D or placebo and found that both vitamin D doses increased positive affect and decreased negative affect compared with placebo. Gloth et al. (1999) assigned 15 people to either 100,000 IU of vitamin D or broad-spectrum light therapy for 1 month and found an increase in serum 25OHD level was significantly associated with improvement in depressive symptoms. However, Harris and Dawson-Hughes (1993) randomized 250 middle-aged and older women to treatment with 400 IU of vitamin D per day of vitamin D plus 377 mg of calcium per day or to calcium alone for 1 year and found no treatment-related changes in seasonal mood as assessed by the Profile of Mood States (POMS) questionnaire.

Observational studies Among four cross–sectional studies on small population groups (n < 50) that evaluated associations between serum 25OHD level and evidence for clinical diagnosis of depression in women (Michelson et al., 1996; Herran et al., 2000; Eskandari et al., 2007) or men and women (Schneider et al., 2000), only Eskandari et al. (2007) found a significant association between serum 25OHD level and diagnosis of depression and Michelson et al. (1996) found a significant association with calcitriol level. Another large population-based cross–sectional study among middle-aged and elderly Chinese also found, after controlling for confounders and geographic location, no significant associations between serum 25OHD level (grouped by tertile) and symptoms of clinical depression (Pan et al., 2009). In contrast to the cross–sectional studies, Hoogendijk et al. (2008) found, in a cohort study in the Netherlands, a significantly lower mean serum 25OHD level (47.5 nmol/L) among individuals with both major and minor depression compared with a mean level of 55 nmol/L among those who did not have depression.

Although some observational studies support an association between low measures of vitamin D exposure and risk for cognitive impairment or changes in mood, results have been inconsistent, and the majority of studies were cross–sectional in study design, including possible selection bias or other confounding factors that diminish the quality ranking of the studies. In addition, few or no clinical trials were identified to support biological plausibility. As a result of the many shortcomings in study design and quality of observational evidence and the paucity of high-quality evidence from RCTs identified by the committee, the findings for neuropsychological indicators are inconclusive. The committee’s review of the available evidence for either associations or a causal relationship between vitamin D and calcium and risk for cognitive disorders shows a lack of sufficient evidence to support DRI development.