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.

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.

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.

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.

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.

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.

In Northern Europe, the disease occurs after winter housing. But in Australia and New Zealand, where the cows are not housed, the disease occurs in similar conditions, when the animal enters lush, grass-dominant pastures. In North America, grass tetany occurs most commonly when range stock are moved onto lush early pasture or when housed stock are turned out onto such pasture in the spring. A second high-risk period may occur in the fall. Although cereal grasses (e.g. winter wheat) and crested wheatgrass may be especially conducive to grass tetany, the problem can also occur with several other grass species. "Winter tetany" may occur with some silages, low-magnesium grass hays, or corn stover.

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.

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.

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.

There is an increased risk that statin (cholesterol-reducing drugs) will cause myopathy (muscle weakness) in individuals with MADD.

Anesthesia has the potential to cause malignant hyperthermia, an uncontrolled increase in body temperature, and permanent muscle damage in patients with MADD. Individuals with MADD are advised to notify their anesthesiologist about their condition prior to surgery.

In most cases where myopathy is present with MADD, a second muscle disease is present and symptoms are worse than either disease in isolation.

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

It is important for MADD patients to maintain strength and fitness without exercising or working to exhaustion. Learning this balance may be more difficult than normally, as muscle pain and fatigue may be perceived differently from normal individuals.

Symptomatic relief from the effects of MADD may sometimes be achieved by administering ribose orally at a dose of approximately 10 grams per 100 pounds (0.2 g/kg) of body weight per day, and exercise modulation as appropriate. Taken hourly, ribose provides a direct but limited source of energy for the cells. Patients with myoadenylate deaminase deficiency do not retain ribose during heavy exercise, so supplementation may be required to rebuild levels of ATP.

Creatine monohydrate could also be helpful for AMPD patients, as it provides an alternative source of energy for anaerobic muscle tissue and was found to be helpful in the treatment of other, unrelated muscular myopathies.

HSH was originally believed to be an X-linked disorder due to the preponderance of affected males. With the finding that mutations in TRPM6 (on chromosome 9) are causative for the disorder this is no longer the case. Of recent interest, however, is the characterization of a patient with symptoms similar to HSH who has a translocation of the chromosomes 9 and X.

The several different causes of lactic acidosis include:

- Genetic conditions

- Biotinidase deficiency, multiple carboxylase deficiency, or nongenetic deficiencies of biotin

- Diabetes mellitus and deafness

- Fructose 1,6-bisphosphatase deficiency

- Glucose-6-phosphatase deficiency

- GRACILE syndrome

- Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes

- Pyruvate dehydrogenase deficiency

- Pyruvate carboxylase deficiency

- Drugs

- Linezolid

- Phenformin

- Metformin

- Isoniazid toxicity

- Propofol

- Propylene glycol (D-lactic acidosis)

- Nucleoside reverse transcriptase inhibitors

- Abacavir/dolutegravir/lamivudine

- Emtricitabine/tenofovir

- Potassium cyanide (cyanide poisoning)

- Fialuridine

- Other

- Impaired delivery of oxygen to cells in the tissues (e.g., from impaired blood flow (hypoperfusion))

- Bleeding

- Polymyositis

- Ethanol toxicity

- Sepsis

- Shock

- Advanced liver disease

- Diabetic ketoacidosis

- Excessive exercise (overtraining)

- Regional hypoperfusion (e.g., bowel ischemia or marked cellulitis)

- Cancers such as Non-Hodgkin's and Burkitt lymphomas

- Pheochromocytoma

The underlying cause determines the prognosis of lactic acidosis. In sepsis, elevated lactate levels correlate with mortality. The mortality of lactic acidosis in people taking metformin was previously reported to be 50%, but in more recent reports this was closer to 25%.

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

HSH is caused by decreased intestinal magnesium reabsorption through TRPM6 channels. When expressed in cells, TRPM6 produces outwardly rectifying currents with the outward portion composed of Na ions and the inward portion of divalent cations (particularly magnesium and calcium). Inward flow of sodium ions is blocked by extracellular divalent cations. Increased intracellular magnesium concentrations also decrease current through TRPM6 channels. There are currently more than 30 known mutations in TRPM6 that are associated with HSH and these mutations are spreading throughout the gene (table 1). Of the eight HSH mutations that have been tested, none have shown to produce whole-cell current. The S141L mutation, one of the few missense mutations, has been of particular interest to researchers. They have found that it prevents coassembly with TRPM7 (and presumably other TRPM6 subunits) and lacks the ability to traffic to the membrane. Whether other mutants are able to traffic properly to the surface or coassemble has not yet been further studied.

While the hypomagnesemia in patients with HSH is a direct result of TRPM6 mutations, hypocalcemia is an indirect, secondary result. Parathyroid gland secretion of PTH can be altered by changes in serum magnesium levels. The decreased serum magnesium levels seen in HSH result in decreased PTH secretion. PTH, in turn, controls the availability of serum calcium. Decreasing PTH levels cause a decrease in calcium availability in serum and, thus, the neurological symptoms of HSH.

Hypophosphatemia is caused by the following three mechanisms:

- Inadequate intake (often unmasked in refeeding after long-term low phosphate intake)

- Increased excretion (e.g. in hyperparathyroidism, hypophosphatemic rickets)

- Shift from extracellular to intracellular space. This can be seen in treatment of diabetic ketoacidosis, refeeding, short-term increases in cellular demand (e.g. hungry bone syndrome) and acute respiratory alkalosis.

Snakes that consume a diet largely composed of goldfish and feeder minnows are susceptible to developing thiamine deficiency. This is often a problem observed in captivity when keeping garter and ribbon snakes that are fed a goldfish-exclusive diet, as these fish contain thiaminase, an enzyme that breaks down thiamine.

Polioencephalomalacia (PEM) is the most common thiamine deficiency disorder in young ruminant and nonruminant animals. Symptoms of PEM include a profuse, but transient, diarrhea, listlessness, circling movements, star gazing or opisthotonus (head drawn back over neck), and muscle tremors. The most common cause is high-carbohydrate feeds, leading to the overgrowth of thiaminase-producing bacteria, but dietary ingestion of thiaminase (e.g., in bracken fern), or inhibition of thiamine absorption by high sulfur intake are also possible. Another cause of PEM is "Clostridium sporogenes" or "Bacillus aneurinolyticus" infection. These bacteria produce thiaminases that will cause an acute thiamine deficiency in the affected animal.

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.

During pregnancy and breastfeeding, women must ingest enough nutrients for themselves and their child, so they need significantly more protein and calories during these periods, as well as more vitamins and minerals (especially iron, iodine, calcium, folic acid, and vitamins A, C, and K). In 2001 the FAO of the UN reported that iron deficiency afflicted 43 percent of women in developing countries and increased the risk of death during childbirth. A 2008 review of interventions estimated that universal supplementation with calcium, iron, and folic acid during pregnancy could prevent 105,000 maternal deaths (23.6 percent of all maternal deaths).

Frequent pregnancies with short intervals between them and long periods of breastfeeding add an additional nutritional burden.

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.