The sunshine vitamin

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Post by Neil McKellar-Stewart04 Dec 2010

As summer warms up many of us head for the shade. Australians have a good track record for adopting sun protection strategies; however, as the latest cancer data from NSW shows1, melanoma is the still the most common cancer for males aged 25 to 54.

Risk factors for melanoma include over-exposure to ultraviolet (UV) radiation and sunburn (especially if you have skin that burns easily), older age, and, significantly for PLHIV, being immunosuppressed.

But we do need to get some sunlight to stay healthy. Vitamin D, the ‘sunshine vitamin’, is an essential hormone which we get through exposure to sunlight and via certain foods.


Vitamin D comes in two forms: vitamins D2 and D3.
Vitamin D2 is found in plants and is the product of ultraviolet B (UVB) irradiation of a compound found in plant leaves. We receive very little vitamin D2 in our diet, although it is sometimes added to foods as a supplement.

Vitamin D3 is a product of UVB irradiation of human skin and is the major source of vitamin D in our bodies.

Vitamin D3 can also be supplied through diet in the form of oily fish, vitamin D3 fortified foods or as a supplement.

The vitamin D story in the human body starts in our skin, where UVB radiation converts the cholesterol in cell membranes into vitamin D3.

This circulates to the liver and is our major circulating form of vitamin D.

How much we have in the blood reflects our vitamin D intake both from dietary sources and production within the body. In the kidneys, it plays a vital role in maintaining bone and muscle health by regulating calcium metabolism.

The vitamin D story does not end with bone and muscle health. Directly or indirectly, it regulates over 200 genes. Vitamin D receptors are present in most human tissues, including blood vessel walls, smooth muscle, breast, colon, prostate and heart tissue.

These receptors enable cells throughout the body to produce and use vitamin D to undertake a range of functions including stimulating production of cytokines to destroy infections, maintaining normal cell growth, stimulating the production of insulin to control blood sugar levels, and regulating blood pressure.

There is an emerging body of evidence suggesting that low vitamin D status increases the risk of colon and possibly other cancers, hypertensionheart attack, cardiovascular infections and diabetes.2


Vitamin D levels are measured in nano-moles per litre (nmol/L). There issome debate about what level is sufficient and what is deficient. In Australia3, mild deficiency is in the range 25–50 nmol/L, and moderate and severe deficiency as vitamin D levels below 25 nmol/L and below 12.5 nmol/L respectively.

It is commonly accepted that ‘insufficient’ is in the range 50-75 nmol/L. Increasingly medical authorities are suggesting that the optimal (‘sufficient’) level should be at least 75 nmol/L4.


Recent research reports have flagged vitamin D-deficiency as an important issue for PLHIV.

A UK study5 was conducted between June and December 2008 (the northern hemisphere autumn-winter) of a large, ethnically diverse urban population of 1041 adults living with HIV and showed that over nine out of ten had insufficient vitamin D levels. Nearly three-quarters were vitamin D-deficient, with 34.2% severely deficient.

The factors associated with lower levels of vitamin D were black race, winter and currently being on efavirenz. Those including efavirenz in their current treatment were twice more likely to have severe vitamin D-deficiency than those on other regimes.

Another study of 211 PLHIV in the Swiss HIV Cohort Study6 was undertaken at three intervals: just before HIV treatment was commenced, after 12 months of continuous treatment and again after 18 months. Study participants commenced treatment either in autumn or spring.

The percent age of PLHIV with vitamin D-deficiency was 42-52% in spring and 14-18% in autumn. This difference reflects the effect of summer when vitamin D is stored and where higher levels are expected in autumn, and winter when vitamin D is not produced by sun exposure and levels are accordingly lower in spring.

Similar results were reported in a US study7 of young adults with HIV (87% with vitamin D levels below 37.5 nmol/L); in Milan, Italy in a study of 68 PLHIV, 25% had vitamin D levels below 45 nmol/L; and in Spain in a small study of 30 men with HIV, 86% had vitamin D levels below 25 nmol/L.

A number of these studies suggest that the use of efavirenz in treatment regimes is associated with increased risk of vitamin D deficiency. In a recent study8 of 87 PLHIV in Ohio, researchers investigated the change in vitamin D levels after participants commenced their first HAART. They found that six to twelve months after commencing efavirenz the average change in vitamin D levels was -12.5 nmol/L (or a drop of 20%). People on regimes not including efavirenz experienced no drop in levels.

People who used efavirenz were nearly twice as likely to develop severe vitamin D deficiency.

