamin D are correlated with depressed feelings and are found in patients who have been diagnosed with depression.

Vitamin D deficiency is typically diagnosed by measuring the concentration of the 25-hydroxyvitamin D in the blood, which is the most accurate measure of vitamin D status.

- Deficiency: <20 ng/mL

- Insufficient: 20–29 ng/mL

- Normal: 30–100 ng/mL

Vitamin D levels falling within this normal range prevent clinical manifestations of vitamin D insufficiency as well as vitamin D toxicity from taking in too much vitamin D.

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.

The classic symptoms of pellagra are diarrhea, dermatitis, dementia, and death ("the four Ds").

A more comprehensive list of symptoms includes:

- High sensitivity to sunlight

- Aggression

- Dermatitis, alopecia (hair loss), edema (swelling)

- Smooth, beefy red glossitis (tongue inflammation)

- Red skin lesions

- Insomnia

- Weakness

- Mental confusion

- Ataxia (lack of coordination), paralysis of extremities, peripheral neuritis (nerve damage)

- Diarrhea

- Dilated cardiomyopathy (enlarged, weakened heart)

- Eventually dementia

J. Frostig and Tom Spies (acc. to Cleary and Cleary) described more specific psychological symptoms of pellagra as:

- Psychosensory disturbances (impressions as being painful, annoying bright lights, odors intolerance causing nausea and vomiting, dizziness after sudden movements)

- Psychomotor disturbances (restlessness, tense and a desire to quarrel, increased preparedness for motor action)

- Emotional disturbances

Despite clinical symptoms, blood level of tryptophan or urinary metabolites such as 2-pyridone/N-methylniacinamide ratio <2 or NAD/NADP ratio in red blood cells could be used to diagnose pellagra. Diagnosis could be confirmed after rapid improvements in the symptoms in patients using high doses of niacin (250–500 mg/day) or niacin enriched food.

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.

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.

Pellagra is a disease caused by a lack of the vitamin niacin (vitamin B). Symptoms include inflamed skin, diarrhea, dementia, and sores in the mouth. Areas of the skin exposed to either sunlight or friction are typically affected first. Over time affected skin may become darker, stiff, begin to peel, or bleed.

There are two main types of pellagra, primary and secondary. Primary pellagra is due to a diet that does not contain enough niacin and tryptophan. Secondary pellagra is due to a poor ability to use the niacin within the diet. This can occur as a result of alcoholism, long term diarrhea, carcinoid syndrome, Hartnup disease, and a number of medications such as isoniazid. Diagnosis is typically based on symptoms and may be assisted by urine testing.

Treatment is with either niacin or nicotinamide supplementation. Improvements typically begin within a couple of days. General improvements in diet are also frequently recommended. Decreasing sun exposure via sunscreen and proper clothing is important while the skin heals. Without treatment death may occur. It occurs most commonly in the developing world, specifically sub-Saharan Africa.

In other 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 mucous membrane of the gastrointestinal tract. Post-mortem studies in rhesus monkeys fed a riboflavin-deficient diet revealed about one-third the normal amount of riboflavin was present in the liver, which is the main storage organ for riboflavin in mammals. Riboflavin deficiency in birds results in low egg hatch rates.

Hypervitaminosis is a condition of abnormally high storage levels of vitamins, which can lead to toxic symptoms. Specific medical names of the different conditions are derived from the vitamin involved: an excess of vitamin A, for example, is called hypervitaminosis A.

Hypervitaminoses are primarily caused by fat-soluble vitamins (D, E, K and A), as these are stored by the body for longer period than the water-soluble vitamins.

Generally, toxic levels of vitamins stem from high supplement intake and not from natural food. Toxicities of fat-soluble vitamins can also be caused by a large intake of highly fortified foods, but natural food rarely deliver dangerous levels of fat-soluble vitamins. The Dietary Reference Intake recommendations from the United States Department of Agriculture define a "tolerable upper intake level" for most vitamins.

Overt clinical signs are rarely seen among inhabitants of the developed countries. The assessment of Riboflavin status is essential for confirming cases with unspecific symptoms where deficiency is suspected.

- Glutathione reductase is a nicotinamide adenine dinucleotide phosphate (NADPH) and FAD-dependent enzyme, and the major flavoprotein in erythrocyte. The measurement of the activity coefficient of erythrocyte glutathione reductase (EGR) is the preferred method for assessing riboflavin status. It provides a measure of tissue saturation and long-term riboflavin status. In vitro enzyme activity in terms of activity coefficients (AC) is determined both with and without the addition of FAD to the medium. ACs represent a ratio of the enzyme’s activity with FAD to the enzyme’s activity without FAD. An AC of 1.2 to 1.4, riboflavin status is considered low when FAD is added to stimulate enzyme activity. An AC > 1.4 suggests riboflavin deficiency. On the other hand, if FAD is added and AC is < 1.2, then riboflavin status is considered acceptable. Tillotson and Bashor reported that a decrease in the intakes of riboflavin was associated with increase in EGR AC. In the UK study of Norwich elderly, initial EGR AC values for both males and females were significantly correlated with those measured 2 years later, suggesting that EGR AC may be a reliable measure of long-term biochemical riboflavin status of individuals. These findings are consistent with earlier studies.

