P O S I TI O N S T A T E ME N T
Vitamin D and adult bone health in Australia and New Zealand:
Working Group of the Australian and New Zealand Bone and Mineral Society,
Endocrine Society of Australia and Osteoporosis Australia*
significant number of Australians are deficient in vitamin
D. Indeed, it is a fallacy that Australians receive adequate
• A significant number of Australians are deficient in vitamin D
Avitamin D from casual exposure to sunlight. Here, we — it is a fallacy that Australians receive adequate vitamin D
outline the causes and outcomes of vitamin D deficiency, the
people who are at risk, and recommendations for management ofdeficiency. • People at high risk of vitamin D deficiency include elderly
people (particularly those in residential care), people with skin
The Medical Journal of Australia ISSN: 0025-
conditions where avoidance of sunlight is advised, those with
D 1 March 2005 182
dark skin (particularly if veiled), and those with malabsorption. • Exposure of hands, face and arms to one-third of a minimal
vittamin D3), formed in the skin through the
erythemal dose (MED) of sunlight (the amount that produces
action of ultraviolet (UV) light on 7-dehydrocholesterol to produce
a faint redness of skin) most days is recommended for
adequate endogenous vitamin D synthesis. However,
• Ergocalciferol (vitamin D2), produced by UV irradiation of the
deliberate sun exposure between 10:00 and 14:00 in summer
plant steroid ergosterol. Ergosterol is the major form of supple-
(11:00–15:00 daylight saving time) is not advised.
mental vitamin D currently available in Australia. • If this sun exposure is not possible, then a vitamin D
supplement of at least 400 IU (10 µg) per day is
1,25-Dihydroxyvitamin D
Vitamin D3 and D2, made in the skin or ingested, are transported
• In vitamin D deficiency, supplementation with 3000–5000 IU
to the liver and metabolised to 25-hydroxyvitamin D (25-OHD),
ergocalciferol per day (Ostelin [Boots]; 3–5 capsules per day)
the major circulating form. Further hydroxylation occurs in the
kidney to form the highly biologically active 1,25-dihydroxyvita-
• Larger-dose preparations of ergocalciferol or cholecalciferol
min D (1,25-(OH)2D). This compound promotes:
are available in New Zealand, Asia and the United States and
absorption of calcium and phosphate from the small intestine;
would be useful in Australia to treat moderate to severe
extracellular calcium homeostasis, directly and through its
vitamin D deficiency states in the elderly and those with poor
absorption; one or two annual intramuscular doses of
300 000 IU of cholecalciferol have been shown to reverse vitamin D deficiency states.
University of New South Wales, Sydney, NSW. Terrence H Diamond, MRCP, FRACP, Associate Professor of Medicine,
Sources of vitamin D Exposure to sunlight: For people living in Australia and New
Garvan Institute of Medical Research, St Vincent’s Hospital and
Zealand, the main source of vitamin D is through exposure to
University of New South Wales, Sydney, NSW.
sunlight. It has been shown that whole body exposure to 10–15
John A Eisman, PhD, FRACP, Professor and Director, Bone and Mineral
minutes of midday sun in summer (about 1 minimal erythemal
dose [MED], or the amount of sun exposure which just produces a
University of Sydney, NSW. Rebecca S Mason, MB BS, PhD, Associate Professor, Department of
faint redness of skin) is comparable to taking 15 000 IU (375 µg) of
Physiology and Institute for Biomedical Research.
vitamin D (cholecalciferol) orally.n this basis, exposure of
hands, face and arms (around 15% of body surface) to around 1/3
Caryl A Nowson, PhD, DipNutDiet, Associate Professor, School of
MED should produce around 1000 IU of vitamin D (cholecalcif-
erol). The amount of sun exposure to produce 1/3 MED varies with
The University of Melbourne, Geelong, VIC.
latitude, season, time of day and skin type (.
Julie A Pasco, BSc(Hons), PhD, DipEd, Senior Research Fellow,
Less vitamin D is synthesised in winter, in those who have dark
Department of Clinical and Biomedical Sciences, Barwon Health.
skin or are older, and in those who dress with little potential for
University of Sydney and Royal North Shore Hospital, NSW.
skin exposure to sunlight for cultural reasons or for sun protection.
Philip N Sambrook, MD, LLB, FRACP, Professor of Rheumatology.
