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.

Hypervitaminosis D is a state of vitamin D toxicity. The normal range for blood concentration is 30.0 to 74.0 nanograms per milliliter (ng/mL).

Vitamin D deficiency has become a worldwide health epidemic with clinical rates on the rise. In the years of 2011-12, it was estimated that around 4 million adults were considered deficient in Vitamin D throughout Australia. The Australian Bureau of Statistics (ABS) found 23%, or one in four Australian adults suffer from some form of Vitamin D deficiency. Outlined throughout the article are the causes of increase through subgroups populations, influencing factors and strategies in place to control deficiency rates throughout Australia.

An excess of vitamin D causes abnormally high blood concentrations of calcium, which can cause overcalcification of the bones, soft tissues, heart and kidneys. In addition, hypertension can result.Symptoms of vitamin D toxicity may include the following:

- Dehydration

- Vomiting

- Decreased appetite

- Irritability

- Constipation

- Fatigue

- Muscle weakness

- Metastatic calcification of the soft tissues

Hypervitaminosis D symptoms appear several months after excessive doses of vitamin D are administered. In almost every case, a low-calcium diet combined with corticosteroid drugs will allow for a full recovery within a month. There is a theory that some of the symptoms of vitamin D toxicity are actually due to vitamin K depletion. One animal experiment has demonstrated that co-consumption with vitamin K reduced adverse effects, but this has not been tested in humans.

A vitamin deficiency can cause a disease or syndrome known as an avitaminosis or hypovitaminosis. This usually refers to a long-term deficiency of a vitamin. When caused by inadequate nutrition it can be classed as a "primary deficiency", and when due to an underlying disorder such as malabsorption it can be classed as a "secondary deficiency". An underlying disorder may be metabolic as in a defect converting tryptophan to niacin. It can also be the result of lifestyle choices including smoking and alcohol consumption.

Examples are vitamin A deficiency, folate deficiency, scurvy, vitamin D deficiency, vitamin E deficiency, and vitamin K deficiency. In the medical literature, any of these may also be called by names on the pattern of "hypovitaminosis" or "avitaminosis" + "[letter of vitamin]", for example, hypovitaminosis A, hypovitaminosis C, hypovitaminosis D.

Conversely hypervitaminosis is the syndrome of symptoms caused by over-retention of fat-soluble vitamins in the body.

- Vitamin A deficiency can cause keratomalacia.

- Thiamine (vitamin B1) deficiency causes beriberi and Wernicke–Korsakoff syndrome.

- Riboflavin (vitamin B2) deficiency causes ariboflavinosis.

- Niacin (vitamin B3) deficiency causes pellagra.

- Pantothenic acid (vitamin B5) deficiency causes chronic paresthesia.

- Vitamin B6

- Biotin (vitamin B7) deficiency negatively affects fertility and hair/skin growth. Deficiency can be caused by poor diet or genetic factors (such as mutations in the BTD gene, see multiple carboxylase deficiency).

- Folate (vitamin B9) deficiency is associated with numerous health problems. Fortification of certain foods with folate has drastically reduced the incidence of neural tube defects in countries where such fortification takes place. Deficiency can result from poor diet or genetic factors (such as mutations in the MTHFR gene that lead to compromised folate metabolism).

- Vitamin B12 (cobalamin) deficiency can lead to pernicious anemia, megaloblastic anemia, subacute combined degeneration of spinal cord, and methylmalonic acidemia among other conditions.

- Vitamin C (ascorbic acid) short-term deficiency can lead to weakness, weight loss and general aches and pains. Longer-term depletion may affect the connective tissue. Persistent vitamin C deficiency leads to scurvy.

- Vitamin D (cholecalciferol) deficiency is a known cause of rickets, and has been linked to numerous health problems.

- Vitamin E deficiency causes nerve problems due to poor conduction of electrical impulses along nerves due to changes in nerve membrane structure and function.

- Vitamin K (phylloquinone or menaquinone) deficiency causes impaired coagulation and has also been implicated in osteoporosis

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.

Symptoms include bruising, petechiae, hematomas, oozing of blood at surgical or puncture sites, stomach pains; risk of massive uncontrolled bleeding; cartilage calcification; and severe malformation of developing bone or deposition of insoluble calcium salts in the walls of arteries. In infants, it can cause some birth defects such as underdeveloped face, nose, bones, and fingers.

Vitamin K is changed to its active form in the liver by the enzyme Vitamin K epoxide reductase. Activated vitamin K is then used to gamma carboxylate (and thus activate) certain enzymes involved in coagulation: Factors II, VII, IX, X, and protein C and protein S. Inability to activate the clotting cascade via these factors leads to the bleeding symptoms mentioned above.

