Maternal Diet, Behaviour and Offspring Skeletal Health

Abstract

Osteoporotic fracture has a major impact upon health, both in terms of acute and long term disability and economic cost. Peak bone mass, achieved in early adulthood, is a major determinant of osteoporosis risk in later life. Poor early growth predicts reduced bone mass, and so risk of fracture in later life. Maternal lifestyle, body build and 25(OH) vitamin D status predict offspring bone mass. Recent work has suggested epigenetic mechanisms as key to these observations. This review will explore the role of the early environment in determining later osteoporotic fracture risk.

DNA methylation and the social gradient of osteoporotic fracture: A conceptual model

“…Importantly, chronic stress up-regulates immune function and inflammatory responses in a way that is epigenetically determined although it is presently unclear whether this is mediated by the HPA axis, the sympathetic nervous system or both. Specific to bone, Goodfellow et al suggest plausibility for an increased expression of glucocorticoid receptors to result in an increased sensitivity of osteoblasts to cortisol, which might influence a reduction in BMD during the life course [42]. [15] Although there are limited data specifically pertaining to associations between social determinants, DNAm and osteoporotic fracture risk in adults, each of the examples highlighted above (placental calcium transporters and alterations to neuroendocrine-immune network set-points) is likely to be influenced by SEP ( Fig., Box 2).…”

Bone loss in adult offspring induced by low-dose exposure to teratogens

“…Epidemiological studies have now provided compelling evidence suggesting that inadequate maternal nutrition during pregnancy may be one of the risk factors for age-related bone loss and fractures [2][3][4]. Those observations are supported by experimental studies demonstrating that offspring of females fed with a restricted protein diet or a highly saturated fat diet exhibit altered bone microarchitecture indicative of bone loss [5,6].…”

Enhancement of osteogenesis post‐splenectomy does not attenuate bone loss in ovariectomized rats

“…Osteoporosis is a multifactorial metabolic skeletal disease characterized by a decline in bone mass and alterations in the microarchitectural integrity of bone, resulting in the loss of mechanical strength and an increased risk of fracture. 5 The immune system has been reported to be intimately involved in regulation of bone homeostasis and remodeling. 6 Evidence suggested that bone resorption and formation were modulated by the immune system through complex interactions involving T and B lymphocytes, dendritic cells, cytokines, and cell-cell interactions.…”