Overview

Vitamin D is a fat-soluble vitamin that was isolated in 1930 and named calciferol. Since then more metabolites have been found, and the two major forms of this vitamin are now known to be vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol). Vitamin D is actually a hormone precursor, which can be manufactured by the body. Therefore, in a classical sense, it is not actually an essential nutrient. However, since the disease rickets is related to vitamin D deficiency, it has been traditionally classified as a vitamin.

Vitamin D is known as the “sunshine” vitamin. It is formed in the body by the action of the sun’s ultraviolet rays on the skin, converting the biological precursor 7-dehydroergosterol (found in animals and humans) into vitamin D3. Vitamin D3 is converted in the liver to 25-hydroxycholecalciferol (25-HCC) which is five times more active than vitamin D3. 25-HCC is then converted in the kidneys to 1,25-dihydroxycholecalciferol (1,25-HCC) which is 10 times more potent than vitamin D3. The active 1,25-HCC form of vitamin D is also called calcitrol. Since calcitrol is produced in the kidney and functions elsewhere in the body, it is considered a hormone, with the intestines and bone as its target.

Dosage Info

Dosage Range

Dosages that have been used in clinical studies range from 200IU (5mcg) to 10,000IU (250mcg) daily. (1) , (2) It is important to note that based on the presence of hypercalcemia (2.75mmol/L or 11mg/dL) at a given dose, The Food and Nutrition Board of the National Academy of Sciences states that 95 mcg of vitamin D per day is the lowest observed adverse effect level reported. (3)

Most Common Dosage

400IU (10mcg) daily.

40IU = 1mcg

Dosage Forms

Capsules, tablets, and liquid.

Adult RDI

10mcg

Adult ODA

5-10mcg

RDA

Interactions and Depletions

Depletions

Active Forms

Vitamin D2 (ergocalciferol), vitamin D3 (cholecalciferol), calcitrol (1,25 dihydroxy cholecalciferol).

Absorption

Vitamin D is absorbed from both the jejunum and/or ileum and bile is necessary for this process.

Toxicities & Precautions

General

Vitamin D can be toxic. Excessive intake of this nutrient results in hypercalcemia which causes calcium deposits in soft tissues such as kidneys, arteries, heart, ears, and lungs. Signs of vitamin D toxicity include headache, weakness, nausea and vomiting, and constipation.

Functions in the Body

Bones and Teeth

The most active form of vitamin D, 1,25-dihydroxycholecalciferol, requires the intestinal absorption of calcium and phosphorus, which are important for the development of bones and teeth. (4) For this reason, vitamin D is an important growth nutrient for infants and children.

Bones

Involved in both the formation (mineralization) of bone, as well as in the mobilization (de-mineralization) of bone. (5) Vitamin D is considered a cost effective form of prevention for hip fractures. (6)

Immune System

The active form of vitamin D enhances the immune system by stimulating the activity of macrophages.

Neuromuscular

There is new evidence to suggest that Vitamin D plays a role in neuromuscular functioning in older adults and this role may have an effect on both functional performance and the risk of falls. (7) , (8)

Clinical Applications

Hearing Loss

Vitamin D deficiency can cause hearing loss and supplementation can result in partial reversal. (9)

Rickets

Two types of metabolic defects have been discovered which are treatable with regular vitamin D supplementation. (10)

Crohn’s Disease

Patients are frequently deficient due to vitamin D malabsorption. (11)

Psoriasis

Topical and oral use of 1,25-dihydroxy-D3 can be effective. (12)

Scleroderma

High-dose 1,25 (OH)2 D3 is an effective treatment for some patients. (13)

Epilepsy

Most anticonvulsant drugs interfere with vitamin D which requires vitamin D supplementation. (14)

Symptoms and Causes of Deficiency

Rickets is the classical childhood vitamin D deficiency disease. Insufficient deposition of calcium phosphate into the bone matrix creates bones that are not strong enough to withstand the ordinary stresses and strains of weight bearing. In adults, vitamin D deficiency can result in osteomalacia and osteoporosis.

