Osteoporosis is one of the most prevalent skeletal disorders and has enormous public health consequences due to the morbidity and mortality of the resulting fractures. This article discusses the developmental origins of osteoporosis and outlines some of the modifiable and non-modifiable risk factors in both intrauterine and postnatal life that contribute to the later onset of osteoporosis. Evidence for the effects of birth size and early growth in both preterm and term born infants are discussed and the role of epigenetics within the programming hypothesis is highlighted. This review provides compelling evidence for the developmental origins of osteoporosis and highlights the importance of osteoporosis prevention at all stages of the life course. Osteoporosis is one of the most prevalent skeletal disorders and has a similar lifetime risk to coronary heart disease [ 3 ]. It affects approximately 3 million people in the UK and worldwide, an osteoporotic fracture occurs every 3 seconds [ 4 ].
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In older adults, the genetic effect has been reported in women only. However, in younger adults, this influence may only be present in men. The association between MTHFR genotype and spine BMD was attenuated particularly in girls by high maternal dietary intakes of vitamin B 6 and folate during pregnancy but not by child dietary intakes at 7 yr. To the extent that these findings reflect known influences of CT MTHFR genotype on plasma homocysteine levels, our results suggest that the latter is an important regulator of spinal BMD in childhood. Homocysteine is one of the suspected biological mechanisms by which BMD may be reduced. Its metabolism is not only affected by folate levels and the MTHFR gene but also by other B vitamins that act as cofactors.