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.

Magnesium (Mg) deficiency is a detrimental plant disorder that occurs most often in strongly acidic, light, sandy soils, where magnesium can be easily leached away. Magnesium is an essential micro nutrient found from 0.2-0.4% dry matter and is necessary for normal plant growth. Excess potassium, generally due to fertilizers, further aggravates the stress from the magnesium deficiency, as does aluminium toxicity.

Magnesium has an important role in photosynthesis because it forms the central atom of chlorophyll. Therefore, without sufficient amounts of magnesium, plants begin to degrade the chlorophyll in the old leaves. This causes the main symptom of magnesium deficiency, chlorosis, or yellowing between leaf veins, which stay green, giving the leaves a marbled appearance. Due to magnesium’s mobile nature, the plant will first break down chlorophyll in older leaves and transport the Mg to younger leaves which have greater photosynthetic needs. Therefore, the first sign of magnesium deficiency is the chlorosis of old leaves which progresses to the young leaves as the deficiency continues. Magnesium also is a necessary activator for many critical enzymes, including ribulosbiphosphate carboxylase (RuBisCO) and phosphoenolpyruvate carboxylase (PEPC), both essential enzymes in carbon fixation. Thus low amounts of Mg lead to a decrease in photosynthetic and enzymatic activity within the plants. Magnesium is also crucial in stabilizing ribosome structures, hence, a lack of magnesium causes depolymerization of ribosomes leading to pre-mature aging of the plant. After prolonged magnesium deficiency, necrosis and dropping of older leaves occurs. Plants deficient in magnesium also produce smaller, woodier fruits.

Magnesium deficiency may be confused with zinc or chlorine deficiencies, viruses, or natural ageing since all have similar symptoms. Adding Epsom salts (as a solution of 25 grams per liter or 4 oz per gal) or crushed dolomitic limestone to the soil can rectify magnesium deficiencies. For a more organic solution, applying home-made compost mulch can prevent leaching during excessive rainfall and provide plants with sufficient amounts of nutrients, including magnesium.

Magnesium deficiency is a nutritional deficiency which can affect both plants and animals

Magnesium deficiency may refer to:

- Magnesium deficiency (plants)

- Magnesium deficiency (medicine)

- For the specific condition of low blood magnesium levels, see Hypomagnesemia

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.

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.

Manganese (Mn) deficiency is a plant disorder that is often confused with, and occurs with, iron deficiency. Most common in poorly drained soils, also where organic matter levels are high. Manganese may be unavailable to plants where pH is high.

Affected plants include onion, apple, peas, French beans, cherry and raspberry, and symptoms include yellowing of leaves with smallest leaf veins remaining green to produce a ‘chequered’ effect. The plant may seem to grow away from the problem so that younger

leaves may appear to be unaffected. Brown spots may appear on leaf surfaces, and severely affected leaves turn brown and wither.

Prevention can be achieved by improving soil structure. Do not over-lime.

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.

Grass tetany or hypomagnesemic tetany, also known as grass staggers and winter tetany, is a metabolic disease involving magnesium deficiency, which can occur in such ruminant livestock as beef cattle, dairy cattle and sheep, usually after grazing on pastures of rapidly growing grass, especially in early spring.

Although many people with a defective AMPD gene are asymptomatic, others may have symptoms such as exercise intolerance, muscle pain, and muscle cramping.

- Fatigue

- MADD lowers aerobic power output, so increased anaerobic power is needed to perform the same amount of work.

- Without myoadenlyate deaminase, heavy activity causes adenosine to be released into the cell or perfused into the surrounding tissues. Fatigue and sedation after heavy exertion can be caused by excess adenosine in the cells which signals muscle fiber to feel fatigued. In the brain, excess adenosine decreases alertness and causes sleepiness. In this way, adenosine may play a role in fatigue from MADD.

- Recovery from over-exertion can be hours, days or even months. In cases of rhabdomyolysis, which is the rapid breakdown of muscle fibers, time to recovery is dependent on duration and intensity of original activity plus any excess activity during the recovery period.

- Muscle pain

- Muscle pain from MADD is not well understood, but is partially due to high levels of lactate. Increased levels of free adenosine temporarily decrease pain, allowing over-exertion without awareness. The over exertion can cause mild to severe cases of rhabdomyolysis, which is painful.

- Adenosine mediates pain through adenosine receptors. MADD causes an increase of free adenosine during heavy activity which may cause exercise-induced muscle pain. Over time, excess free adenosine down-regulates primary A1 adenosine receptors, leading to increased muscle pain. Secondary receptors (A3) increase peripheral inflammation, which also increases pain.

- Muscle cramping

- The cause of cramping is unknown, but may be related to elevated lactate, increased calcium signaling across the sarcoplasmic reticulum caused by membrane instability from reduced levels of ATP, or increased levels of free adenosine.

- Muscle weakness

- Muscle weakness is not a major symptom, though the progressive effects of chronic muscle damage from rhabdomyolysis will eventually cause significant weakness. Similarly, the long-term metabolic effects may result in nerve damage.