Vitamin D deficiency can result from inadequate dietary intake, insufficient exposure to sunlight, which reduces the body’s synthesis of vitamin D, and kidney or liver malfunctions, which inhibit the conversion of vitamin D to its metabolically active forms.

Dietary Sources

Vitamin D does not occur in significant amounts in many foods. It occurs in small and highly variable amounts in butter, cream, egg yolks, and liver. Milk fortified with vitamin D is the major source of this nutrient in the United States. Both the American Dietetic Association and Dietitians of Canada have developed food guidelines for vegetarians that offer the best possible non-meat sources of nutrients. (16)

References

  1. View Abstract: Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr. May1999;69(5):825-6.
  2. View Abstract: Vieth R, Chan PC, MacFarlane GD. Efficacy and safety of vitamin D3 intake exceeding the lowest observed adverse effect level. Am J Clin Nutr. Feb2001;73(2):288-94.
  3. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride; Washington, DC: National Academy Press; 1999:282. Book available at: http://books.nap.edu/books/0309063507/html/index.html.
  4. View Abstract: Outila TA, Karkkainen MU, Lamberg-Allardt CJ. Vitamin D status affects serum parathyroid hormone concentrations during winter in female adolescents: associations with forearm bone mineral density. Am J Clin Nutr. Aug2001;74(2):206-10.
  5. View Abstract: Hampson G, et al. Effects of dietary improvement on bone metabolism in elderly underweight women with osteoporosis: a randomised controlled trial. Osteoporos Int. 2003 Sep;14(9):750-6. Epub 2003 Aug 05.
  6. View Abstract: Lilliu H, et al. Calcium-vitamin D3 supplementation is cost-effective in hip fractures prevention. Maturitas. 2003 Apr 25;44(4):299-305.
  7. View Abstract: Allain TJ, Dhesi J. Hypovitaminosis D in older adults. Gerontology. 2003 Sep-Oct;49(5):273-8.
  8. View Abstract: Latham NK, et al. Effects of vitamin D supplementation on strength, physical performance, and falls in older persons: a systematic review. J Am Geriatr Soc. 2003 Sep;51(9):1219-26.
  9. View Abstract: Brookes GB. Vitamin D Deficiency and Deafness: 1984 Update. Am J Otol. Jan1985;6(1):102-07.
  10. View Abstract: Takeda E, et al. Vitamin D-dependent Rickets Type I and Type II. Acta Paediatr Jpn. Aug1997;39(4):508-13.
  11. View Abstract: Andreassen H, et al. Regulators of Calcium Homeostasis and Bone Mineral Density in Patients with Crohn’s Disease. Scand J Gastroenterol. Oct1998;33(10):1087-93.
  12. View Abstract: Morimoto S, et al. Inverse Relation Between Severity of Psoriasis and Serum 1,25-dihydroxy-vitamin D Level. J Dermatol Sci. Jul1990;1(4):277-82.
  13. View Abstract: Humbert P, et al. Treatment of Scleroderma with Oral 1,25-dihydroxyvitamin D3: Evaluation of Skin Involvement Using Non-invasive Techniques. Results of an Open Prospective Trial. Acta Derm Venereol. Dec1993;73(6):449-51.
  14. View Abstract: Shafer RB, et al. Calcium and Folic Acid Absorption in Patients Taking Anticonvulsant Drugs. J Clin Endocrinol Metab. Dec1975;41(06):1125-29.
  15. View Abstract: Latham NK, et al. Effects of vitamin D supplementation on strength, physical performance, and falls in older persons: a systematic review. J Am Geriatr Soc. 2003 Sep;51(9):1219-26.
  16. View Abstract: Messina V, A new food guide for North American vegetarians. Can J Diet Pract Res. 2003 Summer;64(2):82-6.