Vitamin D supplementation in infancy is recommended to prevent rickets. At the population level, its effects on bone mineralisation are largely unknown. We aimed to explore whether adherence to national vitamin D supplementation guidelines (10 µg/d up to the age of 2 years), supplementation at the ages of 5 and 7 years, and serum 25-hydroxyvitamin D (s-25(OH)D) at various time points associated with bone mineral density (BMD) at the age of 7 years in the Odense Child Cohort, Denmark (n 1194). High adherence was defined as supplementation with 10 µg of vitamin D 6–7 times per week during ≥80 % of the observation time. s-25(OH)D was analysed using LC-MS/MS. Total-body-less-head (TBLH) BMD was measured by dual-energy X-ray absorptiometry. At the median age of 18·1 months, 53·9 % (n 475/881) reported high adherence. The median s-25(OH)D was 64·7, 78·8, 46·0 and 71·8 nmol/l in early pregnancy, late pregnancy, cord blood and at 5 years, respectively. The mean TBLH BMD at the median age of 7·1 years was 0·613 (SD 0·049) g/cm2 (z-score +0·363 (SD 0·824)). In adjusted analyses, vitamin D supplementation up to 18 months, and at 5 and 7 years, was not associated with TBLH BMD. Similarly, no robust associations were found between TBLH BMD and s-25(OH)D at any time point. No associations were found for TBLH bone mineral concentration or bone area. In this population with relatively high s-25(OH)D concentrations, no consistent associations were found between adherence to vitamin D supplementation recommendations or vitamin D status in pregnancy or childhood, and bone mineralisation at the age of 7 years.

Breast-feeding has been associated with later bone health, but results from previous studies are inconsistent. We examined the associations of breast-feeding patterns and timing of introduction of solids with bone mass at the age of 6 years in a prospective cohort study among 4919 children. We collected information about duration and exclusiveness of breast-feeding and timing of introduction of any solids with postnatal questionnaires. A total body dual-energy X-ray absorptiometry scan was performed at 6 years of age, and bone mineral density (BMD), bone mineral content (BMC), area-adjusted BMC (aBMC) and bone area (BA) were analysed. Compared with children who were ever breast-fed, those never breast-fed had lower BMD (−4·62 mg/cm2; 95 % CI −8·28, −0·97), BMC (−8·08 g; 95 % CI −12·45, −3·71) and BA (−7·03 cm2; 95 % CI −12·55, −1·52) at 6 years of age. Among all breast-fed children, those who were breast-fed non-exclusively in the first 4 months had higher BMD (2·91 mg/cm2; 95 % CI 0·41, 5·41) and aBMC (3·97 g; 95 % CI 1·30, 6·64) and lower BA (−4·45 cm2; 95 % CI −8·28, −0·61) compared with children breast-fed exclusively for at least 4 months. Compared with introduction of solids between 4 and 5 months, introduction <4 months was associated with higher BMD and aBMC, whereas introduction between 5 and 6 months was associated with lower aBMC and higher BA. Additional adjustment for infant vitamin D supplementation did not change the results. In conclusion, results from the present study suggest that ever breast-feeding compared with never breast-feeding is associated with higher bone mass in 6-year-old children, but exclusive breast-feeding for 4 months or longer was not positively associated with bone outcomes.

Children's vitamin D intake and status can be optimised to meet recommendations. We investigated if nutritionally balanced school meals with weekly fish servings affected serum 25-hydroxyvitamin D (25(OH)D) and markers related to bone in 8- to 11-year-old Danish children. We conducted an explorative secondary outcome analysis on data from 784 children from the OPUS School Meal Study, a cluster-randomised cross-over trial where children received school meals for 3 months and habitual lunch for 3 months. At baseline, and at the end of each dietary period, 25(OH)D, parathyroid hormone (PTH), osteocalcin (OC), insulin-like growth factor-1 (IGF-1), bone mineral content (BMC), bone area (BA), bone mineral density (BMD), dietary intake and physical activity were assessed. School meals increased vitamin D intake by 0·9 (95 % CI 0·7, 1·1) μg/d. No consistent effects were found on 25(OH)D, BMC, BA, BMD, IGF-1 or OC. However, season-modified effects were observed with 25(OH)D, i.e. children completing the school meal period in January/February had higher 25(OH)D status (5·5 (95 % CI 1·8, 9·2) nmol/l; P = 0·004) than children completing the control period in these months. A similar tendency was indicated in November/December (4·1 (95 % CI –0·12, 8·3) nmol/l; P = 0·057). However, the effect was opposite in March/April (–4·0 (95 % CI –7·0, –0·9) nmol/l; P = 0·010), and no difference was found in May/June (P = 0·214). Unexpectedly, the school meals slightly increased PTH (0·18 (95 % CI 0·07, 0·29) pmol/l) compared with habitual lunch. Small increases in dietary vitamin D might hold potential to mitigate the winter nadir in Danish children's 25(OH)D status while higher increases appear necessary to affect status throughout the year. More trials on effects of vitamin D intake from natural foods are needed.

Infants of diabetic mothers may have low arachidonic acid (AA) and develop obesity and insulin resistance in adulthood. The present study tested the effect of maternal diabetes and AA supplementation on offspring body composition, bone mass and glucose tolerance from 4 to 12 weeks. Rat dams were randomised into six groups using a 3 × 2 design. The rat dams were treated using the following treatments: saline-placebo, streptozotocin-induced diabetes (STZ) with glucose controlled at < 13 mmol/l (STZ/GC) or poorly controlled at 13–20 mmol/l (STZ/PC) using insulin, and fed either a control or an AA (0·5 % of fat) diet throughout reproduction. Weaned offspring were fed regular chow. Measurements included offspring body composition, bone and oral glucose tolerance testing (OGTT) plus liver fatty acids of dam and offspring. Comparable to saline-placebo offspring, the STZ/GC offspring had greater (P < 0·03) whole body and regional bone area than STZ/PC offspring. Maternal glucose negatively correlated (P < 0·05) with offspring whole body bone area and mineral content at 4 weeks in all offspring, and with tibia area in males at 12 weeks. Maternal liver DHA negatively (P < 0·03) correlated with femur and tibia mineral content and tibia mineral density of female offspring at 12 weeks. Offspring from AA-supplemented dams had higher (P = 0·004) liver AA at 4 weeks. Liver AA at 4 weeks positively (P = 0·05) correlated with lumbar spine mineral density in males. OGTT was not affected by maternal treatment or diet. These results suggest that maternal glucose control has long-term consequences to bone health of adult offspring. Skeletal growth appears more sensitive to maternal hyperglycaemia than glucose tolerance.