placebo controls (Pittas et al., 2007a). Although the findings of this study are in agreement with a previous secondary analysis of data from the NHS cohort (see below: Pittas et al., 2006), the study is limited by the small number of outcomes measured compared with the total cohort; thus, an unintended bias cannot be ruled out. In addition, the study was designed for skeletal outcomes as the primary analysis. When the totality of the evidence was considered, the negative findings from the clinical trials for an effect of vitamin D or calcium on risk for type 2 diabetes together with the lack of significant evidence from either the AHRQ reviews or the meta-analysis by Pittas et al. (2007b) compelled the committee to conclude that there was not sufficient evidence to establish a causal relationship.
Low serum 25OHD levels have been implicated in metabolic syndrome, abdominal obesity, and hyperglycemia.
In a prospective cohort analysis of data from NHS, women were followed for 20 years to examine associations between vitamin D and calcium intake and risk for type 2 diabetes (Pittas et al., 2006). A significant inverse association was found between total vitamin D intake and calcium intake and risk for type 2 diabetes. A separate analysis of the association between risk for type 2 diabetes and dairy food consumption found that women who consumed three or more dairy servings per day were at lower risk compared with those who consumed less than one dairy serving per day. These findings suggest that risk for type 2 diabetes is associated with vitamin D or dairy food intake. A small cohort study in obese and overweight individuals found that in addition to a significant inverse association between serum 25OHD level and weight and waist circumference there was a weak inverse relationship with hemoglobin A1c. However, no association between serum 25OHD level and any other indicators of type 2 diabetes or metabolic syndrome were observed (McGill et al., 2008).
In other observational evidence reviewed, a cross–sectional survey of Polynesian and white adult populations in New Zealand found a significantly lower serum 25OHD level in subjects with newly diagnosed diabetes and impaired glucose tolerance compared with controls. In addition, among the control groups, the native New Zealand populations (Maori and Pacific Islanders) were found to have significantly lower serum 25OHD levels compared with Europeans. The authors speculated that the low serum 25OHD level in the native populations explained, in part, the higher prevalence of diabetes in those groups (Scragg et al., 1995). Isaia et al. (2001), in a cross–sectional study in Italy, found that postmenopausal women diagnosed with type 2 diabetes had significantly higher body mass indexes (BMIs), lower activity scores, higher prevalence of serum 25OHD