Manganese is a component of some enzymes and stimulates the development and activity of other enzymes. Manganese superoxide dismutase (MnSOD) is the principal antioxidant in mitochondria. Several enzymes activated by manganese contribute to the metabolism of carbohydrates, amino acids, and cholesterol.

A deficiency of manganese causes skeletal deformation in animals and inhibits the production of collagen in wound healing.

Manganese is found in leafy green vegetables, fruits, nuts, cinnamon and whole grains. The nutritious kernel, called wheat germ, which contains the most minerals and vitamins of the grain, has been removed from most processed grains (such as white bread). The wheat germ is often sold as livestock feed. Many common vitamin and mineral supplement products fail to include manganese in their compositions. Relatively high dietary intake of other minerals such as iron, magnesium, and calcium may inhibit the proper intake of manganese.

Diagnosis typically occurs during the first 6 months of life due to characteristic neurological symptoms. These symptoms include muscle spasms, tetany, and seizures. Laboratory testing indicates hypomagnesemia (decreased serum magnesium levels), hypocalcemia (decreased serum calcium levels), and little to no measurable parathyroid hormone levels. Diagnosis is confirmed with these symptoms and can be further solidified with genetic sequencing of the TRPM6 gene.

Adenosine monophosphate deaminase deficiency type 1, also called myoadenylate deaminase deficiency (MADD), is a recessive genetic metabolic disorder that affects approximately 1–2% of populations of European descent. It appears to be considerably rarer in Asian populations. The genetic form is caused by a defect in the gene for AMP deaminase though there is also an acquired form of AMP deficiency.

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.

Hypomagnesemia with secondary hypocalcemia (HSH) is an autosomal recessive genetic disorder affecting intestinal magnesium absorption. Decreased intestinal magnesium reabsorption and the resulting decrease in serum magnesium levels is believed to cause lowered parathyroid hormone (PTH) output by the parathyroid gland. This results in decreased PTH and decreased serum calcium levels (hypocalcemia). This manifests in convulsions and spasms in early infancy which, if left untreated, can lead to mental retardation or death. HSH is caused by mutations in the TRPM6 gene.

Progressive symptoms may include grazing away from the herd, irritability, muscle twitching, staring, incoordination, staggering, collapse, thrashing, head thrown back, and coma, followed by death. However, clinical signs are not always evident before the animal is found dead.

The condition results from hypomagnesemia (low magnesium concentration in blood) which may reflect low magnesium intake, low magnesium absorption, unusually low retention of magnesium, or a combination of these. Commonly, apparent symptoms develop only when hypomagnesemia is accompanied by hypocalcemia (blood Ca below 8 mg/dL).

Low magnesium intake by grazing ruminants may occur especially with some grass species early in the growing season, due to seasonally low magnesium concentrations in forage dry matter. Some conserved forages are also low in magnesium and may be conducive to hypomagnesemia.

High potassium intake relative to calcium and magnesium intake may induce hypomagnesemia. A K/(Ca+Mg) charge ratio exceeding 2.2 in forages has been commonly considered a risk factor for grass tetany. Potassium fertilizer application to increase forage production may contribute to an increased K/(Ca+Mg) ratio in forage plants, not only by adding potassium to soil, but also by displacing soil-adsorbed calcium and magnesium by ion exchange, contributing to increased susceptibility of calcium and magnesium to leaching loss from the root zone during rainy seasons. In ruminants, high potassium intake results in decreased absorption of magnesium from the digestive tract.

Trans-aconitate, which accumulates in some grasses, can be a risk factor for hypomagnesemia in grazing ruminants. (Tetany has been induced in cattle by administration of trans-aconitate and KCl, where the amount of KCl used was, by itself, insufficient to induce tetany.) Relatively high levels of trans-aconitate have been found in several forage species on rangeland sites conducive to hypomagnesemia. Although at least one rumen organism converts trans-aconitate to acetate, other rumen organisms convert trans-aconitate to tricarballylate, which complexes with magnesium. Using rats as an animal model, oral administration of tricarballylate has been shown to reduce an animal's magnesium retention. Potassium fertilizer application results in increased concentration of aconitic acid in some grass species.

Hypophosphatemia is an electrolyte disturbance in which there is an abnormally low level of phosphate in the blood. The condition has many causes, but is most commonly seen when malnourished patients (especially chronic alcoholics) are given large amounts of carbohydrates, which creates a high phosphorus demand by cells, removing phosphate from the blood ("refeeding syndrome"). Because a "decrease" in phosphate in the blood is sometimes associated with an "increase" in phosphate in the urine, the terms hypophosphatemia and "phosphaturia" are occasionally used interchangeably; however, this is improper since there exist many causes of hypophosphatemia besides overexcretion and phosphaturia, and in fact the most common causes of hypophosphatemia are not associated with phosphaturia.

