|Article||Vitamin D: Believe the hype, IHP, March 2008|
|Article||The Most Recent Vitamin D Research, NMJ, , 2012 March|
|Article||The role of vitamin D3 in autoimmune disorders ,2008 Winter/Spring Vital Link|
Vitamin D is a fat-soluble micronutrient. By definition, it is really more of a hormone than a vitamin because it is produced in the body, but nonetheless it is considered a vitamin. Vitamin D3 is made in the body after exposure to ultraviolet light. After sunlight changes the precursor vitamin D into vitamin D3 (cholecalciferol) it is transported to the liver where it undergoes a second conversion, yielding a more potent form of vitamin D. It is then transported to the kidney to be converted to the most potent form of vitamin D known as 1,25-dihydryoxycholecalciferol (1,25-(OH)2D3). Kidney and liver dysfunction can impair conversion of vitamin D to its active forms. Due to the importance of ultraviolet light in its conversion, the further one lives from the equatorial regions, the more dependent one becomes on exogenous vitamin D3 sources such as dietary sources and supplementation.
The following foods have the highest concentration of vitamin D. For a more expansive list on food sources of specific nutrients visit Health Canada's Dietary Reference Intakes for Vitamins or USDA's National Nutrient Database
Other food sources include:
Uses and Associated Conditions
The following are the primary uses of Vitamin D.
- Rickets and Subclinical Rickets: Rickets is a form of vitamin D3 deficiency that may be found in children. Symptoms of subclinical rickets include: head sweating, hair tenderness (noticed when hair is brushed), and legs giving out. Deficiency of vitamin D can be caused by dairy allergies, strict vegetarianism, excessive sunscreen use, or decreased sun exposure. Both a lack of dietary calcium and vitamin D3 are responsible.
- Osteomalacia: Osteomalacia is the adult-form of vitamin D3 deficiency. It causes softening of the bones, inadequate mineralization of the bone matrix, and accelerated bone loss. Eventually it can lead to muscle weakness or diffuse aches, and bone pain and tenderness.
|Article||The role of vitamin D3 in autoimmune disorders, Vital Link; 2008 Winter/Spring|
|Article||Vitamin D: Applications in autoimmunity and infectious disease, IHP, , Feb/March 2010|
|Article||Vitamin D Part II, IHP, , April/May 2010|
|Article||Vitamin D Part III: Perinatal applications, IHP,  June/July 2010|
|Article||Vitamin D Part IV: Hyperproliferative disorders, IHP, September 2010|
- GERD is associated with Vitamin D deficiency. Increasing Vitamin D status can help to alleviate the systems of heartburn and GERD.
- Hypertension is lowered with Vitamin D supplementation.
- Rheumatoid Arthritis: supplementation with Vitamin D can decrease the risk of rheumatoid arthritis and can result in significant improvement in symptoms due to the immunomodulating potential of Vitamin D.
- Osteoporosis: bone density decreases, bones become fragile, and the risk of fracture increases. Long-term deficiencies in calcium, magnesium and vitamin D can eventually lead to osteoporosis.
- Multiple Sclerosis: Vitamin D deficiency as a risk factor for MS was first postulated in the late 1970s/early 1980s due to its ability to modulate the immune system. Much epidemiological research has since been done to show the connection between vitamin D deficiency and increased MS risk. This link has been made because MS is more prevalent in individuals living in higher latitude locations where UVB exposure is decreased resulting in a decrease in vitamin D concentrations. This phenomenon is not observed, however, in those who eat vitamin D-rich fatty fish regularly. One study using 7 million U.S. military personnel showed that individuals in the highest quintile for serum 25-hydroxyvitamin D levels had 62% lower odds than those in the lowest quintile. The conclusion made was that serum vitamin D status is a predictor of MS risk. In a prospective study with 200 000 U.S. women, a 30 year follow-up showed that those with an increased dietary intake of vitamin D were associated with a decreased incidence of MS. In fact, the incidence was 33% lower in women in the highest quintile of vitamin D intake vs. those in the lowest quintile. It was also lower in women taking a modest amount of vitamin D via supplementation. More randomized trials are needed to determine the safety and efficacy of wide scale, large dose, long-term vitamin D supplementation for the prevention of MS. Vitamin D exposure appears to be particularly important in adolescence and early adulthood in terms of MS risk. Vitamin D does not appear to serve as much of a therapeutic role in MS as it does a preventive role. However, there appears to be some evidence to suggest that vitamin D levels are lower in individuals during relapses and vitamin D may aid in slowing the progression of the disease .
|Article||Effectiveness of Vitamin D in the Treatment of Mood Disorders: A Literature Review J Orthomolecular Med 2012;Vol26(3)|
- Mental Illness: Vitamin D deficiency has also been linked to mental illness. Supplementation has been shown to be helpful in seasonal affective disorder (SAD) and may even be helpful for individuals with chronic depression and schizophrenia.
- Diabetes. Supplementation with Vitamin D from cod liver oil during childhood and pregnancy reduces risk of Type I Diabetes.
