Phosphorus deficiency is a plant disorder associated with insufficient supply of phosphorus. Phosphorus refers here to salts of phosphates (PO), monohydrogen phosphate (HPO), and dihydrogen phosphate (HPO). These anions readily interconvert, and the predominant species is determined by the pH of the solution or soil. Phosphates are required for the biosynthesis of genetic material as well as ATP, essential for life. Phosphorus deficiency can be controlled by applying sources of phosphorus such as bone meal, rock phosphate, manure, and phosphate-fertilizers.

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.

Calcium (Ca) deficiency is a plant disorder that can be caused by insufficient level of available calcium in the growing medium, but is more frequently a product of low transpiration of the whole plant or more commonly the affected tissue. Plants are susceptible to such localized calcium deficiencies in low or non-transpiring tissues because calcium is not transported in the phloem. This may be due to water shortages, which slow the transportation of calcium to the plant, poor uptake of calcium through the stem, or too much nitrogen in the soil.

Acidic, sandy, or coarse soils often contain less calcium. Uneven soil moisture and overuse of fertilizers can also cause calcium deficiency. At times, even with sufficient calcium in the soil, it can be in an insoluble form and is then unusable by the plant or it could be attributed to a "transport protein". Soils containing high phosphorus are particularly susceptible to creating insoluble forms of calcium.

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.

Severe zinc deficiency is rare, and is mainly seen in persons with acrodermatitis enteropathica, a severe defect in zinc absorption due to a congenital deficiency in the zinc carrier protein ZIP4 in the enterocyte. Mild zinc deficiency due to reduced dietary intake is common. Conservative estimates suggest that 25% of the world's population is at risk of zinc deficiency. Zinc deficiency is thought to be a leading cause of infant mortality.

Providing micronutrients, including zinc, to humans is one of the four solutions to major global problems identified in the Copenhagen Consensus from an international panel of economists.

The most widely used potassium fertilizer is potassium chloride (muriate of potash). Other inorganic potassium fertilizers include potassium nitrate, potassium sulfate, and monopotassium phosphate. Potassium-rich treatments suitable for organic farming include feeding with home-made comfrey liquid, adding seaweed meal, composted bracken, and compost rich in decayed banana peels. Wood ash also has high potassium content. Adequate moisture is necessary for effective potassium uptake; low soil water reduces K uptake by plant roots. Liming acidic soils can increase potassium retention in some soils by reducing leaching; practices that increase soil organic matter can also increase potassium retention.

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 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.

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.

Potassium deficiency, also known as potash deficiency, is a plant disorder that is most common on light, sandy soils, because potassium ions (K) are highly soluble and will easily leach from soils without colloids. Potassium deficiency is also common in chalky or peaty soils with a low clay content. It is also found on heavy clays with a poor structure.

All plants require sufficient supplies of macronutrients for healthy growth, and nitrogen (N) is a nutrient that is commonly in limited supply. Nitrogen deficiency in plants can occur when organic matter with high carbon content, such as sawdust, is added to soil. Soil organisms use any nitrogen to break down carbon sources, making N unavailable to plants. This is known as "robbing" the soil of nitrogen. All vegetables apart from nitrogen fixing legumes are prone to this disorder.

Nitrogen deficiency can be prevented in the short term by using grass mowings as a mulch, or foliar feeding with manure, and in the longer term by building up levels of organic matter in the soil. Sowing green manure crops such as grazing rye to cover soil over the winter will help to prevent nitrogen leaching, while leguminous green manures such as winter tares will fix additional nitrogen from the atmosphere.

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.

Zinc deficiency in children can cause delayed growth and has been claimed to be the cause of stunted growth in one third of the world's population.

Fertilisers like ammonium phosphate, calcium ammonium nitrate, urea can be supplied. Foliar spray of urea can be a quick method.

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

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.

Iron (Fe) deficiency is a plant disorder also known as "lime-induced chlorosis". It can be confused with manganese deficiency. A deficiency in the soil is rare but iron can be unavailable for absorption if soil pH is not between about 5 and 6.5. A common problem is excessive alkalinity of the soil (the pH is above 6.5). Also, iron deficiency can develop if the soil is too waterlogged or has been overfertilised. Elements like calcium, zinc, manganese, phosphorus, or copper can tie up iron if they are present in high amounts.

Iron is needed to produce chlorophyll, hence its deficiency causes chlorosis. For example, iron is used in the active site of glutamyl-tRNA reductase, an enzyme needed for the formation of 5-Aminolevulinic acid which is a precursor of heme and chlorophyll.

Cobalt poisoning is intoxication caused by excessive levels of cobalt in the body. Cobalt is an essential element for health in animals in minute amounts as a component of Vitamin B. A deficiency of cobalt, which is very rare, is also potentially lethal, leading to pernicious anemia.

Vitamin D natural selection hypotheses:

Rickets is often a result of vitamin D3 deficiency. The vitamin D natural selection hypothesis suggests that vitamin D production from sunlight is a selective force for human skin color variation. The correlation between human skin color and latitude is thought to be the result of positive selection to varying levels of solar ultraviolet radiation. Northern latitudes have selection for lighter skin that allows UV rays to produce vitamin D from 7-dehydrocholesterol. Conversely, latitudes near the equator have selection for darker skin that can block the majority of UV radiation to protect from toxic levels of vitamin D, as well as skin cancer.

