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Vitamin D (Calciferol)

Nutrient Names: Vitamin D, calciferol.
Synonyms: 1,25-Dihydroxyvitamin D, calciferol, calcipotriol, cholecalciferol (vitamin D3), ergocalciferol (vitamin D2), irradiated ergocalciferol, ergosterol (provitamin D2), activated/irradiated ergosterol (vitamin D2).
Related Substance: Calcitriol is also the name of a drug that is the active (1,25-dihydroxycholecalciferol) form of vitamin D.

Summary Table
nutrient description

Chemistry and Forms

Vitamin D is the generic term for compounds that exhibit the biological activity of calciferol: vitamin D2(ergocalciferol), vitamin D3(cholecalciferol), 1α(OH)D3(alfacalcidol), 25(OH)D3(calcifediol, calcidiol), 1,25(OH)2D3(calcitriol), and dihydrotachysterol.

Physiology and Function

Vitamin D functions as both a fat-soluble vitamin and a hormone. From dietary sources, vitamin D is absorbed from the small intestine in the presence of bile and is transported into the circulation via the lymph in chylomicrons (similar to vitamin A transport). Vitamin D can also be synthesized in the skin as a result of direct exposure to the ultraviolet light in sunlight (UVB radiation) through the conversion of 7-dehydrocholesterol to cholecalciferol (vitamin D3). This ability of animals to produce vitamin D from a cholesterol derivative makes the nutrient a “conditionally essential” vitamin. On entering the circulation from either the diet or the skin, vitamin D3is bound to the vitamin D–binding protein and transported to the liver. Two successive hydroxylations of vitamin D, first in the liver (to 25-hydroxycholecalciferol) and then in the kidneys, produce the hormonally active form, calcitriol, or 1,25-dihydroxycholecalciferol (1,25-dihydroxyvitamin D3), in coordination with the parathyroid glands and calcium-sensitive parathyroid hormone (PTH, parathormone) secretion.

Calcitriol binds to the vitamin D receptor (VDR), a nuclear transcription factor that regulates gene expression. When the calcitriol/VDR complex subsequently combines with the retinoic acid X receptor (RXR), the resulting VDR/RXR heterodimer can interact with the vitamin D–responsive elements (VDREs) within the DNA. This interaction between the VDR/RXR heterodimer and a VDRE alters the rate of transcription of a related gene and thereby regulates the activity of vitamin D–dependent calcium transporters in the small intestine, osteoblasts in bone, and the 1-hydroxylase enzyme in the kidneys. Defects in the vitamin D receptor lead to hypocalcemic vitamin D–resistant rickets, congenital total lipodystrophy, and persistent müllerian duct syndrome. Research suggests that bone may be more responsive to exercise in some genotypes of VDR than in others, 1 and that gene-environment interactions such as leisure physical activity and VDR genotype may play a role in maintaining the bone mineral density (BMD) at the lumbar spine in active postmenopausal women, especially in older active women. 2

The vitamin D endocrine system is responsible for maintaining tight regulation of serum calcium levels within the narrow range critical to bone metabolism and healthy functioning of the nervous system. Calcitriol mediates the intestinal absorption and blood levels of calcium and phosphorus. It facilitates mineral deposition into bone, modulates bone mineralization and demineralization, and enhances muscle strength and balance. Vitamin D is necessary to calcium absorption and increases the absorption of calcium from the intestine (by stimulating the synthesis of calcium-binding protein and the epithelial calcium channel) and maintains serum calcium levels in the normal range; thus increasing resorption of calcium from bone as well as facilitating calcium storage in the bones. Consequently, even though it initially causes bone resorption, the net effect is to increase calcium deposition in the bone. In addition to promoting calcium absorption, calcitriol mediates the intestinal absorption of phosphorus, possibly magnesium and zinc as well, and may promote renal tubule phosphate resorption. Vitamin D is stored in body fat.

Vitamin D also plays many important roles in hormonal regulation and immune function. It helps maintain adequate blood levels of insulin and may assist the metabolism of sugar. Vitamin D may also assist healthy thyroid function, and the active form of vitamin D3may have a mechanism of action similar to thyroid hormone. Vitamin D and VDRs participate in the regulation of cell growth and development, particularly white blood cells and epithelial cells. In particular, the presence of VDRs in T lymphocytes suggests that vitamin D facilitates the development, activity, and response of T cells against antigens (and in autoimmune disorders).

nutrient in clinical practice

Known or Potential Therapeutic Uses

Vitamin D is used to prevent osteoporosis and osteoporotic fractures, and intake is associated with reduced risk of breast cancer, colorectal cancer, prostate cancer, as well as cancers of the lung, skin (melanoma), colon, and bone. Administration of vitamin D in conjunction with bisphosphonate therapy (e.g., alendronate, risedronate, or etidronate) or exogenous hormone therapy (e.g., HRT) may enhance clinical outcomes in preventing and treating osteoporosis. A range of autoimmune diseases, particularly type 1 diabetes mellitus, rheumatoid arthritis, and multiple sclerosis, may be responsive to integrative therapeutics employing vitamin D, especially when they involve a VDR gene polymorphism. Calcitriol, the active metabolite of vitamin D, has been found to inhibit the growth of human prostate cancer cells in vitro; however, findings from preliminary human trials have been disappointing for its use (or that of analogs) as part of innovative protocols in the treatment of hormone-refractory prostate cancer.

Historical/Ethnomedicine Precedent

The physiological parameters of vitamin D may be premised on the ancient origins of humans in equatorial Africa. The high level of exposure to sun inherent to such an interaction with the environment may play a fundamental role in the high susceptibility for insufficiency or deficiency among modern humans less exposed to the sun, especially for dark-skinned individuals, because melanin acts as an ultraviolet absorber.

Possible Uses

Atherosclerosis, autoimmune diseases, breast cancer, burns, cancer prevention, celiac disease, digestive system cancers (oral, esophageal, stomach, pancreas, colorectal; risk reduction, especially in individuals with dark skin), Crohn's disease, depression (particularly seasonal affective disorder), diabetes mellitus, epilepsy, falls (prevention, especially in the elderly), fractures (especially in the elderly), hearing loss, hyperparathyroidism (secondary), hypertension, hypoparathyroidism, migraine headaches, multiple sclerosis, obesity, osteoarthritis, osteomalacia, osteoporosis, prevention of vitamin D deficiency, prostate cancer, psoriasis, rheumatoid arthritis (risk reduction), rickets, scleroderma, skin cancer (risk reduction), tuberculosis.

Deficiency Symptoms

Rickets, osteomalacia, osteoporosis, and fracture risk remain the most obvious and well-known outcomes associated with vitamin D deficiency. Researchers have increasingly expressed concern that the low levels of vitamin D found in a large percentage of Americans and Europeans may be associated with increased risk of a range of conditions, including cancer, heart disease, hypertension, diabetes, multiple sclerosis, and diminished immune status. The classic groups known for increased risk of deficiency are breast-fed infants, individuals on vegetarian diets, the elderly, individuals with fat malabsorption or chronic kidney disease, and individuals with compromised sun exposure due to lifestyle, climate, season, or cultural practices. Other significant etiologies include alcoholism, burns (and burn scarring), Crohn's disease, Cushing's disease, dark skin, decreased consumption of vitamin D, hypothyroidism, anticonvulsant drug therapy, kidney or liver disease, malabsorption (as in celiac disease or after intestinal surgery), ulcerative colitis, and vitamin D–resistant rickets. Vitamin D receptor polymorphic alleles have been linked to diabetes mellitus and colon cancer. 3,4Low dietary calcium intake may enhance the phenotypic expression of VDR gene polymorphisms. 5

Awareness of previously unrecognized vitamin D deficiency and its implications in long-term pathological processes has been growing in recent years. 6,7Chapuy et al. 8 (1997) reported that one of seven adults may be deficient in vitamin D. Similarly, a study in 1998 by Thomas et al. 9 found that 37% of the total group surveyed were deficient in vitamin D, even though their reported diets should have provided the currently recommended levels of vitamin. This study also found that 42% of hospitalized patients under age 65 were deficient in vitamin D. Overall, vitamin D inadequacy has been reported in up to 57% of general medicine inpatients in the United States. 10 Spanish researchers found that healthy postmenopausal women in modern societies have an extremely high prevalence of vitamin D deficiency. 11 Likewise, young adults exhibit an unexpectedly high incidence of vitamin D insufficiency. 12 Vitamin D deficiencies may also raise the risk of prostate cancer by disrupting the relationship between androgens and VDR in prostate cells. 13

Dietary Sources

Cod liver oil, oily cold-water fish (salmon, mackerel, herring), butter, egg yolks, vitamin D–fortified milk, and orange juice.

Most vitamin D in humans is derived from endogenous synthesis subsequent to sun exposure rather than from dietary sources. Vitamin D is found primarily in foods of animal origin, unless they are fortified. Cod liver oil is considered an excellent dietary source. Vegetables are usually low in vitamin D, although mushrooms, if irradiated, can be a significant source of vitamin D. Milk used to make cheese or yogurt is usually not fortified with vitamin D. Human milk contains the 25-hydroxycholecalciferol form of D, possibly to compensate for the limited ability of the liver in infants to achieve the first hydroxylation of cholecalciferol. The vitamin D content in human milk varies with maternal sun exposure and vitamin D intake.

Sunshine

With exposure to ultraviolet light, the skin synthesizes vitamin D. It is estimated that 20 minutes, with face and arms exposed, will stimulate about 600 to 1000 IU per day, during spring, summer, and fall in temperate regions, and year-round in tropical and subtropical regions. Enough sun or UVB exposure to produce minimal skin erythema (known as the minimal erythemic dose ) can produce 10,000 to 20,000 IU in about an hour. Adequate amounts of vitamin D can theoretically be synthesized and stored in fat to carry an individual through the winter. In temperate latitudes, above 35° to 50°, a minimum of 15 minutes of sun exposure on the arms, face, and hands three times per week in the morning or late afternoon during the spring, summer, and fall is needed to avoid vitamin D deficiency at the end of winter. However, research indicates that, in actuality, many individuals in higher latitudes, especially with seasonal clothing, overcast climates, and minimal time outdoors, do not receive adequate sun exposure to avoid compromised vitamin D status. Sun exposure with sunscreen significantly prevents skin synthesis of vitamin D.

Dosage Forms Available

Capsules, injection (IM), liquid, tablets. Intramuscular (IM) form is not available in the United States.

Oral dosing (with meals) is preferred, but malabsorption associated with gastrointestinal, liver, or biliary disease may necessitate IM injection.

Nutrient Preparations Available

Cholecalciferol (vitamin D3) is more potent and bioavailable than ergocalciferol (D2).

Dosage Range

Adult

Dietary: The adequate intake of vitamin D (cholecalciferol, or vitamin D3) is 5 µg (200 IU) per day for adults age 19 to 50 years, 10 µg (400 IU) for adults age 51 to 70 years, and 15 µg (600 IU) for adults 71 years and older.

Supplemental/Maintenance: 10 µg (400 IU) per day. However, in some cases this may be unnecessary, given consistent adequate direct exposure to the sun, usually 20 minutes per day. Supplement with cod liver oil if 25(OH)D levels are low (1 tsp per 50 pounds of body weight). One tablespoon of cod liver oil provides approximately 1200 IU (30 µg) of vitamin D3.

A dose of 20 µg (800 IU) per day for individuals, especially the elderly, not adequately exposed to sunlight or living in farther northern or southern latitudes.

Pharmacological/Therapeutic: 800 to 2000 IU per day, including dietary sources, under supervision of a physician or health care professional experienced in nutritional therapeutics. 14,15Dosages used in clinical studies range from 5 µg (200 IU) to 250 µg (10,000 IU) daily. Significantly higher doses are often used in the treatment of secondary hypoparathyroidism, vitamin D–resistant rickets, nutritional rickets and osteomalacia, and familial hypophosphatemia.

Toxic: The current official tolerable upper intake level (UL) is 50 µg (2000 IU) per day. However, many experts in the field strongly support raising the UL to at least 4000 IU, and 10,000 IU may be tolerable for most individuals, but such a daily dose should be medically monitored.

Adverse effects have been reported at concentrations ranging from 250 to 1250 µg (10,000-50,000 IU) per day.

Pediatric (<18 years)

Dietary: The adequate intake (AI) of vitamin D (cholecalciferol, or vitamin D3) is 5 µg (200 IU) per day for infants and children up to 18 years.

