Vitamin D is increasingly recognised to play an important role in normal muscle function. Low vitamin D status is associated with an increased risk of falls and proximal weakness. Since vitamin D deficiency is very common, and the signs are non-specific, it is important to maintain a high index of suspicion of vitamin D deficiency in patients with muscle pain and weakness, and it is simple to measure serum 25(OH) vitamin D. Therapy is cheap, safe and effective, but sometimes a larger dose may be needed, and, as shown in our case report, willingness of people to pay for an over the counter medication can be an issue. Following a striking case report that demonstrates muscle defects in severe vitamin D deficiency, we discuss clinical studies examining specific effects of vitamin D on physical performance, muscle strength and falls. Finally, we present an overview of molecular mechanisms that explain vitamin D’s biological effects on muscle.

Case report

Mrs. H was a 51 year old woman who presented for management of her type 2 diabetes. She complained of muscle pain in all large muscle groups. She noted difficulty hanging out the washing and on ‘bad days’ difficulty brushing her hair. She complained of calf pain with walking one block which improved with rest. Her other past medical history included a fractured leg after falling down a flight of stairs, gastro-oesophageal reflux and hypercholesterolemia. She had no known allergies, but had one past episode of anaphylaxis for which a trigger was not identified. Mrs. H did not smoke or drink alcohol. Her medications were metformin 1 g bd and gliclazide 80 mg, 2 tablets bd but these were not taken regularly. Her HbA1c was poorly controlled at 9.5%. She had no known retinopathy, nephropathy or neuropathy or macrovascular complications of diabetes. She was born in Turkey and had been resident in Australia for many years. Mrs. H did not wear hajib (veil) but did cover her arms and legs, and wore a headscarf. She did report low sun exposure. On examination her weight was 103.5 kg and her height 155.5 cm, giving her a BMI of 42.8 kg/m2 . Blood pressure was 128/79 mmHg and her after-lunch blood glucose level was 12.6 mmol/l. Her foot architecture, pedal pulses and capillary refill were normal. There was no muscle tenderness to palpation but power was 4/5 in all proximal muscle groups. Distal power was normal (5/5). Reflexes were present and brisk, with down-going plantar responses. There was no loss of sensation present, and pedal blood supply was normal. On being asked to stand, she had to use her hands to help her to stand from an office chair. The timed up and go test was administered, and the time was 14 s to stand, walk across the room (3 m), turn and walk back and sit down. Although reference values for TUAG in subjects < 65 yrs have not been reported, a time of 14 s in this subject (age 51 yrs) is very abnormal. In older subjects, 10 s or less to perform timed up and go test is considered normal (Podsiadlo and Richardson, 1991). She was requested to have serum vitamin D measured, with other blood tests and to commence vitamin D supplementation at 2000–۳۰۰۰ IU per day. Serum 25(OH) vitamin D was 12 nmol/l. Serum corrected calcium and phosphate were normal (2.28 mmol/l and 1.39 mmol/l respectively). Magnesium was low at 0.61 mmol/L. She returned to clinic for her next visit, and again complained of muscle pains and weakness. On questioning, she said she had not commenced vitamin D treatment.