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Vitamin D

Author: Vanessa Ngan, Staff Writer, 2005.


What is vitamin D?

Vitamin D is made up from a group of fat-soluble vitamins that exist in several forms.

  • Vitamin D2 (ergocalciferol or calciferol) is made from inactive provitamin ergosterol in plants by the action of sunlight (UV radiation).
  • Vitamin D3 (cholecalciferol/colecalciferol) is present in small amounts in some foods such as oily fish (salmon, sardines and mackerel), eggs, meat (particularly liver) and foods fortified with vitamin D. More importantly cholecalciferol is made in the skin by the action of sunlight (mostly UVB) on a cholesterol-derived compound (7-dehydrocholesterol).
  • 1,25 dihydroxycholecalciferol (calcitriol) is the biologically active hormonal form of vitamin D, which is used by the body to form and maintain healthy strong bones. Calcitriol is converted from cholecalciferol (vitamin D3) in the liver and kidney.

Hence, the skin is of unique importance in the synthesis, storage and release of vitamin D into circulation.

What is the relationship between vitamin D and sun exposure?

It is well established that sunshine is a significant source of vitamin D as UVB rays from sunlight trigger vitamin D3 manufacture in the skin. However, there is little information available about how much sunlight is necessary to make enough vitamin D3 to maintain adequate serum calcitriol levels to form and maintain healthy, strong bones. On the other hand, there is much evidence around about the dangers of over exposure to sunlight and its role in causing skin cancer. There has been much discussion about how to achieve a balance between exposing oneself to enough sunlight to maintain adequate vitamin D levels and avoiding an increase in the risk of skin cancer.


  1. In most situations, sun protection to prevent skin cancer is required during times when the UV index (UVI) is raised. At such times when the UVI is higher than or equal to 3, sensible sun protection behaviour is warranted and is unlikely to put people at risk of vitamin D deficiency.
    When the UVI is low (1 or 2) no sun protection is required.
  2. During the summer months most people should be able to achieve adequate vitamin D (blood 25-hydroxy vitamin D) levels through regular, short incidental outdoor UV exposure outside peak UV times.
    As an example, someone who burns easily in the sun (skin type 1 or 2) may only need 5 minutes of sun exposure each day before 11am and after 4pm (to the face, hands and forearms) to achieve adequate vitamin D levels whereas someone who tans more easily or has darker skin (skin type 5 or 6) will need more time e.g., up to 20 minutes.
    Deliberate exposure at peak UV times is not recommended as this increases the risk of skin cancer, eye damage, and photo-aging.
    It is thought that vitamin d production is most effective while taking exercise.
    There is no advantage in spending longer in the sun, as it does not increase the production of vitamin d beyond the initial amount.
    During winter, particularly in southern New Zealand (or Northern Europe), when UV radiation levels are dramatically lower, vitamin D status may drop below adequate levels. Additional measures to achieve adequate vitamin D status may be required particularly for those at risk of vitamin D deficiency. Summer levels of vitamin D influence winter levels of vitamin D because body stores decline in winter.
  3. Certain people are at high risk of skin cancer. They include individuals who have had skin cancer, have received an organ transplant or are highly sun sensitive. People at high risk need to have more rigorous sun protection practices and should therefore discuss their vitamin D requirements with their medical practitioner to determine if dietary supplementation rather than sun exposure is necessary.
  4. Some groups in the community are at increased risk of vitamin D deficiency. These include the elderly, babies of vitamin D deficient mothers, people who are housebound or are in institutional care, people with darker skin types, those who avoid sun exposure due to photosensitivity disorders, and those who cover their skin for religious or cultural reasons.
    People with higher risk of vitamin D deficiency should discuss their status with their medical practitioner.
  5. People who have darker skin (skin types 5 and 6) are at higher risk of vitamin D insufficiency and at lower risk of skin cancer.
    This may have implications for the health of Maori, Asian and Pacific communities.

During winter months, vitamin D production is reduced. However, the body can rely on tissue stores of vitamin D for between 30 and 60 days assuming levels are adequate prior to winter. As summer approaches and more sunlight hours are available, vitamin D is produced by the skin to rebuild depleted stores.

What does vitamin D deficiency cause?

The classic vitamin D deficiency diseases are rickets and osteomalacia.

