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Researcher, Children’s Hospital Research Institute of Manitoba; Associate Professor, Pediatric Endocrinology, Department of Pediatrics and Child Health, University of Manitoba
1985 Doctor of Medicine University of Toronto
1989 The Royal College of Physicians and Surgeons (Canada) Pediatrics
1991 Subspecialty Certification in Pediatric Endocrinology, Royal College of Physicians and Surgeons (Canada)
2010 Masters in Epidemiology, London School of Hygiene and Tropical Medicine
For years, my research has focused on calcium homeostasis and bone physiology and their associated disorders. I am particularly interested in defining optimal vitamin D intake for healthy Canadian children. My work assessing vitamin D adequacy in the paediatric population includes novel functional outcomes, such as muscle strength, balance and body composition. These studies determined that 400IU/day of vitamin D is sufficient for normal bone mineralization and accrual in healthy children.
Recent grants have used population-based studies of term and pre-term infants to assess vitamin D supplementation rates and the association between the recent increase in exclusive breastfeeding and the incidence of rickets. These results point to the fact that we need to engage parents early and often, particularly younger parents and those with lower education levels to promote vitamin D in infancy.
As part of our efforts to define vitamin D adequacy, our group has also been developing normative data for minerals and other analytes, particularly in healthy infants, where there is a real paucity of such data. Our data was just published; ongoing collaboration with the CALIPER study will ramp up in Winnipeg. Longstanding collaborative projects also assess bone health in children with chronic diseases and those exposed to prolonged glucocorticoids.
With funding through CIHR, our European-Canadian collaborative team is also examining the causes of hypercalcemia and hypercalciuria in children. We have been using a candidate gene approach and sensitive metabolomics investigations by LC-MS/MS to help unravel the relationship between these disorders and mutations in CYP24A1, the enzyme responsible for degrading vitamin D metabolites to inactive forms. These efforts have recently demonstrated a role for CYP24A1 mutations in milder cases of hypercalcuria and nephrocalcinosis in Canadian children.
Lastly, now that new Canadian growth charts have been developed (2014 WHO growth charts for Canada), detailed validation studies are ongoing.