In a recent European study9 of PLHIV who were on treatment using NNRTIs, NRTIs and PIs drugs and who switched to the new PI darunavir, vitamin D deficiency was present in 170 out of 221 people (77%). Deficiency was strongly associated with use of efavirenz. In fact, 25% of participants using efavirenz had severe vitamin D deficiency (compared to 15% using PIs). Ninety six weeks after the switch to darunavir, increases in vitamin D levels were significantly greater (around 30% increase) for those who stopped using efavirenz compared to other NNRTIs or NRTIs.

All the above studies were conducted in the northern hemisphere, most at latitudes of at least 40° north amongst urban populations where sunlight exposure might be expected to be less than that experienced by most Australians. (The only Australian capital more than 40° south is Hobart.) There are some comparable data from an Australian study into bone mineral density. This study10 of 153 PLHIV (mainly white-skinned males) in Sydney in January-April 2007 found that 12% had vitamin D levels below 35 nmol/L (deficient).

While this is less than that reported from the northern hemisphere, it is still significant. In a very small study11 of twelve darkskinned African-born migrants with HIV living in Melbourne, ten were found to ave vitamin D levels below 54 nmol/L, while results from a larger cross-sectional study12 of over 500 patients with vitamin D levels measured between March 2009 to March 2010 in Melbourne, revealed that 39.1% had deficient levels (below 50 nmol/L) and 73.3% had insufficient levels (below 75 nmol/L)


Vitamin D-deficiency occurs in a significant portion of PLHIV, possibly as a result of HIV itself, and almost certainly as a result of HIV treatments, as well as the usual risk factors for vitamin D deficiency (age, skin colour, UVB exposure). So it is a health issue all of us need to consider.

  • Do you spend very little time outdoors, especially in winter?
  • are you dark-skinned?
  • Do you wear clothing which leaves very little exposed skin?
  • is one of your HiV treatments efavirenz (Stocrin and also in the combination pill atripla)?

If you answered ‘Yes’ to any of these questions it might pay to ask your doctor whether your vitamin D levels have been checked recently.

If your level is less than 50 nmol/L or ‘deficient’ you may need to take action to increase it, either by sensible sun exposure and/or vitamin D supplementation. But discuss either strategy with your doctor, especially before you commence taking vitamin D supplements.

The best way to ensure that you have the optimal vitamin D levels is to get outside and get some sensible sun exposure. Adequate exposure to the right kind of sunlight is essential.

The amount of vitamin D produced in your skin depends on many factors: length of exposure, latitude, time of day, season, amount of shade, the amount of your body exposed to the light, your skin pigmentation, your body mass index, and amount of body fat13.

In Australia, we receive lots of longer wavelength UVA light (the type that causes skin damage as it penetrates deeply into our skin). Our skies are clear of pollution and cloud much of the time. What is needed is exposure to short wavelength UVB radiation.

Recent research14 commissioned by the Cancer Council Queensland suggests that we can receive sufficient UVB radiation by spending time in shaded sunlight where we can see at least 40% of the sky. The amount of time will vary by latitude and season. The simple table above should help, but remember:

  • Sun exposure under shade during the middle of the day otherwise in full sunlight on either side of the peak UVA periods before 10am and after 3pm.
  • Around 15% of your body exposed: face, hands, arms and, if possible, shoulders.
  • No sun protection for the short period you are getting your vitamin D, but definitely cover up if you head for the beach or for outdoor activities.
  • If you are red or burn you have definitely had too much. Reduce your exposure. A very faint pink ‘glow’ 24 hours after exposure is okay – this is called a minimal erythemal dose.
  • If you are dark-skinned you may need slightly more.
  • If you have to cover our face or head for ultural reasons, make ure your hands are xposed and perhaps ncrease the length of time.
  • If you are housebound, ry and get outside to an pen balcony or garden area.
    UVB radiation does ot pass through glass but he nasty burning UVA oes. So, sitting behind lass in the full sun will urn you and do nothing or your vitamin D intake.
  • You don’t need to get nto the sunshine each ay. Vitamin D is stored the fat in your body so just ensure that you get enough spread over a week.
  • Daily exposure of five minutes in summer (as indicated above) should produce a daily dose of at least 1000 international units (iU) of vitamin D3 sufficient for most people.


Your doctor or complementary therapist can advise you whether you need a supplement or not. If you are severely deficient you may require up to 3000 iU of vitamin D3 per day for up to three months. A daily dose of 800-1000 iU may be sufficient if you are unable to get sufficient sunlight exposure.

