Polymorphisms in the vitamin D receptor and their associations with risk of schizophrenia and selected anthropometric measures

The association between vitamin D levels and skeletal growth has long been recognized. However, exposure to low levels of vitamin D during early life is also known to alter brain development, and is a candidate risk factor for schizophrenia. This study examines the association between four polymorphisms in the vitamin D receptor (VDR) and 1) risk of schizophrenia, and 2) three anthropometric variables (height, head size, and head shape). Four single-nucleotide polymorphisms (SNPs; rs10735810/FokI, rsl544410/BsmI, rs7975232/ApaI, and rs731236/TaqI) in the VDR gene were genotyped in 179 individuals with schizophrenia and 189 healthy controls. No significant associations were detected between any of the four VDR SNPs and risk of schizophrenia. Patients were slightly but significantly shorter compared to controls. Of the four SNPs, only rs10735810/FokI was associated with any of the anthropometric measures: the M4 isoform of this SNP was significantly associated with larger head size (P = 0.002). In light of the evidence demonstrating a role for vitamin D during brain development, the association between polymorphisms in VDR and brain development warrants closer scrutiny.

What are the policy implications of the evidence on cannabis and psychosis?

Objective: To explore the implications for mental health services, for health education about the risks of cannabis use, and for public policy toward cannabis use of observational evidence that cannabis use is a contributory cause of psychosis. Method: Using comparative analyses of similar evidence for the harmful effects of alcohol, tobacco, and amphetamine use, we considered the relation between observational evidence and action on cannabis. We examined arguments on the grounds of public health prudence for discouraging cannabis use by young individuals. With the assumption that the relation may be causal, we considered recommendations for policy in mental health services, health education, and public policy toward cannabis. Results: The observational evidence and biological plausibility of the hypothesis that cannabis is a contributory cause of psychosis is at least as strong as evidence for causal relations between heavy alcohol and amphetamine use and psychosis. On public health grounds, there is a good case for discouraging cannabis use among adolescents and young adults. It remains uncertain how best to discourage use and at whom campaigns to reduce cannabis use should be targeted. Conclusions: We should discourage young adults seeking treatment in mental health services from using cannabis and inform them of the probable mental health risks of cannabis use, especially of early and frequent use. We must exercise caution in liberalizing cannabis laws in ways that may increase young individuals' access to cannabis, decrease their age of first use, or increase their frequency of cannabis use. We should consider the feasibility of reducing the availability of high-potency cannabis products.