An anecdote often cited to support this hypothesis is that Arctic populations whose skin is relatively darker for their latitude, such as the Inuit, have a diet that is historically rich in vitamin D. Since these people acquire vitamin D through their diet, there is not a positive selective force to synthesize vitamin D from sunlight.

Environment mismatch:

Ultimately, vitamin D deficiency arises from a mismatch between a populations previous evolutionary environment and the individual’s current environment. This risk of mismatch increases with advances in transportation methods and increases in urban population size at high latitudes.

Similar to the environmental mismatch when dark-skinned people live at high latitudes, Rickets can also occur in religious communities that require long garments with hoods and veils. These hoods and veils act as sunlight barriers that prevent individuals from synthesizing vitamin D naturally from the sun.

In a study by Mithal et al., Vitamin D insufficiency of various countries was measured by lower 25-hydroxyvitamin D. 25(OH)D is an indicator of vitamin D insufficiency that can be easily measured. These percentages should be regarded as relative vitamin D levels, and not as predicting evidence for development of rickets.

Asian immigrants living in Europe have an increased risk for vitamin D deficiency. Vitamin D insufficiency was found in 40% of non-Western immigrants in the Netherlands, and in more than 80% of Turkish and Moroccan immigrants.

The Middle East, despite high rates of sun-exposure, has the highest rates of rickets worldwide. This can be explained by limited sun exposure due to cultural practices and lack of vitamin D supplementation for breast-feeding women. Up to 70% and 80% of adolescent girls in Iran and Saudi Arabia, respectively, have vitamin D insufficiency. Socioeconomic factors that limit a vitamin D rich diet also plays a role.

In the United States, vitamin D insufficiency varies dramatically by ethnicity. Among males aged 70 years and older, the prevalence of low serum 25(OH) D levels was 23% for non-Hispanic whites, 45% for Mexican Americans, and 58% for non-Hispanic blacks. Among women, the prevalence was 28.5%, 55%, and 68%, respectively.

A systematic review published in the Cochrane Library looked at children up to three years old in Turkey and China and found there was a negative association between vitamin D and rickets. In Turkey children getting vitamin D had only a 4% chance of developing rickets compared to children who received no medical intervention. In China, a combination of vitamin D, calcium and nutritional counseling was linked to a decreased risk of rickets.

With this evolutionary perspective in mind, parents can supplement their nutritional intake with vitamin D enhanced beverages if they feel their child is at risk for vitamin D deficiency,

Exposure to cobalt metal dust is most common in the fabrication of tungsten carbide. Another potential source is wear and tear of metal-on-metal hip prostheses; however, this is a relatively uncommon phenomenon with 18 reported cases being documented in the medical literature.

Boron deficiency is a common deficiency of the micronutrient boron in plants. It is the most widespread micronutrient deficiency around the world and causes large losses in crop production and crop quality. Boron deficiency affects vegetative and reproductive growth of plants, resulting in inhibition of cell expansion, death of meristem, and reduced fertility.

Plants contain boron both in a water-soluble and insoluble form. In intact plants, the amount of water-soluble boron fluctuates with the amount of boron supplied, while insoluble boron does not. The appearance of boron deficiency coincides with the decrease of water-insoluble boron. It appears that the insoluble boron is the functional form while the soluble boron represents the surplus.

Boron is essential for the growth of higher plants. The primary function of the element is to provide structural integrity to the cell wall in plants. Other functions likely include the maintenance of the plasma membrane and other metabolic pathways.

Boric acid (16.5%boron), borax (11.3% boron) or SoluBor (20.5% boron) can be applied to soils to correct boron deficiency. Typical applications of actual boron are about 1.1 kg/hectare or 1.0 lb/acre but optimum levels of boron vary with plant type. Borax, Boric Acid or Solubor can be dissolved in water and sprayed or applied to soil as a dust. Excess boron is toxic to plants so care must be taken to ensure correct application rate and even coverage. Leaves of many plants are damaged by boron; therefore, when in doubt, only apply to soil. Application of boron may not correct boron deficiency in alkaline soils because even with the addition of boron, it may remain unavailable for plant absorption. Continued application of boron may be necessary in soils that are susceptible to leaching such as sandy soils. Flushing soils containing toxic levels of boron with water can remove the boron through leaching.

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.

Maternal deficiencies may be the cause of overt bone disease from before birth and impairment of bone quality after birth. The primary cause of congenital rickets is vitamin D deficiency in the mother's blood, which the baby shares. Vitamin D ensures that serum phosphate and calcium levels are sufficient to facilitate the mineralization of bone. Congenital rickets may also be caused by other maternal diseases, including severe osteomalacia, untreated celiac disease, malabsorption, pre-eclampsia, and premature birth. Rickets in children is similar to osteoporosis in the elderly, with brittle bones. Pre-natal care includes checking vitamin levels and ensuring that any deficiencies are supplemented.

Also exclusively breast-fed infants may require rickets prevention by vitamin D supplementation or an increased exposure to sunlight.

In sunny countries such as Nigeria, South Africa, and Bangladesh, there is sufficient endogenous vitamin D due to exposure to the sun. However, the disease occurs among older toddlers and children in these countries, which in these circumstances is attributed to low dietary calcium intakes due to a mainly cereal-based diet.

Those at higher risk for developing rickets include:

- Breast-fed infants whose mothers are not exposed to sunlight

- Breast-fed infants who are not exposed to sunlight

- Breast-fed babies who are exposed to little sunlight

- Adolescents, in particular when undergoing the pubertal growth spurt

- Any child whose diet does not contain enough vitamin D or calcium