Primary hypophosphatemia is the most common cause of nonnutritional rickets. Laboratory findings include low-normal serum calcium, moderately low serum phosphate, elevated serum alkaline phosphatase, and low serum 1,25 dihydroxy-vitamin D levels, hyperphosphaturia, and no evidence of hyperparathyroidism.

Other rarer causes include:

- Certain blood cancers such as lymphoma or leukemia

- Hereditary causes

- Liver failure

- Tumor-induced osteomalacia

Hypocalcaemia, also spelled hypocalcemia, is low calcium levels in the blood serum. The normal range is 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L) with levels less than 2.1 mmol/L defined as hypocalcemia. Mildly low levels that develop slowly often have no symptoms. Otherwise symptoms may include numbness, muscle spasms, seizures, confusion, or cardiac arrest.

Common causes include hypoparathyroidism and vitamin D deficiency. Others causes include kidney failure, pancreatitis, calcium channel blocker overdose, rhabdomyolysis, tumor lysis syndrome, and medications such as bisphosphonates. Diagnosis should generally be confirmed with a corrected calcium or ionized calcium level. Specific changes may be seen on an electrocardiogram (ECG).

Initial treatment for severe disease is with intravenous calcium chloride and possibly magnesium sulfate. Other treatments may include vitamin D, magnesium, and calcium supplements. If due to hypoparathyroidism, hydrochlorothiazide, phosphate binders, and a low salt diet may also be recommended. About 18% of people who are in hospital have hypocalcemia.

Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids. Symptoms in humans include all those of typical metabolic acidosis (nausea, vomiting, generalized muscle weakness, and rapid breathing).

The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect due to the decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers,reduced calcium lowers the threshold for depolarization. The symptoms can be recalled by the mnemonic "CATs go numb" - convulsions, arrhythmias, tetany, and numbness in the hands and feet and around the mouth.

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid.

Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness.

The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death.

Potomania, also known as beer potomania, beer drinker's potomania, and beer drinker's hyponatremia, is a specific hypo-osmolality syndrome related to massive consumption of beer, which is poor in solutes and electrolytes. With little food or other sources of electrolytes, consumption of large amounts of beer or other dilute alcoholic drinks leads to electrolyte disturbances, where the body does not have enough of nutrients known as electrolytes, namely sodium, potassium, and magnesium. The symptoms of potomania are similar to other causes of hyponatremia and include dizziness, muscular weakness, neurological impairment and seizures, all related to hyponatremia and hypokalaemia. While the symptoms of potomania are similar to other causes of hyponatremia and acute water intoxication, it should be considered an independent clinical entity because of its often chronic nature of onset, pathophysiology, and presentation of symptoms.

Physiological plant disorders are caused by non-pathological conditions such as poor light, adverse weather, water-logging, phytotoxic compounds or a lack of nutrients, and affect the functioning of the plant system. Physiological disorders are distinguished from plant diseases caused by pathogens, such as a virus or fungus. While the symptoms of physiological disorders may appear disease-like, they can usually be prevented by altering environmental conditions. However, once a plant shows symptoms of a physiological disorder it is likely that that season’s growth or yield will be reduced.

Symptoms of beriberi include weight loss, emotional disturbances, impaired sensory perception, weakness and pain in the limbs, and periods of irregular heart rate. Edema (swelling of bodily tissues) is common. It may increase the amount of lactic acid and pyruvic acid within the blood. In advanced cases, the disease may cause high-output cardiac failure and death.

Symptoms may occur concurrently with those of Wernicke's encephalopathy, a primarily neurological thiamine-deficiency related condition.

Beriberi is divided into four categories as follows. The first three are historical and the fourth, gastrointestinal beriberi, was recognized in 2004:

- "Dry beriberi" specially affects the peripheral nervous system

- "Wet beriberi" specially affects the cardiovascular system and other bodily systems

- "Infantile beriberi" affects the babies of malnourished mothers

- "Gastrointestinal beriberi" affects the digestive system and other bodily systems

Poor growth and a variety of disorders such as leaf discolouration (chlorosis) can be caused by a shortage of one or more plant nutrients. Poor plant uptake of a nutrient from the soil (or other growing medium) may be due to an absolute shortage of that element in the growing medium, or because that element is present in a form that is not available to the plant. The latter can be caused by incorrect pH, shortage of water, poor root growth or an excess of another nutrient. Plant nutrient deficiencies can be avoided or corrected using a variety of approaches including the consultation of experts on-site, the use of soil and plant-tissue testing services, the application of prescription-blend fertilizers, the application of fresh or well-decomposed organic matter, and the use of biological systems such as cover crops, intercropping, improved fallows, ley cropping, permaculture, or crop rotation.

Nutrient (or mineral) deficiencies include:

- Boron deficiency

- Calcium deficiency

- Iron deficiency

- Magnesium deficiency

- Manganese deficiency

- Molybdenum deficiency

- Nitrogen deficiency

- Phosphorus deficiency

- Potassium deficiency

- Zinc deficiency