Therefore, serum vitamin D levels are lower in winter than in
The University of Melbourne and Royal Melbourne Hospital, VIC. John D Wark, PhD, FRACP, Professor of Medicine.
summer Short exposures may be more efficient at producing
Reprints will not be available from the authors. Correspondence: Dr
vitamin D. Once previtamin D3 (a chemical precursor of vitamin
Julie A Pasco, Department of Clinical and Biomedical Sciences, Barwon
D3) and vitamin D3 (cholecalciferol) have been formed, continued
Health, The University of Melbourne, PO Box 281, Geelong, VIC 3220.
exposure to UV results in their degradation to relatively inert over-
MJA • Volume 182 Number 6 • 21 March 2005 P O S I TI O N S T A T E ME N T
tively). Radiation in the UVB range is responsible for skin carcino-
1 Recommended sun exposure times (minutes) which
genesis as well as the conversion of 7-dehydrocholesterol into
result in 1/3 MED for people with moderately fair skin*
previtamin D3. Glass blocks UVB rays and therefore prevents
at different times of day
previtamin D3 synthesis. Concerns were raised that sunscreen usemay cause vitamin D deficiency, especially among older people.
Yet sunscreens are essential to prevent skin damage with longer
periods of sun exposure. For incidental sun exposures (< ½ MED),
it may be reasonable to omit the sunscreen for the time required. Groups at risk of vitamin D deficiency
Older people who are institutionalised or housebound are at a
particularly high risk of vitamin D deficiency. For example, up to
80% of women and 70% of men living in hostels or nursing homes
in Victoria, New South Wales and Western Australia were frankly
deficient in vitamin D, and 97% had a 25-OHD level below themedian value of the healthy reference range.here also appears
to be a significant prevalence of mild vitamin D deficiency in
younger adults, particularly during winter.
Groups for whom low vitamin D levels have been documented
• older people in low- and high-level residential care; • older people admitted to hospital • patients with hip fracture; • dark-skinned women (particularly if veiled);d
* Exposure times for people with highly pigmented skin would be 3–4 times greater.3
• mothers of infants with rickets (particularly if dark-skinned and
† Based on the relationship 1 MED = 200 J/m2 effective or 2 standard erythemal
doses for people with type I or II (sensitive) skin. Data for Australian cities were obtained from Gies et al,4 using measured averages of MED/h over the 2 months listed, for a minimum of 5 years in the
Vitamin D deficiency and bone
period 1996–2003, except Hobart, which used data from 1 year.
Circulating 25-OHD and 1,25-(OH)2D levels decrease with age.
Times for New Zealand were calculated from ultraviolet data averaged over 2
This may be a result of age-related factors, such as reduced
years provided by the National Institute of Water and Atmospheric Research. ‡ 11:00 or 15:00 daylight saving time, respectively.
capacity to produce vitamin D, diminished sunlight exposure,reduced intake, decline in renal function, disorders associated withabnormal gut function, or reduced synthesis or enhanced degrada-tion of 25-OHD .
It is therefore prudent to expose hands, face and arms to 1/3
MED of sunlight most daysshows approximate exposure
Mild vitamin D deficiency: Defined as serum 25-OHD levels in the
times for various regions, months and skin types. But there is a
range 25–50 nmol/L, mild deficiency leads to increased parathy-roid hormone secretion and high bone turnover.
caveat: deliberate exposure to sunlight between 10:00 and 14:00(or 11:00 and 15:00 daylight saving time) in the summer months
Moderate vitamin D deficiency: Defined as serum 25-OHD levels
is not advised. If adequate sunlight exposure to generate sufficient
of 12.5–25 nmol/L,oderate deficiency has been associated
endogenous cholecalciferol is not possible, then a vitamin D
with reduced bone density, high bone turnoved increased
supplement of at least 400 IU (10 µg) per day is recommended.
risk of hip fracture in older peopleSevere vitamin D deficiency: Serum 25-OHD levels of Diet:Vitamin D3 is found in small quantities in a few foods, such
< 12.5 nmol/L, resulting in osteomalacia, are rare in Australia and
as fatty fish (North Sea salmon, herring and mackerel). Liver, eggs
New Zealand. Patients with severe deficiency may present with
and fortified foods, such as margarine and some low-fat milks, also
bone and muscle pains, weakness and pseudofractures. Bone
contain very small amounts of vitamin D.