Rickets occurs in children who are vitamin D deficient and is a bone disease characterised by softening and weakening of the bones. There is a loss of calcium and phosphate from the bones, which eventually causes destruction of the supportive matrix. vitamin D deficiency is not only caused by lack of sunlight exposure but may arise from other factors including:

  • Dietary lack of vitamin D, especially in people on vegetarian diets who do not drink milk products or foods of animal origin. People with milk allergy or lactose intolerance are also at risk.
  • Associated medical conditions that affect the absorption of vitamin D from the digestive tract.
  • Kidney disorders that prevent the conversion of vitamin D3 to its active hormone form.

In adults, vitamin D deficiency can lead to osteomalacia, which results in muscular weakness, bone pain and bone fractures. Initially symptoms of muscle weakness and bone pain may be subtle and go undetected. Long-term uncorrected vitamin D deficiency can lead to osteoporosis.

Recently some studies have been published that suggest possible beneficial effects of sun exposure in the prevention or improvement of outcome of a number of diseases including breast, prostate and colorectal cancer, autoimmune diseases such as non-Hodgkin lymphoma and multiple sclerosis, cardiovascular disease and diabetes. The mechanisms mediating the association are still under investigation. There is insufficient evidence at present to make any recommendations related to vitamin D and these diseases, however, recommendations should be reviewed when new evidence becomes available.

Who is at risk of vitamin D deficiency?

For most people, consuming vitamin D containing foods or vitamin D fortified foods and adequate sunlight exposure is sufficient for maintaining healthy vitamin D levels. However, there are several groups of individuals that may require dietary supplements and/or monitoring of vitamin D levels to ensure they do not become deficient. However, the blood tests can be misleading, as the normal level may depend on the time of year – one needs a high level at the end of summer to ensure vitamin stores will last through the winter. A low level at the end of winter might be quite normal. The blood tests are also quite expensive (about $50 a test in New Zealand).

  • Older people – as people age (>50 years) the skin cannot synthesise vitamin D3 as efficiently and the kidney is less able to convert vitamin D3 to its active form. It has been estimated that as many as 30-40% of older adults with hip fractures are vitamin D insufficient.
  • People with limited sun exposure – people who wear robes and head covering for religious reasons, homebound or office-bound individuals, people living in northern Europe or southern New Zealand.
  • Darker skinned individuals – these people have high melanin pigment content, which actually reduces the skin’s ability to produce vitamin D from sunlight.
  • Some people develop skin disease in sites exposed to the sun, and must therefore avoid it.
  • Exclusively breast-fed infants – vitamin D requirements are not met by human (breast) milk alone. In the US, after 2 months of age, supplementation is recommended unless the infant is weaned to receive vitamin D fortified milk formula. In Australia and New Zealand, it is thought that very short periods of UV exposure before 10am and after 4pm will provide the infant with enough sunlight to maintain healthy vitamin D levels even with the use of sun protection.
  • Vitamin D levels are lower in the obese and those with metabolic and insulin resistance syndromes.
  • Fat malabsorption disorders – vitamin D is a fat-soluble vitamin so individuals who have reduced ability to absorb dietary fat are at risk.

Normal regular sunscreen usage has not been associated with Vitamin D insufficiency in the majority of studies (Matsouka et al 1987, Farrerons et al 2001, Marks et al 1995, Norval et al 2009). This may be because insufficient sunscreen is applied and sunscreen users may expose themselves to more sun than non-users (Im et al 2010).

What is the dose of supplemental vitamin D?

Supplemental vitamin D can be taken in two forms: vitamin D2 and vitamin D3.

  • Vitamin D2 (ergocalciferol): the dose is 400 to 1000 iu per day.
  • Vitamin D3 (colecalciferol): the usual dose is 1.25 mg (50,000 iu) once monthly.

Can you get too much vitamin D?

Too much vitamin D can cause toxicity that results in nausea, vomiting, poor appetite, constipation, weakness and weight loss. It can also raise blood calcium levels, causing mental status changes such as confusion and heart rhythm abnormalities.