Supplemental/Maintenance: One teaspoon of cod liver oil per 50 lb/wt. Sun exposure of 20 minutes daily is adequate and preferable. Do not give cod liver oil when sun exposure is being implemented.

Pharmacological/Therapeutic

  • Premature infants: 10 to 20 µg (400-800 units) per day, up to 750 µg (30,000 IU) per day.
  • Infants and healthy children: 10 µg (400 IU) per day.

Significantly higher doses are often used in the treatment of hypoparathyroidism, nutritional rickets and osteomalacia, vitamin D–resistant rickets, and familial hypophosphatemia. Vitamin D receptor defects, specifically tissue resistance to vitamin D, or vitamin D–dependent rickets (VDDR), are usually treated with 20 µg/day of the bioactive form, calcitriol, or 5 mg/day of the dietary form, vitamin D2, plus oral calcium and phosphate. 16

Toxic: UL for infants (0-12 months) is 25 µg (1000 IU) per day and for children (1-18 years) is 50 µg (2000 IU) per day.

Note: Requirements depend on the exposure of a person's skin to ultraviolet radiation. The intensity of exposure is also a factor. The latitude determines how much exposure to sunlight the person requires to synthesize adequate levels of vitamin D. Pollution, clouds, and skin color also affect an individual's ability to produce vitamin D. The darker the skin, the less vitamin D will be produced (up to 95% blocked). However, with longer exposure times, even with the darkest skin color, sufficient levels of vitamin D are produced. Glass and topical sunscreens block UV light.

Laboratory Values

Laboratory assessment of vitamin D status has been in a state of controversy and evolution in recent years, particularly since the effects of mild vitamin D deficiency or insufficiency have become more widely recognized.

Plasma 25(OH)-Vitamin D

This assay reflects body reserves. Plasma levels less than 25 nmol/L indicate deficiency.

However, results from laboratories doing 25-hydroxyvitamin D (25-OHD) tests vary widely. 17 Reference ranges from most labs are too low. Optimal serum levels of 25-OHD to avoid increases in PTH are at least 20 ng/mL, 18 but may actually be in the range of 45 to 55 ng/mL (115-140 nmol/L). Heaney et al. 19,20suggest that the appropriate serum 25-OHD level is 32 ng/mL. 8 Concurrent parathyroid tests (PTH) may elucidate equivocal laboratory findings because one could expect a high PTH if there is a low vitamin D concentration in the blood.

Plasma 1,25(OH)2-Vitamin D

This assay measures the active form of the vitamin. As 25-OHD levels drop, PTH secretion increases (secondary hyperparathyroidism), which maintains the 1,25(OH)2-vitamin D level in the normal range. For this reason, measuring the 25-OHD level is necessary to diagnose vitamin D deficiency or insufficiency. Normal 1,25(OH)2D levels are 48 to 100 pmol/L.

Also, measure serum calcium, blood urea nitrogen (BUN), and phosphorus every 1 to 2 weeks; and monitor bone density regularly until stabilized.

Serum calcium concentration times phosphorus concentration should not exceed 70 mg/dL to avoid ectopic calcification; ergocalciferol levels: 10 to 60 ng/mL; serum calcium: 9 to 10 mg/dL; phosphorus: 2.5 to 5.0 mg/dL.

safety profile

Overview

Vitamin D is generally well tolerated, and excessive doses from sunlight exposure or dietary source are considered highly improbable, if not impossible. Its UL of 50 µg (2000 IU) per day reflects that vitamin D has long been considered the most likely of all vitamin supplements to cause toxicity. Although a revised consensus has developed in recent years among researchers and some clinicians, regulatory and institutional guidelines are only gradually beginning to respond to and integrate the new data into their recommendations.