For most Australians, adequate vitamin D is unlikely to be
achieved through diet alone. Intake is estimated as 2–3 µg/day
2 Recommended adequate intake (AI) for vitamin D from
(< 100 IU). Recommended dietary intakes are currently under
the US Food and Nutrition Board6*
review in Australia. Daily reference intakes for vitamin D devisedby the Food and Nutrition Board of the Institute of Medicine of the
United States National Academy of Science6 are shown in.
These are similar to the recommendations of the Food and
Agriculture Organization of the United Nations (FAO). Sunscreens
* AIs are recommended levels of dietary intake when there are limited data on the relationship between intake and deficiency. AIs cover the needs of adults
Broad-spectrum sunscreens protect the skin against UVA and UVB
radiation (wavelengths, 320–400 nm and 290–320 nm, respec-
MJA • Volume 182 Number 6 • 21 March 2005 P O S I TI O N S T A T E ME N T
histomorphometry shows classic findings of thickened unmineral-
3 Causes of vitamin D deficiency
ised seams, increased osteoclast surfaces, smearing of tetracyclinelabels and prolonged mineralisation lag times. Cortical thinning
Reduced intake or synthesis of cholecalciferol
occurs because of secondary hyperparathyroidism. • Reduced sunlight exposure: ageing, veiling, illness, immobility • Reduced synthesis from a given ultraviolet exposure: ageing, dark Vitamin D deficiency, muscle function and falls • Combined with low consumption of foods with high vitamin D
Vitamin D deficiency is an independent predictor of falls in older
women in residential care in Australia.t is also linked with falls
Disorders associated with abnormal gut function and
and fragility fractures in both women and older men
Australia, a randomised clinical trial of vitamin D supplementation
• Small bowel disorders: coeliac disease, sprue, inflammatory bowel
in non-institutionalised people is required to determine whether
disorders, infiltrative disorders (eg, lymphoma, granuloma,
falls and fracture can be prevented in this group. • Pancreatic insufficiency: chronic pancreatitis, cystic fibrosis Vitamin D supplementation • Biliary obstruction: primary biliary cirrhosis, external biliary
drainage (eg, treatment for obstructive jaundice or after surgical
Some calcium supplements and multivitamin preparations
contain vitamin D, but the levels of 32–200 IU per tablet are too
Reduced synthesis or enhanced degradation of 25-OHD
low to treat vitamin D deficiency. • • Chronic hepatic disorders: hepatitis, cirrhosis
Halibut or cod liver oil capsules contain 400 IU of cholecalcif-
Drugs: rifampicin, perhaps multiple anticonvulsant drug therapy
3) per capsule. However, although these are cheap
(0.08 cents each), they also contain vitamin A (4000 IU), whichmay not be beneficial (epidemiological studies suggest that vitamin
available in Australia, and there is concern about inducing hyper-
A excess may be associated with an increased fracture risk
calcaemia or hypercalciuria if excessive doses are used. Vitamin D3
The single pure vitamin D preparation in Australia is Ostelin
appears more effective than D2 in raising serum 25-OHD level.
1000 (Boots), which contains ergocalciferol (vitamin D2) (1000 IU
• Calcitriol (1,25-(OH)
or 25 µg) and costs about 24 cents per capsule.
patients with deprivational vitamin D deficiency as it has a narrow
A larger dose (50 000 IU) of cholecalciferol is available in New
therapeutic window, may result in hypercalcaemia or hypercalciu-
ria and does not increase serum 25-OHD levels.
Some commercial 25-OHD assays do not measure 25-OHD2
(the vitamin D2 form) as well as they measure 25-OHD3 (thevitamin D3 form) and may not be optimal for monitoring replace-
Vitamin D intoxication produces hypercalcaemia (with anorexia,nausea, polyuria, constipation, weakness, weight loss, headache,
Dosages required to treat moderate to severe vitamin D
depression, vague aches, stiffness, soft tissue calcification, nephro-
calcinosis, hypertension and anaemia). In severe cases, hypercal-
Vitamin D is stored in fat and muscle and slowly released,
caemia may lead to irreversible renal and heart failure or coma
particularly during winter.n vitamin D-deficient patients, it is
necessary to replete the vitamin D stores. While the daily
• Vitamin D toxicity can be caused by excess oral intake through
requirement for vitamin D is 400–600 IU, a larger dose is needed
supplementatio but not by prolonged exposure of the skin to
to treat patients with deficiency. As vitamin D is distributed in the
body fat compartment, which is larger than the plasma and
• No clinical or biochemical evidence of toxicity has been noted
extracellular fluid compartment, large doses are needed before
with doses up to 4 000 IU (100 µg) daily.30 Although there is little
changes in serum 25-OHD are seen. This may explain the lag
evidence for toxicity with high-dose injections (300 000 IU) at
time seen with vitamin D supplements before normalisation of
intervals of not less than 3–6 monthse safety of such
serum 25-OHD levels. Vitamin D status should be assessed 3–4
supraphysiological doses is yet to be established.
