Vitamin D No Defense Against Dementia or MS

Summary: Researchers report they have found little convincing evidence to support the claim vitamin D is a neuroprotective agent.

Source: University of Adelaide.

New research from South Australian scientists has shown that vitamin D (also commonly known as the sunshine vitamin) is unlikely to protect individuals from multiple sclerosis, Parkinson’s disease, Alzheimer’s disease or other brain-related disorders.

The findings, released today in the science journal Nutritional Neuroscience reported that researchers had failed to find solid clinical evidence for vitamin D as a protective neurological agent.

“Our work counters an emerging belief held in some quarters suggesting that higher levels of vitamin D can impact positively on brain health,” says lead author Krystal Iacopetta, PhD candidate at the University of Adelaide.

Based on a systematic review of over 70 pre-clinical and clinical studies, Ms Iacopetta investigated the role of vitamin D across a wide range of neurodegenerative diseases.

“Past studies had found that patients with a neurodegenerative disease tended to have lower levels of vitamin D compared to healthy members of the population,” she says.

“This led to the hypothesis that increasing vitamin D levels, either through more UV and sun exposure or by taking vitamin D supplements, could potentially have a positive impact. A widely held community belief is that these supplements could reduce the risk of developing brain-related disorders or limit their progression.”

“The results of our in-depth review and an analysis of all the scientific literature however, indicates that this is not the case and that there is no convincing evidence supporting vitamin D as a protective agent for the brain,” she says.

Ms Iacopetta believes that the idea of vitamin D as a neuro-related protector has gained traction based on observational studies as opposed to evaluation of all the clinical evidence.

“Our analysis of methodologies, sample sizes, and effects on treatment and control groups shows that the link between vitamin D and brain disorders is likely to be associative – as opposed to a directly causal relationship,” she explains.

“We could not establish a clear role for a neuroprotective benefit from vitamin D for any of the diseases we investigated.”

Mark Hutchinson, Director of the ARC Centre of Excellence for Nanoscale BioPhotonics (CNBP) and Professor at the University of Adelaide worked with Ms Iacopetta on the research and findings.

“This outcome is important and is based on an extremely comprehensive review and analysis of current data and relevant scientific publications,” Professor Hutchinson says.

“We’ve broken a commonly held belief that vitamin D resulting from sun exposure is good for your brain.”

Interestingly, Professor Hutchinson notes that there may be evidence that UV light (sun exposure) could impact the brain beneficially, in ways other than that related to levels of vitamin D.

“There are some early studies that suggest that UV exposure could have a positive impact on some neurological disorders such as multiple sclerosis,” he says. “We have presented critical evidence that UV light may impact molecular processes in the brain in a manner that has absolutely nothing to do with vitamin D.”

a brain
Ms Iacopetta believes that the idea of vitamin D as a neuro-related protector has gained traction based on observational studies as opposed to evaluation of all the clinical evidence. image is in the public domain.

“We need to complete far more research in this area to fully understand what’s happening,” says Professor Hutchinson.

“It may be that sensible and safe sun exposure is good for the brain and that there are new and exciting factors at play that we have yet to identify and measure.”

“Unfortunately however, it appears as if vitamin D, although essential for healthy living, is not going to be the miracle ‘sunshine tablet’ solution for brain-disorders that some were actively hoping for.”

About this neuroscience research article

Researchers involved in this systematic review are affiliated with the University of Adelaide, the University of South Australia and the ARC Centre of Excellence for Nanoscale BioPhotonics (CNBP).

Source: Mark Hutchinson – University of Adelaide
Publisher: Organized by
Image Source: image is in the public domain
Original Research: Abstract for “Are the protective benefits of vitamin D in neurodegenerative disease dependent on route of administration? A systematic review” by Krystal Iacopetta, Lyndsey E. Collins-Praino, Femke T. A. Buisman-Pijlman, Jiajun Liu, Amanda D. Hutchinson & Mark R. Hutchinson in Nutritional Neuroscience. Published July 9 2018.

Cite This Article

[cbtabs][cbtab title=”MLA”]University of Adelaide”Vitamin D No Defense Against Dementia or MS.” NeuroscienceNews. NeuroscienceNews, 10 July 2018.
<>.[/cbtab][cbtab title=”APA”]University of Adelaide(2018, July 10). Vitamin D No Defense Against Dementia or MS. NeuroscienceNews. Retrieved July 10, 2018 from[/cbtab][cbtab title=”Chicago”]University of Adelaide”Vitamin D No Defense Against Dementia or MS.” (accessed July 10, 2018).[/cbtab][/cbtabs]


Are the protective benefits of vitamin D in neurodegenerative disease dependent on route of administration? A systematic review

Background: The clinical and preclinical exploration of the therapeutic properties of vitamin D have significantly increased in the past decade, owing to the growing associative evidence suggesting vitamin D is neuroprotective. However, whether depletion of vitamin D contributes to the onset of neurological disorders or is a symptom of neurological disease has yet to be defined. Much remains unclear about the causal role of vitamin D and the method of use and forms of vitamin D.

Objectives: We sought to quantitatively assess if neuroprotective benefits from vitamin D in neurodegenerative diseases are dependent on route of administration: comparing the effect of endogenously sourced vitamin D from UV exposure to exogenously derived vitamin D through synthetic supplementation.

Design: We systematically searched PubMed, Embase and PsycInfo databases which included both pre-clinical and clinical studies investigating vitamin D in neurodegenerative diseases. Articles were subject to strict inclusion criteria and objectively assessed for quality. Additionally, Medline data was analysed to identify trends in topic publications and linguistic characteristics of papers.

Results: From a total of 231 screened articles, we identified 73 appropriate for review based on inclusion criteria: original studies that investigated vitamin D levels or levels of vitamin D supplementation in neurodegenerative diseases or investigated past/present sun exposure in disease cohorts. Results indicate there is insufficient evidence to comprehensively reflect on a potential neuroprotective role for vitamin D and if this was dependent on route of administration. The majority of current data supporting neuroprotective benefits from vitamin D are based on pre-clinical and observational studies. Solid evidence is lacking to support the current hypothesis that the beneficial effect of UV exposure results from the synthesis of vitamin D. Sun exposure, independent of vitamin D production, may be protective against multiple Sclerosis, Parkinson’s disease and Alzheimer’s disease. Yet, further research is required to elucidate the beneficial mechanism of actions of UV exposure. The literature of vitamin D and amyotrophic lateral sclerosis was limited, and no conclusions were drawn. Therefore, in cases where UV-derived vitamin D was hypothesized to be the beneficial mediator in the neuroprotective effects of sun exposure, we propose results are based only on associative evidence.

Conclusion: On the basis of this systematic review, strong recommendations regarding therapeutic benefits of vitamin D in neurodegenerative disease cannot be made. It is unclear if vitamin D mediates a protective benefit in neurodegenerative disease or whether it is an associative marker of UV exposure, which may contribute to as of yet unidentified neuroprotective factors.

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