- Cancer: Vitamin D may also protect against some forms of cancer, namely colon, colorectal, and prostate cancers.
- Inflammatory Conditions: Vitamin D has been shown to decrease inflammation and can be helpful in inflammatory conditions such as hypertension, heart disease, autoimmune disease, and diabetes.
Deficiency in children can lead to rickets characterized by an inability to calcify the bone matrix leading to:
- softening of the skull bones
- bowing of legs
- spinal curvature
- increased joint size
Deficiency in adults can lead to a osteomalacia.
Deficiency is commonly seen in the elderly due to decreased sun exposure and can lead to:
Low levels of serum Vitamin D may be indicative of inflammation, not of body stores.
Excess vitamin D is typically due to high-dose supplementation over an extended period of time. Excess symptoms are not typically a result of sunlight exposure.
Excessive intake over an extended period of time may lead to:
- increased thirst
- increased urination
- failure to gain weight in children
More extreme consequences include:
- potentially death
Acute overdose symptoms include:
- increased urinary frequency
- loss of appetite
- muscle weakness
- calcification of the heart, blood vessels, and lungs
- Symptoms resolve after overdosing is discontinued.
Many of the adverse effects are a result of increased serum calcium as a result of high levels of vitamin D.
|Article||25-Hydroxyvitamin D Levels and Mortality, NMJ, , 2012 October|
25-Hydroxyvitamin D is only one of more than 50 vitamin D metabolites identified. Vitamin D nutritional status may be a function of complex interactions between many different vitamin D metabolites.
Common Deficiency Tests: 
- Serum 25-Hydroxyvitamin D - a low level indicates a deficiency
- Urine Bone-Specific Peptide - a high level indicates a deficiency
|Article||The vitamin D gap: Estimating an adequate intake of vitamin D, IHP, , Feb/March 2010|
- Sunlight exposure of 5 - 15 minutes 2 - 3 times a week between 10 a.m. and 3 p.m. in spring, summer, and autumn is frequently sufficient for most people in order to maintain adequate Vitamin D levels. .
- Vitamin D supplementation is available as D2 (ergocalciferol) and D3 (cholecalciferol).
- Calcitriol is the prescription form of vitamin D (1,25-(OH)2D3) and is about 10 times as potent as vitamin D2 or D3 
- The recommended dosages varies based on age and health status. To determine what your specific requirements are talk to your naturopathic doctor or other trained medical professional.
- Infants (under 6 months): 300 I.U.
- Child (6 months-10 years): 400 I.U.
- Adolescent and Adult: 800 - 1200 I.U.
- Pregnancy and Lactation: 800 I.U.
- Children: 2000-3000 I.U./day may cause toxicity symptoms in some children. Some hypersensitive children may experience toxicity symptoms at 1000 I.U./day. Most cases of toxicity involve intake of 25 000- 60 000 I.U./day for 1-4 months. Toxicity symptoms are related to hypercalcemia and may include: headaches, weakness, nausea, vomiting, constipation, polyuria, polydipsia, diarrhea, and calcification of soft tissues, such as kidneys, lungs, tympanic membrane, or ears.
- Adults: no reported concerns
- Seniors: no reported concerns
- Pregnancy and Breastfeeding: Vitamin D enters breast milk and is considered compatible at usual dosage levels.
- Special Populations: Individuals with sarcoidosis or other granulomatous disease and certain types of lymphoma may quickly convert vitamin D to its active D3 form if supplemented. Elevated levels of activated vitamin D3 increases ones risk of hypercalcemia.
- Contraindications: hypercalcemia, hyperparathyroidism (primary), hypersensitivity to cholecalciferol, malabsorption syndrome, sarcoidosis, granulomatous disease, lymphoma, evidence of vitamin D toxicity.
- Precautions: Administer with caution to those with impaired renal function, heart disease, renal stones, or arteriosclerosis.
- Drug Interactions include:
- Supportive or Beneficial:
- Allopurinol - Drug may increase 1,25(OH)2D levels, especially with supplementation.
- Androgen-Deprivation Therapy - Concomitant vitamin D and calcium can counter skeletal impact of deficiency patterns associated with prostate cancer treatment, decreased sex hormones, and ADT, especially when used with bisphosphonates. Co-adminster vitamin D and calcium.
- Bisphosphonates - Synergistic interaction. Vitamin D assists calcium absorption and both enable bisphosphonates in maintaining bone mineralization, including with hormone replacement therapy (HRT). Co-administer vitamin D. Administer calcium but separate from drug.
- Hormone Replacement Therapy (HRT): Estrogen-Containing and Synthetic Estrogen and Progesterone Analog Medications - Synergistic interaction, especially with osteoporosis. Vitamin D assists calcium absorption, and both enable estrogen in inhibiting osteoclastic activity and bone resorption and maintaining bone mineralization. Progestins may counter benefit. Co-administer vitamin D and calcium.
- Raloxifene - Synergistic interaction. Vitamin D assists calcium absorption and both enable drug in inhibiting bone resorption. Co-administer D3 and calcium.
