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We recently reported that 73% of adolescent girls attending an inner city school in Manchester, UK had hypovitaminosis D (serum 25‐hydroxyvitamin D concentration <30 nmol/l). However, none of the subjects had clinical features of vitamin D deficiency or disturbance of their serum calcium or inorganic phosphate concentrations.1 Rajeswari et al2 have suggested that low dietary calcium intake, which is common in many parts of India, exacerbates symptoms of vitamin D deficiency.
We studied 50 post‐menarchal girls from a state‐run school in Pune, India during February 2006, using a similar protocol to that used previously.1 Informed consent was obtained from parents and the study was approved by the Ethical Committee of the Hirabai Cowasji Jehangir Medical Research Institute. None of the subjects were receiving vitamin D or any other dietary supplements. A 7 day food frequency questionnaire and Gopalan et al's3 tables of the nutrient value of Indian foods were used to estimate daily dietary intake of calcium and vitamin D.
The findings of this study were compared with those of a companion study previously undertaken in Manchester (table 11).). While there are always problems when comparing two cross‐sectional studies, undertaken in different continents and using different biochemical assays, we were surprised to find that the prevalence of hypovitaminosis D in Pune girls (70%) living at latitude 18.34° N (abundant sunshine) was similar to that in Manchester girls (73%) living at latitude 53.4°N. Secondary hyperparathyroidism, low serum calcium concentration, musculoskeletal symptoms and skeletal deformities were also more common among Pune girls. The median dietary calcium intake of Pune girls was 449 (356–538) mg/day, which is lower than the recommended intake for girls of this age in the UK (800 mg/day). Furthermore, the dietary calcium in Pune girls was derived from non‐dairy products, such as vegetables, pulses and cereals, from which only approximately 10% of calcium is absorbed. Thus, the estimated amount of dietary calcium absorbed by Pune girls was only around 58 mg/day, explaining the higher incidence of secondary hyperparathyroidism. High serum parathyroid hormone concentration leads to increased synthesis of 1,25‐dihydroxyvitamin D, which is known to degrade 25‐hydroxyvitamin D to inactive 24,25‐dihydroxyvitamin D, thereby depleting body stores of vitamin D.4 We therefore speculate that cutaneous vitamin D synthesis might have been normal in Pune girls but that their low calcium and high fibre diet led to depletion of body stores of vitamin D. From the results of this and our previous study,1 we conclude that dietary calcium intake should be considered when assessing the adequacy of an individual's vitamin D status.
We thank the participating youngsters, their parents and staff at the Dhole‐Patil school, Pune. We are grateful to Dr Sadanand Naik, Mrs Dhole‐Patil, Mrs Shilpa Shirole, Mrs Shamim Momin and Ms Deepa Pillay for their help with the study.
Competing interests: None declared.