Adverse effects have been reported at concentrations ranging from 250 to 1250 µg/daily. 21 Hypervitaminosis D has generally been associated with intake of 625 to 1500 µg (25,000-60,000 IU) daily for 1 to 4 months, or several years of vitamin D supplementation at 250 to 1250 µg (10,000-50,000 IU) daily, and has never been associated with sun exposure. Published case reports of vitamin D toxicity with hypercalcemia, for which the 25(OH)D concentration and vitamin D dose are known, all involve intake of at least 1000 µg (40,000 IU) per day, and only one case occurred at a level of intake under 40,000 IU/day. 14

However, emerging evidence and the opinions of many vitamin D researchers now suggest that the daily value (DV) of 400 IU for vitamin D, which was based on the amount necessary to prevent rickets in infants (initially given as 5 mL of cod liver oil 100 years ago) is an order of magnitude below the amount necessary for older adults, and those not exposed to sun without sunscreen on a regular basis, to achieve and maintain blood levels of vitamin D that are optimum for bone health and cancer prevention. 15,22-33“Estimates of the population distribution of serum 25(OH)D values, coupled with available dose-response data, indicate that it would require input of an additional 2600 IU/d (65 mcg/d) of oral vitamin D3to ensure that 97.5% of older women have 25(OH)D values at or above desirable levels.” 34 Absent lymphoma or granulomatous disease, which can cause vitamin D sensitivity, it appears that long-term ingestion of greater than 10,000 IU/day is necessary to cause vitamin D toxicity and hypercalcemia.

Nutrient Adverse Effects

General Adverse Effects

Excessive levels of vitamin D intake over an extended period can lead to headaches, kidney stones, and weight loss. Less common symptoms include diarrhea, increased thirst, increased urination, irritability, and failure to gain weight in children. More extreme consequences include blindness, deafness, and potentially death. Elevated vitamin D levels (as well as vitamin D deficiency) may be related to increased risk of prostate cancer. 35 Vitamin D intake increases both calcium and phosphorus absorption. Although the increased levels of calcium associated with enhanced vitamin D status may be an indicator of benefit for those at risk for bone loss, elevated blood levels of calcium may also be associated with increased risk of heart disease. Elevated serum calcium levels induced by hypervitaminosis D are responsible for many of its primary adverse effects.

Acute overdose is associated with increased urinary frequency, nausea, vomiting, loss of appetite, diarrhea, muscle weakness, dizziness, and calcification of heart, blood vessels, and lungs; symptoms reverse after overdosing is discontinued.

Adverse Effects Among Specific Populations

Individuals with sarcoidosis, other granulomatous diseases, and certain types of lymphoma may quickly develop elevated levels of 1,25(OH)2-vitamin D3(the activated form), if supplemented with cholecalciferol or other vitamin D precursor, because of autonomous conversion of 25-OHD to the active hormone, 1,25(OH)2D. Elevated levels of activated vitamin D significantly increase risk of hypercalcemia, which might require treatment with hydration, intravenous bisphosphonates, ketoconazole, hydroxychloroquine (Plaquenil), and corticosteroids, as well as avoidance of dietary sources of vitamins D2and D3and calcium.

Pregnancy and Nursing

Vitamin D enters breast milk and is considered compatible at usual dosage levels.

Infants and Children

Vitamin D intakes of 50 to 75 µg (2000-3000 IU) per day may cause toxicity symptoms in some children. Also, some hypersensitive infants have developed toxicity symptoms at 1000 IU/day.

Most cases of toxicity involve the intake of 625 to 1500 µg (25,000-60,000 IU) per day for 1 to 4 months.

Children taking 250 µg (10,000 IU) per day for 4 months can develop the following toxicity symptoms, related to hypercalcemia: headaches, weakness, nausea and vomiting, constipation, polyuria, polydipsia, diarrhea, and calcification of soft tissues, such as kidneys, lungs, tympanic membrane, or ears.

Contraindications

Hypercalcemia, hyperparathyroidism (primary), hypersensitivity to cholecalciferol or any component of the formulation, malabsorption syndrome, sarcoidosis, granulomatous disease, lymphoma; evidence of vitamin D toxicity. If vitamin D insufficiency or deficiency is documented in a patient with lymphoma, cautious supplementation of vitamin D3with monitoring of blood levels of both forms of vitamin D and calcium may be undertaken. Not all lymphomas will autonomously convert 25-OHD to its activated form, and no predictive tests yet exist for this capability. Successful treatment of the lymphoma with a complete response obviates the risk of vitamin D hyperconversion. Vitamin D sufficiency may decrease risk of relapse in treated lymphoma patients because vitamin D deficiency is associated with increased risk of developing the disease (along with several other cancers, including breast, colon, and prostate).

