Reports of vitamin D deficiency and rickets among Aboriginal people in Canada are not new. In 1984, Godel and Hart  reported on 16 Inuit infants living in high Arctic coastal communities who presented at approximately three months of age with a spectrum of illnesses that included hepatitis, rickets, hemolytic anemia and respiratory infections. Eighty-one per cent of infants had florid rickets and high alkaline phosphatase levels. Extremely low 25-hydroxyvitamin D (25[OH]D) levels of 6.8 nmol/L to 9.4 nmol/L were found in four of seven infants. Similarly, Haworth and Dilling  reported 48 cases of vitamin D-deficient rickets in First Nations communities in Manitoba between 1977 and 1984. A follow-up by Lebrun et al  found a high prevalence of deficiency, much of it related to breastfeeding and lack of supplementation.
More recently, the Canadian Paediatric Surveillance Program reported 104 confirmed cases of rickets in Canada between 2002 and 2004. A high percentage of these patients were of First Nations (13%) or Inuit (12%) descent, with 14% of Middle-Eastern origin . Vitamin D deficiency also continues to be a problem among Aboriginal mothers during pregnancy. This is underlined in a recent report by Weiler et al .
The present statement addresses the advances in knowledge and practice related to vitamin D since the Canadian Paediatric Society statement on vitamin D in 2002  and makes recommendations based on these advances.
The emphasis is no longer solely on preventing rickets, which requires only a relatively small amount of vitamin D supplementation. The focus is now also on the prevention of associated childhood and adult diseases. New findings suggest that adequate vitamin D status in mothers during pregnancy and in their infants may have lifetime implications. These findings modify our knowledge and understanding of vitamin D metabolism, our basis for diagnosis of vitamin D deficiency and our recommendations for supplementation.
It is now clear that vitamin D is involved in the regulation of cell growth, immunity and cell metabolism. Vitamin D receptors are found in most tissues and cells in the body . The interaction of 1,25(OH)2D with these receptors may result in a variety of biological responses influencing disease processes . Vitamin D deficiency has been linked to osteoporosis ; asthma ; autoimmune diseases such as rheumatoid arthritis, multiple sclerosis  and inflammatory bowel diseases ; diabetes ; disturbed muscle function ; resistance to tuberculosis ; and the pathogenesis of specific types of cancer  (evidence level III).
Maternal vitamin D status during gestation and lactation may influence the health status of the child later in life. Bone density in nine-year-old children (evidence level II-3) , the severity of asthma in three-year-old children  (evidence level II-2) and the susceptibility to type 1 diabetes  (evidence level II-2) have been linked to low vitamin D status during fetal life. Intervention trials have demonstrated that supplementation with vitamin D or its metabolites may improve blood glucose levels in diabetics and decrease symptoms of rheumatoid arthritis and multiple sclerosis  (evidence level III).
Dental caries may also have their beginnings in fetal or early newborn life. Studies suggest that infants of mothers who are vitamin D- or calcium-deficient during pregnancy may be at risk for enamel defects in primary and permanent teeth in spite of adequate supplementation later  (evidence level II-3). Aboriginal communities with a high incidence of vitamin D deficiency have an associated high prevalence of caries , although no studies of cause and effect have been carried out.
The purpose of the present update is to explore the implications of the latest research in vitamin D on the health of all Canadian mothers and their infants and to make recommendations based on these findings. A brief review of the nomenclature and metabolism is included for clarity.
Review of the nomenclature and metabolism of vitamin D
Three systems are used interchangeably to measure vitamin D: Metric (ng/mL), International Units (IU) and Molar (nmol/L). 1 IU of vitamin D equals 25 ng (0.025 µg) or 65 pmol. Thus 400 IU of vitamin D equals 10 µg or 26 nmol . Vitamin D3, which is produced in the skin of animals, and Vitamin D2, which is of plant origin, are metabolized in a similar manner, first by 25-hydroxylation in the liver to 25(OH)D2 and D3, inactive but stable forms used for defining vitamin D status, then by 1-hydroxylation in the kidney to 1,25(OH)2D2 and D3, the active but unstable forms.
The definition of vitamin status has been modified as a result of research into the relationship between vitamin D, parathyroid hormone, serum calcium and bone resorption. Optimal plasma 25(OH)D levels have been defined as levels at which parathyroid hormone production  (evidence level II-2) and calcium reabsorption from bone are minimized, and intestinal calcium absorption is stabilized (range 75 nmol/L to 225 nmol/L [30 ng/mL to 90 ng/mL]). Levels greater than 225 nmol/L (90 ng/mL) may be associated with hypercalcemia and calcium deposition in tissues, and levels greater than 500 nmol/L (greater than 200 ng/mL) are considered toxic. Table 1  shows current definitions of 25(OH)D status.