- Experimental balance studies indicate that urinary riboflavin excretion rates increase slowly with increasing intakes, until intake level approach 1.0 mg/d, when tissue saturation occurs. At higher intakes, the rate of excretion increases dramatically. Once intakes of 2.5 mg/d are reached, excretion becomes approximately equal to the rate of absorption (Horwitt et al., 1950) (18). At such high intake a significant proportion of the riboflavin intake is not absorbed. If urinary riboflavin excretion is <19 µg/g creatinine (without recent riboflavin intake) or < 40 µg per day are indicative of deficiency.

The symptoms of chromium deficiency caused by long-term total parenteral nutrition are severely impaired glucose tolerance, weight loss, and confusion. However, subsequent studies questioned the validity of these findings.

Chromium deficiency is a proposed disorder that results from an insufficient dietary intake of chromium. Chromium was first proposed as an essential element for normal glucose metabolism in 1959, and was widely accepted as being such by the 1990s. Cases of deficiency have been claimed in hospital patients who were fed defined liquid diets intravenously for long periods of time.

By the turn of the century, these views were being challenged, with subsequent work suggesting that chromium supplements may present a health risk. In spite of this, dietary supplements containing chromium remain widely available.

Manganese deficiency in humans results in a number of medical problems. Manganese is a vital element of nutrition in very small quantities (adult male daily intake 2.3 milligrams). However, in greater amounts manganese, like most metals, is poisonous when eaten or inhaled.

Overnutrition or hyperalimentation is a form of malnutrition in which the intake of nutrients is oversupplied. The amount of nutrients exceeds the amount required for normal growth, development, and metabolism.

The term can also refer to:

- Obesity, which "usually" occurs by overeating, as well as:

- Oversupplying a "specific" nutrient, such as dietary minerals or vitamin poisoning. This is due to an excessive intake or a nutritional imbalance caused by fad diets.

For mineral excess, see:

- Iron poisoning, and

- Low sodium diet (a response to excess sodium).

Overnutrition may also refers to greater food consumption than appropriate, as well as other feeding procedures such as parenteral nutrition.

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.

Iodine deficiency is a lack of the trace element iodine, an essential nutrient in the diet. It may result in a goiter, sometimes as an endemic goiter as well as cretinism due to untreated congenital hypothyroidism, which results in developmental delays and other health problems. Iodine deficiency is an important public health issue as it is a preventable cause of intellectual disability.

Iodine is an essential dietary mineral; the thyroid hormones thyroxine and triiodothyronine contain iodine. In areas where there is little iodine in the diet, typically remote inland

areas where no marine foods are eaten, iodine deficiency is common. It is also common in mountainous regions of the world where food is grown in iodine-poor soil.

Prevention includes adding small amounts of iodine to table salt, a product known as "iodized salt". Iodine compounds have also been added to other foodstuffs, such as flour, water and milk, in areas of deficiency. Seafood is also a well known source of iodine.

Iodine deficiency resulting in goiter occurs in 187 million people globally as of 2010 (2.7% of the population). It resulted in 2700 deaths in 2013 up from 2100 deaths in 1990.

Iodine deficiency is one of the leading causes of preventable mental handicaps worldwide, producing typical reductions in IQ of 10 to 15 IQ points. It has been speculated that deficiency of iodine and other micronutrients may be a possible factor in observed differences in IQ between ethnic groups: see race and intelligence for a further discussion of this controversial issue.

Cretinism is a condition associated with iodine deficiency and goiter, commonly characterised by mental deficiency, deafness, squint, disorders of stance and gait and stunted growth due to hypothyroidism. Paracelsus was the first to point out the relation between goitrous parents and their mentally disabled children.

As a result of restricted diet, isolation, intermarriage, etc., as well as low iodine content in their food, children often had peculiar stunted bodies and retarded mental faculties, a condition later known to be associated with thyroid hormone deficiency. Diderot, in his 1754 "Encyclopédie", described these patients as "crétins". In French, the term "crétin des Alpes" also became current, since the condition was observed in remote valleys of the Alps in particular. The word "cretin" appeared in English in 1779.

While reporting recent progress towards overcoming iodine-deficiency disorders worldwide, "The Lancet" noted: "According to World Health Organization, in 2007, nearly 2 billion individuals had insufficient iodine intake, a third being of school age." A conclusion was made that the single most preventable cause of intellectual disability is that of iodine deficiency.

Osteomalacia is a generalized bone condition in which there is inadequate mineralization of the bone. Many of the effects of the disease overlap with the more common osteoporosis, but the two diseases are significantly different. There are two main causes of osteomalacia:

1. insufficient calcium absorption from the intestine because of lack of dietary calcium or a deficiency of, or resistance to, the action of vitamin D

2. phosphate deficiency caused by increased renal losses.