Precautions and Warnings

  • Administer with extreme caution in patients with impaired renal function, heart disease, renal stones, or arteriosclerosis.
  • Administer concomitant calcium supplementation.
  • Maintain adequate fluid intake.
  • Avoid hypercalcemia, although not likely in absence of 1,25(OH)2-vitamin D3excess.

Caution may be appropriate with renal function impairment with secondary hyperparathyroidism. However, impaired renal function is often associated with a need to administer prescription vitamin D as well as D3because second hydroxylation of the 25-OH form is lacking. Furthermore, secondary hyperparathyroidism is an indication for D3therapy.

interactions review

Strategic Considerations

Several classes of common pharmacological agents interact with vitamin D and its metabolic processes. These interactions take on greater significance in light of the elevated probability of vitamin D deficiency in many of the patient populations likely to be prescribed the medications under consideration. More broadly, the occurrence of vitamin D deficiency has been recognized as being more widespread than previously believed, and in turn the implications of vitamin D insufficiency for health maintenance and disease prevention have become better understood. Thus, although conventional medical practice and governmental nutritional policies have focused on prevention of short-latency deficiency diseases, vitamin D represents a prime example of the growing awareness of the central role of nutritional factors in health maintenance and prevention of long-latency deficiency diseases. Factors such as lack of time outdoors with significant sunlight exposure, air pollution, cultural practices, and geographic population distribution all add to the subtle but profound significance of seasonal decrease in sunlight availability, even in areas generally considered as “sunny.” 7,9,11,36,37The combined effect of these many factors contributes to what some experts have described as an “epidemic” of vitamin D deficiency, affecting 20% to 60% of the population.

The issues of pervasive vitamin D deficiency status and underutilization of laboratory assessment for 25-hydroxyvitamin D levels influence and limit research design, interpretation, and clinical practice within conventional medicine. For example, in 2005, two randomized controlled trials of calcium carbonate and cholecalciferol (vitamin D3) administration for prevention of fractures in primary care reported widely publicized conclusions that such nutrient supplementation provided no value in preventing fractures. 38,39Such declarations were made despite disclosures that (1) vitamin D levels had been tested in only a small sample of the subjects in one of the studies; (2) vitamin D deficiency appeared to be common within the subject populations, as indicated by responses to vitamin D supplementation; (3) quality control of the supplements was very poor, and compliance was marginal and declined over time (e.g., 63%, or as low as 45%); and (4) the use of calcium carbonate in a population of older and often hypochlorhydric subjects would be considered suboptimal by many, if not most, experienced practitioners of nutritional therapeutics. Digestion of calcium carbonate relies on the integrity of gastric function and the bowel culture to produce the ionizing acids. Thus, gastrointestinal adverse effects, typical of calcium carbonate, were cited as a major factor in greater noncompliance with calcium intake.

In the study in which 1% of the subjects had their vitamin D levels actually measured, there was only a marginal increase after 1 year of supplementation with 800 IU of vitamin D per day (although some supplements, when analyzed, contained as little as 372 IU, mean value, per tablet). Average 25-OHD levels at beginning of the study (15 ng/mL) were in the range of severe deficiency and after 1 year improved only to 24 ng/mL, still well below what many vitamin D researchers consider to be adequate levels (30-40 ng/mL). 40

Subsequently, in a trial involving 944 healthy Icelandic adults, Steingrimsdottir et al. 41 found that with 25-OHD levels below 10 ng/mL, maintaining calcium intake above 800 mg/day appeared to normalize calcium metabolism, as determined by the PTH level, but in individuals with higher 25-OHD levels, no benefit was observed from calcium intake above 800 mg/day. Likewise, Jackson et al. 42 found that the combination of 1000 mg elemental calcium (as calcium carbonate) and 400 IU vitamin D daily did not appreciably reduce risk of hip fracture over 7 years, except in those who took their nutrients regularly. Thus, among adherent women (i.e., those who followed the treatment protocol 80% of the time), the supplements reduced hip fractures by 29%. Nevertheless, the relatively low dose of vitamin D, the use of calcium carbonate (a less-than-optimal form in the opinion of many and one associated with reduced compliance), and the late start and relatively limited duration of supplementation suggest that the treatment protocol was less than adequate (unless consistently adhered to) and thus render these findings less than conclusive. Such studies also indicate the importance of nutrient support throughout adulthood, as opposed to beginning it past midlife. Clearly, further research on calcium and other minerals involved in bone metabolism needs to take into account, and preferably optimize, vitamin D status.