More information is available in the Australian Position Statement on Vitamin D and adult bone health. A range of proprietary vitamin D supplements are available from retail grocery stores and pharmacies. But check with your treating doctor first.

Evidence is still emerging on our need for vitamin D and other supplements and guidelines are in development. So watch this space.

  1. Cancer Institute NSW. Cancer in New South Wales: Incidence and Mortality 2008. Incite: J. Cancer Institute NSW. 2010 Sep; Issue 5. Full text:
    Downloaded 8/10/10
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    Holick MF. Vitamin D deficiency. N Engl J Med. 2007 Jul 19; 357(3): 266-81. Abstract:

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    Bischoff-Ferrari H. Vitamin D: what is an adequate vitamin D level and how much supplementation is necessary? Best Pract Res Clin Rheumatol. 2009 Dec; 23(6): 789-95. Abstract:

    Souberbielle JC, Body JJ, Lappe JM, Plebani M, Shoenfeld Y, Wang TJ, Bischoff-Ferrari HA, Cavalier E, Ebeling PR, Fardellone P, Gandini S, Gruson D, Guérin AP, Heickendorff L, Hollis BW, Ish-Shalom S, Jean G, von Landenberg P, Largura A, Olsson T, Pierrot-Deseilligny C, Pilz S, Tincani A, Valcour A, Zittermann A. Vitamin D and musculoskeletal health, cardiovascular disease, autoimmunity and cancer: Recommendations for clinical practice. Autoimmun Rev. 2010 Sep; 9(11): 709-15. Abstract:

  5. Welz T, Childs K, Ibrahim F, Poulton M, Taylor CB, Moniz CF, Post FA. Efavirenz is associated with severe vitamin D deficiency and increased alkaline phosphatase. AIDS. 2010 Jul 31;24(12):1923-8. Abstract:

    Welz, et al. Efavirenz use is associated with severe Vitamin D deficiency in a large, ethnically diverse urban UK HIV cohort. 5th IAS Conference on HIV Pathogenesis and Treatment: Abstract no. TUPEB186 Abstract:

  6. Mueller NJ, Fux CA, Ledergerber B, Elzi L, Schmid P, Dang T, Magenta L, Calmy A, Vergopoulos A, Bischoff-Ferrari HA; Swiss HIV Cohort Study. High prevalence of severe vitamin D deficiency in combined antiretroviral therapy-naive and successfully treated Swiss HIV patients. AIDS. 2010 May 15; 24(8): 1127-34. Abstract:
  7. Stephensen CB, Marquis GS, Kruzich LA, Douglas SD, Aldrovandi GM, Wilson CM. Vitamin D status in adolescents and young adults with HIV infection. Am J Clin Nutr. 2006 May; 83(5): 1135-41. Full-text:
  8. Brown TT, McComsey GA. Association between initiation of antiretroviral therapy with efavirenz and decreases in 25-hydroxyvitamin D. Antivir Ther. 2010; 15(3): 425-9. Abstract:
  9. 20 Fox J, Peters B, Prakash M, Arribas J, Hill A, Moecklinghoff C. Improvement in Vitamin D Deficiency Following Antiretroviral Regime Change: Results from the MONET Trial. AIDS Res Hum Retroviruses. 2010 Sep 21. Full-text:
  10. Calmy A, Fux CA, Norris R, Vallier N, Delhumeau C, Samaras K, Hesse K, Hirschel B, Cooper DA, Carr A. Low bone mineral density, renal dysfunction, and fracture risk in HIV infection: a cross-sectional study. J Infect Dis. 2009 Dec 1; 200(11): 1746-54. Abstract:
  11. Woolley IJ, Giles ML, Howard JE, Korman TM. Unrecognised vitamin D deficiency: low concentrations in African migrants with HIV in Australia. Sex Health. 2008 Dec;5(4):375-6. Full text:
  12. Price J, Wooley,I, Bailey M, Nyulasi I, Hoy J Traditional and HIV-related factors of Vitamin D insufficiency in Melbourne . Australasian HIV/AIDS Conference 2010. Handbook. p. 91, Paper no. 343
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    Samanek AJ, Croager EJ, Gies P, Milne E, Prince R, McMichael AJ, Lucas RM, Slevin T; Skin Cancer Prevention. Estimates of beneficial and harmful sun exposure times during the year for major Australian population centres. Med J Aust. 2006 Apr 3; 184(7): 338-41. Turnbull DJ, Parisi AV. Latitudinal variations over Australia of the solar UV-radiation exposures for vitamin D3 in shade compared to full sun. Radiat Res. 2010 Mar; 173(3): 373-9. Abstract: