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Q&A With John McGrath

by Hakon Heimer Posted on 17 Feb 2017

In a short email interview with SRF, John McGrath isn't ready to concede the case that prenatal vitamin D levels could create risk for later mental illness. He continues work to explore developmental links between vitamin D and psychotic disorders or autism.

 Q&A With John McGrath

See SRF related news report.

Q: Do these findings in depression influence how you see the prospects for more research into the relationship between vitamin D and psychosis?

A: We have shown in animal models that developmental vitamin D deficiency produces a different phenotype from adult vitamin D deficiency. With respect to psychosis, we are still focused on gestational vitamin D. We are working on new studies in Denmark. We recently published a study based on the Generation R birth cohort that found an association between gestation and cord blood vitamin D concentration, and higher autism-related scores. (Vinkhuyzen et al., 2016)

Q: Will the current randomized trials underway address mental illness links, and do you know when they will be completed?

A: I think some of the studies may include mental health outcomes (e.g., self-report measures), but none have specified mental disorders as a primary outcome. Currently, there is not enough evidence to suggest that adult vitamin D deficiency is a cause of adult-onset mental disorders. My hunch is that vitamin D deficiency may contribute to worse outcomes in those with neuropsychiatric disorders―but this is a "two hit" model. Of course, many people with mental disorders have low vitamin D, and thus they need to have supplements in order to help their bone health and reduce risk of falls (good evidence to support these outcomes). But, we do not expect that the use of vitamin D supplements will "cure" their antecedent mental disorders.

Q: Negative results such as the Jovanova study and last year’s report on fish oil for psychosis-risk patients could make the field less interested in research on fundamental or, as you say, “promiscuous,” molecules (e.g., also folate). Is that justified, and what sort of research do you think we should support on such molecules?

A: The Jovanova study was an observational study, while the recent fish oil study was a Randomized Controlled Trial. It is disappointing that the new RCT does not replicate the findings of the original fish oil study. We would expect nutrition-related augmentation studies to have a small effect size; thus, we do need large studies to detect these weak effects. With respect to prenatal vitamin D and folate, it is not practical or ethical to do RCTs of prenatal interventions and follow up for 20 to 30 years. So if we wish to build an evidence base to justify their use, we will need to look for more proximal outcomes (e.g., autism spectrum disorders) or surrogates―early-onset outcomes. Unfortunately, we currently lack these in schizophrenia research. It will be a challenge for the field.