Notably, the main conventional pharmacological intervention against osteoporosis is antiresorptive drugs, such as bisphosphonates, for which almost every clinical trial has included coadministration of calcium or vitamin D. Moreover, the decontextualization and narrow focus of these studies highlight the shortcomings of standard research methodology and clinical practice to account for the broad factors of aging, lifestyle, activity level, drug depletions, and poor nutritional status characteristic of the populations in question, as well as the complex nature of bone health and its reliance on interdependencies of multiple nutrients and tissues, rather than such a narrow focus on supplemental calcium and vitamin D. As public and practitioner attention on vitamin D grows, it may prove a pivotal issue in expanding perceptions and awareness, analysis, and intervention through a broad integrative model more accurately reflecting patient needs and scientifically comprehending the breadth and complexity of the processes involved. 14,24,28,37

The well-known interactions between vitamin D and pharmaceutical medications cluster into several main groups. The use of calcium and vitamin D appears to enhance the bone-maintaining effectiveness of hormone replacement therapy (HRT) and bisphosphonates, especially for women who already have osteoporosis; this benefit appears greater for women supplementing with calcium citrate than for those using calcium carbonate. Anticonvulsants, particularly phenobarbital and phenytoin, may reduce serum levels of calcidiol (25-hydroxycholecalciferol, calcifediol) by altering hepatic metabolism of vitamin D. Notably, physicians prescribing agents that impair vitamin D function for extended periods (e.g., anticonvulsants, opioids, oral cortiocosteroids) usually do not advise or prescribe adequate countermeasures, whether vitamin D and calcium, bisphosphonates, or the combination, to effectively address the common occurrence of drug-induced decreases in bone mineral density and increased risk of fracture. 43,44Numerous medications that alter fat absorption, such as cholestyramine, colestipol, mineral oil, orlistat, and olestra, can interfere with intestinal absorption of vitamin D. Ketoconazole can reduce serum levels of calcitriol. Conversely, excessive vitamin D intake may, in rare cases, induce hypercalcemia and could theoretically precipitate cardiac arrhythmia in patients receiving cardiovascular medications such as verapamil or digoxin. Moreover, cardiac glycosides could potentially increase toxicity. Thiazide diuretics may increase vitamin D effects. Finally, it is now recognized that cholecalciferol inhibits CYP2C8/9, 2C19, and 2D6, although the full implications of such activity and the potential effects on pharmaceuticals metabolized by these enzymes have yet to be fully investigated and documented.

Because vitamin D toxicity from supplemental sources is a real (though improbable) possibility, health care providers are reminded to counsel their patients to avoid taking more than the recommended amount of vitamin D, and to take it in conjunction with a calcium supplement and possibly a special diet. The encouragement of greater exposure to sunlight (outdoors) cannot be overemphasized. Although contrary to prevailing dogma of the past decade and as yet poorly studied, it is becoming increasingly evident that use of high-potency sunscreens that block UVB may significantly contribute to vitamin D deficit. Oral supplementation can be used to compensate for lack of adequate UV exposure from sunlight. However, significantly higher amounts of supplementation may be necessary than previously believed and currently available in most vitamin preparations. Titrating intake to blood level of 25-OHD is the most reliable way to ensure adequate intake.