months after commencing treatment. Recommendations for
• The contraindication for administration of vitamin D is hyper-
management of vitamin D deficiency states are summarised in
• Cod liver oil also contains vitamin A, which can be toxic at high • High dosages of Ostelin (3000–5000 IU daily for 6–12 weeks)
can be used to replete body stores. Indeed, oral doses of 10 000 IUper day have been given without adverse effects for at least 90 daysin postmenopausal women. Oral dosing can be effective in
individuals with malabsorption, unless it is very severe, but higher
The greatest benefits of vitamin D supplementation are seen in
high-risk vitamin D-deficient individuals with demonstrated
• Higher single doses of 50 000–500 000 IU orally or 300 000–
decreases in bone density. Increases in bone density from 0–4% in
600 000 IU vitamin D3 intramuscularly can effectively treat vita-
vitamin D-insufficient patients and from 10%–40% in vitamin D-
min D deficiency One or two annual intramuscular doses of
deficient patients with osteomalacia have been reported after
300 000 IU of cholecalciferol have been shown to reverse vitamin
optimal treatment with vitamin D. It is unlikely that vitamin D
D deficiency states.Intramuscular preparations are preferable for
supplementation has any role in vitamin D-replete individuals.
malabsorption. However, these formulations are not currently
However, the optimal level of serum 25-OHD is unknown;
MJA • Volume 182 Number 6 • 21 March 2005 P O S I TI O N S T A T E ME N T Acknowledgements 4 Recommendations for management of vitamin D
We thank the many members of the Australian and New Zealand Bone and
deficiency states
Mineral Society (ANZBMS), Osteoporosis Australia (OA), the Endocrine
Society of Australia (ESA) and the Cancer Councils of Australia for theirsuggestions and critical comments; the Australian Radiation Protection and
• Elderly people, particularly in residential care
Nuclear Safety Agency for calculating the data and providing information on
• People with skin cancers or skin-related conditions where
sun exposure times; and Dr Richard McKenzie (National Institute of Water
and Atmospheric Research) for providing the New Zealand data. We also
• Dark-skinned people, particularly veiled women
thank Professor BEC Nordin for critical appraisal of the final draft of theposition statement and Professor GC Nicholson (Chair, Medical and Scien-
• Patients with malabsorption syndromes
tific Affairs Committee, ANZBMS) for commissioning the project on behalf of
ANZBMS. Consensus process: This position statement was developed by a working
• 25-hydroxyvitamin D (25-OHD) (note that not all commercially-
group commissioned by the ANZBMS and OA. The first draft was developed
available assays detect 25-OHD2 [vitamin D2 form] optimally)
by the seven members of the working group with expertise in bone health
and osteoporosis. Drafts were circulated to other experts in the area and also
• Fatty fish, such as mackerel and herring
to the Cancer Council of Victoria for advice on sun exposure recommenda-tions. The subsequent draft was posted on the ANZBMS website for
• Liver
widespread comment and feedback. Suggested revisions were incorporated
• Foods fortified with vitamin D (margarine and some milks)
with consensus from each member of the working party. Further adviceabout sun exposure was provided by the Australian Radiation Protection and
Minimum sun exposure to prevent deficiency
Nuclear Safety Agency. The final manuscript was reviewed by Councils of the
• For most people, exposure of hands, face and arms to 1/3 minimal
ANZBMS, ESA and OA scientific affairs committees. • Older people require more frequent exposure Competing interests
Dietary vitamin D required to prevent deficiency
• At least 200 IU (5 µg) (age < 50 years) or 600 IU (15 µg) (age > 70 • Those with substantial sun avoidance may require higher doses References
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27 Tjellesen L, Hummer L, Christiansen C, Rodbro P. Serum concentration of
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29 Koutkia P, Chen TC, Holick MF. Vitamin D intoxication associated with an
over-the-counter supplement. N Engl J Med 2001; 345: 66-67. (Received 26 Nov 2004, accepted 24 Dec 2004)MJA • Volume 182 Number 6 • 21 March 2005
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