Vitamin D Deficiency

Vitamin D deficiency is common in Australia despite abundant sunshine. Reduced skin synthesis (ageing, veiling, dark skin, indoor lifestyle, sunscreen use), malabsorption, and drugs that accelerate vitamin D breakdown (rifampicin, anticonvulsants) are the main mechanisms. Most Australians cannot get adequate vitamin D from diet alone.

Risk factors

• Older people, especially those in residential care, housebound or hospitalised (thinner skin, less sun exposure).
• Dark-skinned people, particularly if habitually covered — 3–4 times more UV exposure is needed for the same synthesis.
• People who avoid the sun for cultural, medical, occupational or residential reasons, and people with obesity.
• Malabsorptive conditions — coeliac disease, inflammatory bowel disease, cystic fibrosis, biliary obstruction, prior bariatric surgery.
• Chronic kidney disease and renal transplant recipients.
• Anticonvulsant or rifampicin therapy.
• Established osteoporosis or a fragility fracture, or planned antiresorptive/bisphosphonate therapy — adequate vitamin D is needed for these drugs to work.

Clinical presentation

Deficiency is usually asymptomatic and picked up on testing done for one of the risk factors above. When symptomatic, it presents with diffuse bone/muscle aches and proximal muscle weakness, or as osteomalacia. In children, uncorrected deficiency causes rickets. Vitamin D deficiency is also a recognised contributor to falls and fragility fractures in older people through both bone and muscle mechanisms.

Investigations

Routine population screening is not recommended. Test 25-hydroxyvitamin D (25-OHD) — the storage form and the correct test, not 1,25-dihydroxyvitamin D — in patients with any of the risk factors above, or:

• Signs, symptoms or planned treatment of osteoporosis or osteomalacia.
• Raised alkaline phosphatase with otherwise normal liver function tests.
• Hyperparathyroidism, or unexplained hypo-/hypercalcaemia or hypophosphataemia.

Interpret the result against Australian reference thresholds, not an overseas laboratory’s default range — some pathology reports quote higher “sufficiency” cut-offs based on international rather than Australian guidelines. A practical severity scale:

25-OHD	Category
> 50 nmol/L	Adequate
30–50 nmol/L	Mild deficiency
12.5–29 nmol/L	Moderate deficiency
< 12.5 nmol/L	Severe deficiency

A 25-OHD threshold of at least 50 nmol/L at the end of winter is the accepted treatment target for musculoskeletal health, based on parathyroid hormone suppression, bone turnover markers and bone density data rather than a fracture-outcome trial powered on vitamin D level itself.

Check parathyroid hormone and calcium alongside 25-OHD — PTH is usually raised with deficiency, and the treatment goal is to normalise all three. If deficiency persists despite adherent supplementation, investigate for malabsorption (coeliac serology in particular).

Treatment

Choose the dose from severity, not a fixed regimen for everyone:

• Mild–moderate deficiency: cholecalciferol 1000–2000 IU (25–50 micrograms) daily, or an equivalent weekly dose.
• More marked deficiency: cholecalciferol 3000–5000 IU (75–125 micrograms) daily for 6–12 weeks to replete stores, then step down to a maintenance dose of 1000–2000 IU daily.
• Give with or alongside calcium if dietary calcium intake is inadequate — vitamin D and calcium together, not vitamin D alone, is what the falls/fracture-reduction trial evidence supports.

Cholecalciferol (vitamin D3) is preferred to calcitriol for routine treatment. Calcitriol has a narrow therapeutic window and a materially higher risk of hypercalcaemia, and is reserved for deficiency in renal failure — where the kidney cannot activate 25-OHD — with close calcium and renal-function monitoring.

Avoid annual high-dose (“stoss”) therapy. A large Australian trial of annual oral cholecalciferol 500,000 IU in older women at high fracture risk found 26% more fractures than placebo, driven by a 31% higher falls rate in the three months after each dose. Daily, weekly or monthly dosing is preferred; avoid single annual megadoses.

Calcifediol (25-hydroxyvitamin D, brand Vistella) is a newer prescription option — 255 microgram capsules taken monthly (fortnightly for more severe deficiency), approved for adults. It raises 25-OHD faster and more reliably than an equivalent-labelled dose of cholecalciferol in trial data, and may suit patients with malabsorption or obesity, but it is not PBS-listed, costs more than cholecalciferol, and cholecalciferol and calcifediol doses are not interchangeable microgram-for-microgram. It is a second-line option, not a replacement for standard cholecalciferol in routine deficiency.

Safety

Cholecalciferol has a wide safety window; toxicity from sunlight exposure does not occur. No toxicity has been seen with daily doses up to 4000 IU, or with intermittent doses up to 100,000 IU given no more often than three-monthly. Vitamin D toxicity causes hypercalcaemia — anorexia, nausea, constipation, and in more severe cases renal calculi and renal impairment. Serum 25-OHD concentrations above 375 nmol/L are associated with increased adverse effects.

Monitoring

Re-check 25-OHD 3–4 months after starting treatment — vitamin D is fat- and muscle-stored, so serum levels take this long to reflect a dose change; retesting earlier is uninformative. Once a patient is stable on maintenance therapy, annual testing at the end of winter is reasonable only if fracture/falls risk or malabsorption make ongoing monitoring worthwhile — routine indefinite retesting of an asymptomatic, adherent patient adds little.

Prevention

For people without diagnosed deficiency, brief regular sun exposure outside peak UV hours — roughly 5–15 minutes several times a week, tailored to skin type, season and latitude — is a reasonable prevention strategy, balanced against skin cancer risk. Use sun protection whenever the UV index is 3 or above.

Where sun exposure is consistently limited, a maintenance intake of at least 600 IU/day for adults up to 70 years and 800 IU/day beyond 70 is recommended by the Australian and New Zealand bone-health societies’ joint position statement. Standard multivitamins containing only 32–200 IU of vitamin D are inadequate for either prevention in a high-risk person or treatment of established deficiency.

Referral

Most deficiency is managed entirely in general practice. Refer or seek specialist advice for:

• Deficiency that persists despite adherent maximal-dose supplementation — investigate and manage the underlying malabsorptive cause.
• Suspected osteomalacia or rickets, or biochemistry suggesting a primary parathyroid or renal cause rather than simple nutritional deficiency.
• Severe deficiency in a patient with renal failure being considered for calcitriol, which needs close specialist monitoring.