Although some innovative therapeutic strategies are emerging using vitamin D analogs, most examples of such approaches are considered separately in a brief review later.

nutrient-drug interactions
Allopurinol
Androgen-Deprivation Therapy
Anticonvulsant Medications, Including Phenobarbital, Phenytoin, and Valproic Acid
Bisphosphonates
Calcitriol and Vitamin D Analogs
Cholestyramine, Colestipol, and Related Bile Acid Sequestrants
Cimetidine
Corticosteroids, Oral, Including Prednisone
Hormone Replacement Therapy (HRT): Estrogen-Containing and Synthetic Estrogen and Progesterone Analog Medications
Heparin, Unfractionated
Isoniazid and Related Antitubercular Agents
Ketoconazole
Neomycin
Orlistat
Raloxifene
Rifampin
Thiazide Diuretics
Thioridazine
Verapamil and Related Calcium Channel Blockers
Calcitriol and Vitamin D Analogs
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Antacids, Especially Magnesium-Containing Antacids
Calcitonin
Digoxin
Doxorubicin
Flurbiprofen
Hydroxychloroquine
Indapamide

Indapamide (Lozol).

Indapamide is a thiazide-like diuretic, but evidence is lacking as to whether it might enhance the activity of vitamin D in the manner of thiazide diuretics and whether such interaction might rise to the level of clinical significance. Pending clarification by controlled clinical trials, physicians prescribing indapamide are advised to discuss the potential effects of vitamin D supplementation with patients and closely supervise and regularly monitor calcium and vitamin D status in individuals for whom such supplementation may be appropriate for comorbid conditions.

Mineral Oil
Sodium Fluoride
Sucralfate
Warfarin
nutrient-nutrient interactions
Boron
Caffeine
Calcium
Phosphorus
Sodium
Vitamin A
Citations and Reference Literature
  • 1.Tsuritani I, Brooke-Wavell KS, Mastana SS et al. Does vitamin D receptor polymorphism influence the response of bone to brisk walking in postmenopausal women? Horm Res 1998;50:315-319.
  • 2.Blanchet C, Giguere Y, Prud’homme D et al. Association of physical activity and bone: influence of vitamin D receptor genotype. Med Sci Sports Exerc 2002;34:24-31.
  • 3.Slatter ML, Yakumo K, Hoffman M, Neuhausen S. Variants of the VDR gene and risk of colon cancer (United States). Cancer Causes Control 2001;12:359-364.View Abstract
  • 4.Motohashi Y, Yamada S, Yanagawa T et al. Vitamin D receptor gene polymorphism affects onset pattern of type 1 diabetes. J Clin Endocrinol Metab 2003;88:3137-3140.View Abstract
  • 5.Marc J, Prezelj J, Komel R, Kocijancic A. Association of vitamin D receptor gene polymorphism with bone mineral density in Slovenian postmenopausal women. Gynecol Endocrinol 2000;14:60-64.View Abstract
  • 6.Heaney RP. Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr 2003;78:912-919.View Abstract
  • 7.Plotnikoff GA. Vitamin D: the steroid hormone prescription for every patient. Minn Med 2003;86:43-45.View Abstract
  • 8.Chapuy MC, Preziosi P, Maamer M et al. Prevalence of vitamin D insufficiency in an adult normal population. Osteoporos Int 1997;7:439-443.View Abstract
  • 9.Thomas MK, Lloyd-Jones DM, Thadhani RI et al. Hypovitaminosis D in medical inpatients. N Engl J Med 1998;338:777-783.View Abstract
  • 10.Holick MF. High prevalence of vitamin D inadequacy and implications for health. Mayo Clin Proc 2006;81:353-373.View Abstract
  • 11.Mezquita-Raya P, Munoz-Torres M, Luna JD et al. Relation between vitamin D insufficiency, bone density, and bone metabolism in healthy postmenopausal women. J Bone Miner Res 2001;16:1408-1415.
  • 12.Tangpricha V, Pearce EN, Chen TC, Holick MF. Vitamin D insufficiency among free-living healthy young adults. Am J Med 2002;112:659-662.
  • 13.Tuohimaa P, Lyakhovich A, Aksenov N et al. Vitamin D and prostate cancer. J Steroid Biochem Mol Biol 2001;76:125-134.View Abstract
  • 14.Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr 1999;69:842-856.View Abstract
  • 15.Vieth R, Chan PC, MacFarlane GD. Efficacy and safety of vitamin D3 intake exceeding the lowest observed adverse effect level. Am J Clin Nutr 2001;73:288-294.View Abstract
  • 16.Hewison M, O’Riordan JL. Hormone-nuclear receptor interactions in health and disease: vitamin D resistance. Baillieres Clin Endocrinol Metab 1994;8:305-315.
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