Notably, when one examines the lab values in Vitamin K deficiency [see below] the prothrombin time is elevated, but the partial thromboplastin time is normal or only mildly prolonged. This may seem counterintuitive given that the deficiency leads to decreased activity in factors of both the intrinsic pathway (F-IX) which is monitored by PTT, as well as the extrinsic pathway (F-VII) which is monitored by PT. However, factor VII has the shortest half-life of all the factors carboxylated by vitamin K; therefore, when deficient, it is the PT that rises first, since the activated Factor VII is the first to "disappear." In later stages of deficiency, the other factors (which have longer half lives) are able to "catch up," and the PTT becomes elevated as well.

Vitamin K deficiency or hypovitaminosis K is a form of avitaminosis resulting from insufficient vitamin K or vitamin K or both.

Vitamin D plays an important role in which it supports calcium absorption in the body, sustaining good bone health as well as muscle function. When calcium in the body becomes underprovided for normal bodily functions, calcitriol, an active form of Vitamin D, pairs with parathyroid hormone. Together they act to assemble cells in order to increase the calcium stores taken from bone.

The popular term Sunshine vitamin, as it’s often called, is one of the one main sources of achieving sufficient Vitamin D through sunlight on the skin known as D3. The second form is commonly known as D2, which is found in foods such as fatty fish and fortified products like margarine and milk.

Additionally, if you consume vitamin D through your diet, or make vitamin D in your skin from UVB exposure, it is processed through two organs before it becomes activated. Vitamin D is first processed in the liver, before heading to the kidneys where it becomes activated to the form 1-25 dihydroxy vitamin D or alternatively named chemical calcitriol.

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.

Infants with rickets often have bone fractures. This sometimes leads to child abuse allegations. This issue appears to be more common for solely nursing infants of black mothers, in winter in temperate climates, suffering poor nutrition and no vitamin D supplementation. People with darker skin produce less vitamin D than those with lighter skin, for the same amount of sunlight.

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:

Signs and symptoms of rickets can include bone tenderness, and a susceptibility for bone fractures particularly greenstick fractures. Early skeletal deformities can arise in infants such as soft, thinned skull bones – a condition known as craniotabes which is the first sign of rickets; skull bossing may be present and a delayed closure of the fontanelles.

Young children may have bowed legs and thickened ankles and wrists; older children may have knock knees. Spinal curvatures of kyphoscoliosis or lumbar lordosis may be present. The pelvic bones may be deformed. A condition known as rachitic rosary can result as the thickening caused by nodules forming on the costochondral joints. This appears as a visible bump in the middle of each rib in a line on each side of the body. This somewhat resembles a rosary, giving rise to its name. The deformity of a pigeon chest may result in the presence of Harrison's groove.

Hypocalcemia, a low level of calcium in the blood can result in tetany – uncontrolled muscle spasms. Dental problems can also arise.

An X-ray or radiograph of an advanced sufferer from rickets tends to present in a classic way: the bowed legs (outward curve of long bone of the legs) and a deformed chest. Changes in the skull also occur causing a distinctive "square headed" appearance known as "caput quadratum". These deformities persist into adult life if not treated. Long-term consequences include permanent curvatures or disfiguration of the long bones, and a curved back.

Zinc toxicity is a medical condition involving an overdose on, or toxic overexposure to, zinc. Such toxicity levels have been seen to occur at ingestion of greater than 225 mg of zinc. Excessive absorption of zinc can suppress copper and iron absorption. The free zinc ion in solution is highly toxic to bacteria, plants, invertebrates, and even vertebrate fish. Zinc is an essential trace metal with very low toxicity in humans.

Transaldolase deficiency is a disease characterised by abnormally low levels of the Transaldolase enzyme. It is a metabolic enzyme involved in the pentose phosphate pathway. It is caused by mutation in the transaldolase gene (TALDO1). It was first described by Verhoeven et al. in 2001.

Following an oral intake of extremely high doses of zinc (where 300 mg Zn/d – 20 times the US RDA – is a "low intake" overdose), nausea, vomiting, pain, cramps and diarrhea may occur. There is evidence of induced copper deficiency, alterations of blood lipoprotein levels, increased levels of LDL, and decreased levels of HDL at long-term intakes of 100 mg Zn/d. The USDA RDA is 15 mg Zn/d.

There is also a condition called the "zinc shakes" or "zinc chills" or metal fume fever that can be induced by the inhalation of freshly formed zinc oxide formed during the welding of galvanized materials.

Lysosomal acid lipase deficiency (or LAL deficiency or LAL-D), also known as Wolman disease, happens when the body does not produce enough active lysosomal acid lipase (LAL) enzyme. This enzyme plays an important role in breaking down fatty material (cholesteryl esters and triglycerides) in the body. Infants, children and adults that suffer from LAL Deficiency experience a range of serious health problems. The lack of the LAL enzyme can lead to a build-up of fatty material in a number of body organs including the liver, spleen, gut, in the wall of blood vessels and other important organs.

