In India, there is a lack of information about the adequate daily dose of vitamin D3 supplementation in school children. Hence, we undertook this study to evaluate the adequacy and efficacy of different doses of vitamin D3 in schoolchildren. A total of 1008 vitamin D-deficient (VDD) children, aged 6–16 years with serum 25-hydroxyvitamin D (25(OH)D) levels <50nmol/l, were cluster randomised into three groups (A-344, B-341 and C-232) for supplementation (600, 1000 and 2000 IU daily) of vitamin D3 under supervision for 6 months. Of the 1008 subjects who completed the study, 938 (93 %) were compliant. Baseline and post-supplementation fasting blood and urine samples were evaluated for Ca, phosphates, alkaline phosphatase, 25(OH)D and parathormone and urine Ca:creatinine ratio. The mean age of the subjects was 11·7 (sd 2·4) years, and the overall mean baseline serum 25(OH)D level was 24·3 (SD 9·5)nmol/l. Post-supplementation rise in serum 25(OH)D in compliant group was maximum with 2000 IU (70·0 (SD 30·0)nmol/l), followed by 1000 IU (46·8 (SD 22·5)nmol/l) and 600 IU (36·5 (SD 18·5)nmol/l), and serum 25(OH)D levels of ≥50nmol/l were achieved in 71·5, 81·8 and 92·9 % by groups A, B and C, respectively. Secondary hyperparathyroidism decreased from 31·7 to 8·4 % post-supplementation. Two participants developed hypercalciuria, but none developed hypercalcaemia. Children with VDD benefit maximum with the daily supplementation of 2000 IU of vitamin D3. Whether recommendations of 400 IU/d by Indian Council of Medical Research or 600 IU by Indian Academy of Pediatrics or Institute of Medicine would suffice to achieve vitamin D sufficiency in children with VDD remains debatable.

Acceleration of bone remodelling increases the risk of fragility fractures. The objective of the present study was to explore in elderly women whether a vitamin D and Ca-fortified dairy product providing about 17–25 % of the recommended intakes in vitamin D, Ca and proteins would reduce secondary hyperparathyroidism and bone remodelling in a way that may attenuate age-related bone loss in the long term. Thirty-seven institutionalised women, aged 84·8 (sd 8·1) years, with low serum 25-hydroxyvitamin D (5·5 (sd 1·7) ng/ml) were enrolled into a multicentre open trial to consume during 1 month two servings of soft plain cheese made of semi-skimmed milk providing daily 686 kJ (164 kcal), 2·5 μg vitamin D, 302 mg Ca and 14·2 g proteins. The primary endpoint was the change in serum carboxy terminal cross-linked telopeptide of type I collagen (CTX), selected as a marker of bone resorption. Thirty-five subjects remained compliant. Mean serum changes were: 25-hydroyvitamin D, +14·5 % (P = 0·0051); parathyroid hormone (PTH), − 12·3 % (P = 0·0011); CTX, − 7·5 % (P = 0·01); tartrate-resistant acid phosphatase isoform 5b (TRAP 5b), − 9·9 % (P < 0·0001); albumin, +6·2 % (P < 0·0001); insulin-like growth factor-I (IGF-I),+16·9 % (P < 0·0001); osteocalcin, +8·3 % (P = 0·0166); amino-terminal propeptide of type 1 procollagen (P1NP),+19·3 % (P = 0·0031). The present open trial suggests that fortified soft plain cheese consumed by elderly women with vitamin D insufficiency can reduce bone resorption markers by positively influencing Ca and protein economy, as expressed by decreased PTH and increased IGF-I, respectively. The rise in the bone formation marker P1NP could be explained by a protein-mediated increase in IGF-I. Thus, such a dietary intervention might uncouple, at least transiently, bone resorption from bone formation and thereby attenuate age-related bone loss.

Considering the negative effects of secondary hyperparathyroidism (SHPT) in patients with chronic renal failure (CRF), the objective of the present study was to evaluate body composition changes using conventional and vector bioimpedance analysis in patients before and after parathyroidectomy (PTX). Twelve adult patients, mean age 43·4 (sd 12·7) years, were evaluated prior to and 6 months after PTX. Diets were assessed with 3d dietary records, and mean energy, protein, calcium and phosphorus intake were estimated from these inventories. Weight, height, BMI and bioelectrical impedance were measured; and biochemical markers of nutritional status (albumin and total protein) and bone metabolism (calcium, phosphorus and intact parathyroid hormone) were determined. No significant differences were observed in mean energy, protein and phosphorus after surgery. There was a significant increase in calcium intake after PTX (382·3 (sd 209·6) mg to 656·6 (sd 313·8) mg; P<0·05). Mean weight, BMI, conventional bioelectrical impedance measurements, total body fat, lean body mass and total body water were unaffected by surgery. However, the phase angle and reactance significantly increased after PTX (5·0° (sd 1·4) to 5·6° (sd 1·3); 44·1 (sd 15·6) Ω to 57·1 (sd 14·4) Ω, respectively). The high levels of intact parathyroid hormone before surgery had a negative effect on total body fat (r −0·69, P<0·05). After PTX, the mean albumin significantly increased (3·9 (sd 0·4) g/dl to 4·2 (sd 0·6) g/dl; P<0·05). PTX for SHPT is associated with certain changes in laboratory values, dietary intake and body composition. The latter is best seen with bioimpedance vector analysis.