- Addresses Drug-Induced Deficiency:
- Anticonvulsant Medications - Phenytoin and Phenobarbital accelerate vitamin D metabolism in the liver and may reduce serum levels. Thus, drugs may impair mineralization leading to increased risk of bone loss, osteoporosis, osteomalacia, rickets, and fractures. Co-administration of "high-dose" vitamin D and calcium can mitigate drug-induced vitamin depletion and related bone loss.
- Cholestyramine, Colestipol, and Related Bile Acid Sequestrants - Drug decreases lipid digestion and absorption and thereby reduces absorption of vitamin D and fat-soluble nutrients. Risk of deficiency and sequelae. Supplement vitamin D.
- Cimetidine - Drug may inhibit action of vitamin D hydroxylase and could reduce hepatic activation of vitamin D through hydroxylation. Possible risk of deficiency.
- Corticosteroids, oral, including Prednisone - Drug reduces calcium absorption and may increase excretion while decreasing vitamin D availability and lowering serum levels. Increased risk of bone loss, osteoporosis, and fractures with long-term use of oral steroid use. Supplement with vitamin D and calcium.
- Heparin, Unfractionated - Drug is associated with bone loss and may also inhibit formation of 1,25(OH)2D by kidneys. Risks of bone loss and associated nutrient depletion with extended heparin use are significant. Co-administer vitamin D and calcium.
- Isoniazid - Drug can lower levels of both activated vitamin D and calcium levels. It can also reduce corresponding vitamin D metabolites. Drug-induced vitamin D deficiency can produce hypocalcemia and elevate parathyroid hormone. Supplement vitamin D and calcium when drug is used for > 1 month.
- Neomycin - Long-term use of drug decreases absorption and/or increases elimination of many nutrients including vitamin D. Risk of deficiency and sequelae. Supplement multivitamin-mineral.
- Orlistat - Drug binds fat to prevent absorption and can interfere with absorption of vitamin D and other fat-soluble nutrients. Possible risk of significant deficiency. Supplement multivitamin. Separate intake.
- Rifampin - Drug induces cytochrome P450, resulting in decreased plasma levels of 25-hyroxycholecalciferol. Risk of significant deficiency uncertain. Supplement D3 when drug is used >1 month.
- Calcitriol and Vitamin D Analogs - Additive effect from concurrent use would increase risk of vitamin D toxicity, especially since 1,25(OH)2D and analogs bypass renal feedback controls. Generally avoid.
- Thioridazine - Cholecalciferol inhibits hepatic cytochrome P2D6 and may decrease the metabolism of thioridazine. Concurrent use might increase activity and adverse drug effects.
- Verapamil and Related Calcium Channel Blockers - Vitamin D can increase calcium availability, which opposes verapamil's activity as a calcium antagonist. Excess vitamin D might theoretically contribute to hypercalcemia on rare occasions, which in turn might theoretically precipitate cardiac arrhythmia in individuals taking verapamil. Minimal evidence and low probability but potentially severe.
- Ketoconazole - Drug inhibits P450 enzymes to block adrenal steroidogenesis; also inhibits both synthesis of activated vitamin D and its metabolism by 1 alpha-hydroxylase and 24-hydroxylase, thus maintaining 1,25(OH)2 vitamin D levels if it is supplemented. Drug reduces calcium and 1,25-D in hypercalcemia and sarcoidosis. Monitor for vitamin D deficiency with long-term use. Calcitriol may be necessary.
- Thiazide Diuretics - Drug reduces calcium excretion and could potentially lead to hypercalcemia (rare) and changes in vitamin D metabolism. Significance of interaction uncertain. Monitor serum calcium.
- Nutrient Interactions include: 
- Boron - appears to play an important role in converting vitamin D from 25-OHD to its active form, 1,25(OH)2D, thus aiding in calcium absorption.
- Caffeine - High levels of caffeine intake have been linked to bone loss and it is possible that caffeine interacts with vitamin D receptor genotypes.
- Calcium - Vitamin D functions to facilitate intestinal calcium absorption and is part of an overall approach for calcium nourishment and attainment in the body. Excessive intake of vitamin D in some individuals may lead to hypercalcemia and its associated risks.
- Magnesium is required for the proper utilization of Vitamin D. Magnesium deficiency compromises the beneficial action of vitamin D on bone health.
- Phosphorus - Vitamin D may cause an increase in the absorption of phosphorus.
- Vitamin A - Vitamin A antagonizes some of the activity of vitamin D. If given in higher doses, it can reduce the toxic effects of vitamin D. One must also consider vitamin A toxicity in this context.
- Medlineplus 
- Hoffer Abram, Prousky Jonathan (2005) Naturopathic Nutrition, A Guide to Nutrient-Rich Food & Nutritional Supplements for Optimum Health, CCNM Press
- Cutolo M, Otsa K, Uprus M, Paolino S, Seriolo B (2007) Vitamin D in rheumatoid arthritis. Autoimmun Rev.Nov;7(1):59-64. PMID: 17967727.
- Ascherio A, Munger KL, Simon KC. Vitamin D and multiple sclerosis. Lancet Neurol. 2010 Jun;9 (6):599-612.
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