Symptoms:

Osteomalacia in adults starts insidiously as aches and pains in the lumbar (lower back) region and thighs before spreading to the arms and ribs. The pain is symmetrical, non-radiating and accompanied by sensitivity in the involved bones. Proximal muscles are weak, and there is difficulty in climbing up stairs and getting up from a squatting position.

As a result of demineralization, the bones become less rigid. Physical signs include deformities like triradiate pelvis and lordosis. The patient has a typical "waddling" gait. However, these physical signs may derive from a previous osteomalacial state, since bones do not regain their original shape after they become deformed.

Pathologic fractures due to weight bearing may develop. Most of the time, the only alleged symptom is chronic fatigue, while bone aches are not spontaneous but only revealed by pressure or shocks.It differs from renal osteodystrophy, where the latter shows hyperphosphatemia.

The causes of adult osteomalacia are varied, but ultimately result in a vitamin D deficiency:

Fluoride or fluorine deficiency is a disorder which may cause increased dental caries (or tooth decay, is the breakdown of dental tissues by the acidic products released by the "bacterial fermentation of dietary carbohydrates.") and possibly osteoporosis (a bone disorder which leads to a decrease in bone mass, and an increase in bone fragility), due to a lack of fluoride in the diet; however, there are anti-osteoporotic functional food ingredients that can help decrease the risk of osteoporosis fractures. In terms of dietary sources, fish and tea are considered natural sources of fluoride, as well as tap water that has been fluoridated. The extent to which the condition truly exists, and its relationship to fluoride poisoning has given rise to some controversy. Fluorine is not considered to be an essential nutrient, but the importance of fluorides for preventing tooth decay is well-recognized, although the effect is predominantly topical. Prior to 1981, the effect of fluorides was thought to be largely systemic and preeruptive, requiring ingestion. Fluoride is considered essential in the development and maintenance of teeth by the American Dental Hygienists' Association. Fluoride is also essential as it incorporates into the teeth to form and harden teeth enamels so that the teeth are more acid resistant as well as more resistant to cavity forming bacteria. Caries-inhibiting effects of fluoride were first seen in 1902 when fluoride in high concentrations was found to stain teeth and prevent tooth decay.

Fluoride salts, particularly sodium fluoride (NaF), are used in the treatment and prevention of osteoporosis. Symptoms such as fractured hips in the elderly or brittle and weak bones are caused due to fluorine deficiency in the body. Fluoride stimulates bone formation and increases bone density, however bone with excess fluoride content has an abnormal structure resulting in increased fragility. Thus fluoride therapy results in large increases in bone mineral density but the effect on fracture rates, while positive, is small.

Disputes over the essentiality of fluorine date back to the 19th century, when fluorine was observed in teeth and bones. In 1973 a trial found reduced reproduction in mice fed fluorine-deficient diets, but a subsequent investigation determined that this was due to reduced iron absorption.

The defining sign of kwashiorkor in a malnourished child is pitting edema (swelling of the ankles and feet). Other signs include a distended abdomen, an enlarged liver with fatty infiltrates, thinning hair, loss of teeth, skin depigmentation and dermatitis. Children with kwashiorkor often develop irritability and anorexia. Generally, the disease can be treated by adding protein to the diet; however, it can have a long-term impact on a child's physical and mental development, and in severe cases may lead to death.

In dry climates, marasmus is the more frequent disease associated with malnutrition. Another malnutrition syndrome includes cachexia, although it is often caused by underlying illnesses. These are important considerations in the treatment of the patients.

Keshan disease is a congestive cardiomyopathy caused by a combination of dietary deficiency of selenium and the presence of a mutated strain of Coxsackievirus, named after Keshan County of Heilongjiang province, Northeast China, where symptoms were first noted. These symptoms were later found prevalent in a wide belt extending from northeast to southwest China, all due to selenium-deficient soil. The disease peaked in 1960–1970, claiming thousands of lives.

Often fatal, the disease afflicts children and women of child bearing age, characterized by heart failure and pulmonary edema. Over decades, supplementation with selenium reduced this affliction.

It had been linked to the coxsackie B virus. Current research suggests that the lack of selenium results in a more virulent strain of the coxsackievirus becoming the dominant viral species present in the population of virus, but the mechanism of this selection event is unclear.

The disease got its name from the province in which it was discovered: Keshan, China. Since its discovery, it can also be found in New Zealand and Finland. Keshan disease results from a selenium deficiency which is a nutrient we receive in our diet from eating foods that were grown in selenium enriched soils. Because of that factor, Keshan deficiency can be found anywhere that the level of selenium present in the soil is low. An individual with Keshan disease will have an abnormally large heart. Keshan disease can also lead to higher rates of cancer, cardiovascular disease, hypertension, and strokes. In addition, an individual can experience eczema, psoriasis, arthritis, cataracts, alcoholism, and infections.

Copper toxicity, also called copperiedus, refers to the consequences of an excess of copper in the body. Copperiedus can occur from eating acid foods cooked in uncoated copper cookware, or from exposure to excess copper in drinking water or other environmental sources.