The fetal origins of adult disease hypothesis was first suggested in the late 1980’s, where low birth weight was linked to adverse cardiovascular health in adulthood. Additionally, epidemiologic studies have reported that low birth weight humans have bone mineral content (BMC), density (BMD) and bone strength deficits, highlighting the effects an adverse intrauterine environment can have on adult bone phenotypes.
Experimentally, using a rat model of uteroplacental insufficiency, we have reported that both male and female rats born small have slowed growth throughout life with shorter adult femur length. Importantly, deficits in trabecular and cortical BMC, periosteal circumference, endosteal circumference, cortical thickness and bone bending strength are also present in these offspring at age 6 and 12 months. We further investigated this phenotype and determined the effects of calcium supplementation from early adolescence on adult bone phenotypes using both a constant and cyclic mode of calcium delivery. Additionally, we were the first to report changes to maternal skeletal physiology during pregnancy when the mother suffers from uteroplacental insufficiency.
We have investigated the transgenerational transmission of bone deficits across subsequent generations, and also focused on the possible deleterious effects of maternal stress on maternal and offspring bone health. More recently our work has focused on the effects of high fat diet and exercise on bone health and paternal line transmission of programmed bone deficits. This talk will highlight our findings to date related to this novel area of bone research. Determining a potential mechanism and interventions that can rescue these skeletal deficits are of major public health relevance, as we may then be able to reduce the incidence of skeletal diseases such as osteoporosis and fracture risk in adults who were born small.