Abstract
Optimizing skeletal health in early life has potential effects on bone health later in childhood and in adulthood. We aimed to evaluate the existing evidence that maternal exposures during pregnancy have an impact on the subsequent bone health among offspring in young adults aged between 16 and 30 years. The protocol is registered in the International Prospective Register of Systematic Reviews (PROSPERO) (ID: CRD42019126890). The search was conducted up to 2 April 2019. We included seven observational prospective cohort studies that examined the association between maternal dietary factors, vitamin D concentration, age, preeclampsia, and smoking with any bone indices among offspring. The results indicated that high concentrations of maternal vitamin D; low fat intake; and high intakes of calcium, phosphorus, and magnesium may increase the bone mineral density in offspring at age 16. Evidence also suggests that the offspring of younger mothers may have a higher peak bone mass. It remains inconclusive whether there is an influence of preeclampsia or maternal smoking on bone health among young adults. Our assessment of internal validity warrants a cautious interpretation of these results, as all of the included studies were judged to have serious risks of bias. High-quality studies assessing whether prenatal prognostic factors are associated with bone health in young adults are needed.
Highlights
Osteoporosis causes more than 8.9 million fractures annually worldwide, of which more than4.5 million occur in America and Europe [1]
Through the literature search up to 2 April 2019, we identified 3656 records after removing
There was a paucity of high-quality studies, but there is an indication that certain nutritional factors in pregnancy may be beneficial in terms of achieving a higher peak bone mass among the offspring
Summary
Osteoporosis causes more than 8.9 million fractures annually worldwide, of which more than. 4.5 million occur in America and Europe [1]. The overall lifetime risk for a wrist, hip, or vertebral fracture has been estimated to be 30–40% in developed countries [1]. Osteoporosis gives rise to a high global societal and individual disease burden and is associated with significant morbidity and mortality and a reduction in the quality of life [2]. Scientific contributions to the life course perspective of the prevention of osteoporosis have, over the last few decades, been growing considerably. In the Baker hypothesis, it was postulated that the prenatal environment induces long-lasting changes in physiological parameters such as hormonal levels, glucose tolerance, and satiety, a phenomenon known as “development programming”.
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