Sun exposure is unlikely to result in vitamin D toxicity. Other compounds produced in the skin protect the body from synthesising too much vitamin D during periods of prolonged sun exposure. Vitamin D toxicity is likely to occur from overdose of vitamin D supplements. People taking vitamin D supplements should never exceed the recommended dose and should be made aware of the side effects of vitamin D overdose.

Why do dermatologists say unprotected sun exposure is unsafe to boost Vitamin D?

UVB radiation has the dual effect of promoting vitamin D3 synthesis in the skin (which can be further converted to 1,25(OH)2D3) and increasing DNA damage, leading to skin cancer. Thus, although UVR may be an efficient means of providing the nutritional requirement for vitamin D, the advantage to the skin may be countered by the increased risk of mutations.1


  • Childhood is a critical period for reducing ultraviolet exposure and lifetime skin cancer risk.2
  • Responsiveness to UVB radiation varies among individuals, causing some to have low vitamin D status despite abundant sun exposure.3
  • The risks of high sun exposure leading to skin cancer cannot be counteracted by high vitamin D status.4
  • Although sunscreens could almost entirely block the solar-induced production of cutaneous previtamin D3 on theoretical grounds or if administered under strictly controlled conditions, in practice they have not been shown to do so.5
  • Exposure to a small amount of UV results in production of vitamin D without sunburn. Exposure to a higher dose does not result in higher amounts of vitamin D – instead, inactive luminsterol and tachysterol are produced. But exposure to large doses of UV results in sunburn with blistering and peeling.6



  1. Bikl DD. Vitamin D receptor, UVR, and skin cancer: a potential protective mechanism. J Invest Dermatol 2008; 128: 2357–61. PubMed
  2. Dobbinson S, Wakefield M, Hill D, Girgis A, et al. Children's sun exposure and sun protection: prevalence in Australia and related parental factors. J Am Acad Dermatol 2012; 66: 938–47. PubMed
  3. Binkley N, Novotny R, Krueger D, et al. Low vitamin D status despite abundant sun exposure. J Clin Endocrinol Metab 2007; 92: 2130–5. PubMed
  4. van der Pols JC, Russell A, Bauer U, et al. Vitamin D status and skin cancer risk independent of time outdoors: 11-year prospective study in an Australian community. J Invest Dermatol 2013; 133: 637–41. PubMed
  5. Norval M, Wulf HC. Does chronic sunscreen use reduce vitamin D production to insufficient levels? Br J Dermatol 2009; 161: 732–6. PubMed
  6. Gilchrest BA. Sun protection and vitamin D: three dimensions of obfuscation. J Steroid Biochem Mol Biol 2007; 103: 655–63. PubMed
  7. Consensus Statement on Vitamin D and Sun Exposure in New Zealand published 14 March 2012
  8. Rook A, Wilkinson DS, Ebling FJB, Champion RH, Burton JL (eds). Textbook of dermatology, 4th edn. Blackwell Scientific Publications.
  9. Wolpowitz D, Gilchrest BA. The vitamin D questions: how much do you need and how should you get it? J Am Acad Dermatol 2006; 54: 301–17. Medline.
  10. Marks R, Foley P, Jolley D, et al. The effect of regular sunscreen use on vitamin D levels in an Australian population: results of a randomized controlled trial. Arch Dermatol 1995; 131:415–21. PubMed
  11. Matsouka L, Ide L, Wortsman J, et al. Sunscreens suppress cutaneous vitamin D3 synthesis. J Clin Endocrinol Metab 1987; 64: 1165–8. PubMed
  12. Farrerons J, Barnadas M, Rodriguez J, et al. Clinically prescribed sunscreen (sun protection factor 15) does not decrease serum vitamin D concentration sufficiently either to induce changes in parathyroid function or in metabolic markers. Br J Dermatol 1998; 139: 422–7. PubMed
  13. Im SM, Oh BH, Lee YW, et al. The relation between the amount of sunscreen applied and the sun protection factor in Asian skin. J Am Acad Dermatol 2010; 62: 218–22. PubMed
  14. Scragg RK, Stewart AW, McKenzie RL, et al. Sun exposure and 25-hydroxyvitamin D(3) levels in a community sample: Quantifying the association with electronic dosimeters. J Expo Sci Environ Epidemiol 2016 Sep 7. doi: 10.1038/jes.2016.51. [Epub ahead of print] PubMed

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