Very low levels of the LAL enzyme lead to LAL Deficiency. LAL Deficiency typically affects infants in the first year of life. The accumulation of fat in the walls of the gut in early onset disease leads to serious digestive problems including malabsorption, a condition in which the gut fails to absorb nutrients and calories from food. Because of these digestive complications, affected infants usually fail to grow and gain weight at the expected rate for their age (failure to thrive). As the disease progresses, it can cause life-threatening liver dysfunction or liver failure.

Until 2015 there was no treatment, and very few infants with LAL-D survived beyond the first year of life. In 2015 an enzyme replacement therapy, sebelipase alfa was approved in the US and EU. The therapy was additionally approved in Japan in 2016.

Boron deficiency is a pathology which may occur in animals due to a lack of boron. A report given by E. Wayne Johnson et al. at the 2005 Alan D. Leman Swine Conference suggests that boron deficiency produces osteochondrosis in swine that is correctable by addition of 50 ppm of boron to the diet. The amount of boron required by animals and humans is not yet well established.

Megaloblastic anemia (MA) is associated with GSE and is believed to be the result of B and folate deficiency. In GSE, it appears to be associated with the IgA-less phenotype. Unlike other forms of megaloblastic anemia, GSEA MA is not a form of autoimmune gastritis.

Pernicious anemia (PA). Pernicious anemia is associated with GSE and is believed to result primarily from malabsorption phenomena.

Iron-deficiency anemia. Iron-deficiency anemia (IDA) may be the only symptom for CD, detected in subclinical CD and is accompanied by a decrease in serum ferritin levels. This can cause addition problems (see:symptoms of IDA and certain conditions like such as Paterson-Brown Kelly (Plummer-Vinson). Whereas IDA is corrected on GF diet, refractory disease or gluten-sensitive malignancies can cause persistent IDA.

There are two different techniques for the diagnosis of Transaldolase deficiency.

Hypercalcemia is suspected to occur in approximately 1 in 500 adults in the general adult population. Like hypocalcemia, hypercalcemia can be non-severe and present with no symptoms, or it may be severe, with life-threatening symptoms. Hypercalcemia is most commonly caused by hyperparathyroidism and by malignancy, and less commonly by vitamin D intoxication, familial hypocalciuric hypercalcemia and by sarcoidosis. Hyperparathyroidism occurs most commonly in postmenopausal women. Hyperparathyroidism can be caused by a tumor, or adenoma, in the parathyroid gland or by increased levels of parathyroid hormone due to hypocalcemia. Approximately 10% of cancer sufferers experience hypercalcemia due to malignancy. Hypercalcemia occurs most commonly in breast cancer, lymphoma, prostate cancer, thyroid cancer, lung cancer, myeloma, and colon cancer. It may be caused by secretion of parathyroid hormone-related peptide by the tumor (which has the same action as parathyroid hormone), or may be a result of direct invasion of the bone, causing calcium release.

Symptoms of hypercalcemia include anorexia, nausea, vomiting, constipation, abdominal pain, lethargy, depression, confusion, polyuria, polydipsia and generalized aches and pains.

Thromboembolism is a well-described complication of IBD, with a clinical incidence of up to 6% and a three-fold higher risk of disease, and the Factor V Leiden mutation further increases the risk of venous thrombosis. Recent studies describe the co-occurrence between coeliac disease, in which IBD is common in venous thrombosis.

Hypocalcemia is common and can occur unnoticed with no symptoms or, in severe cases, can have dramatic symptoms and be life-threatening. Hypocalcemia can be parathyroid related or vitamin D related. Parathyroid related hypocalcemia includes post-surgical hypoparathyroidism, inherited hypoparathyroidism, pseudohypoparathyroidism, and pseudo-pseudohypoparathyroidism. Post-surgical hypoparathyroidism is the most common form, and can be temporary (due to suppression of tissue after removal of a malfunctioning gland) or permanent, if all parathyroid tissue has been removed. Inherited hypoparathyroidism is rare and is due to a mutation in the calcium sensing receptor. Pseudohypoparathyroidism is maternally inherited and is categorized by hypocalcemia and hyperphosphatemia. Finally, pseudo-pseudohypoparathyroidism is paternally inherited. Patients display normal parathyroid hormone action in the kidney, but exhibit altered parathyroid hormone action in the bone.

Vitamin D related hypocalcemia may be associated with a lack of vitamin D in the diet, a lack of sufficient UV exposure, or disturbances in renal function. Low vitamin D in the body can lead to a lack of calcium absorption and secondary hyperparathyroidism (hypocalcemia and raised parathyroid hormone). Symptoms of hypocalcemia include numbness in fingers and toes, muscle cramps, irritability, impaired mental capacity and muscle twitching.