Vitamin D no defense against dementia

ADELAIDE – 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 on July 8, 2018 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.”

“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.”

Xavier Gruffat, pharmacist, from asked a few questions to Professor Hutchinson about this study:

Xavier Gruffat (Creapharma) – If I understand you correctly, your study shows that the lower levels of vitamin D found in patients with a neurodegenerative disease is the consequence rather than the cause of these diseases?
Prof. Hutchinson – This is our hypothesis – correct

A study published in 2014 in Neurology (here a press relase: by the University of Exeter in the UK showed that the risk of Alzheimer increases by 69% in participants with moderate vitamin D deficiency and increases to 122% in severe deficiency. Does your study explain or show a difference of percentage between low, moderate and severe deficiency of vitamin D and the impact on diseases like Alzheimer?
We propose that sun exposure is good and obviously is associated with vitamin D elevations. However, if sun exposure is good because of the mediator of the effect is vitamin D, then oral supplementation by vitamin D should be able to replace the absence of sun, and benefit the patients. This is where our study has identified that oral vitamin D does not have the same effects and as such vitamin D is a consequence of sun exposure, but other mystery “Sun induced factors” may be responsible for the brain benefits of sun exposure.

Did your study showed any possible difference in the intake of vitamin D, namely between nutritional supplements and sun exposure? Other said, the sun exposure was more efficient against neurodegenerative disease like Alzheimer or multiple sclerosis than intake with supplements, or the opposite?
Our study showed that oral vitamin D supplementation was unable to replace the sun effect for multiple neurodegenerative diseases.

Talking about multiple sclerosis, an interesting study carried out in Iran showed that after the Islamic Revolution, skin exposure to the sun became much rarer. Researchers at Oxford University in the UK found in 2013 that between 1989 and 2006 the number of cases of multiple sclerosis among women in Iran increased by 800%. Therefore, some scientists have investigated the impact of vitamin D in the development of multiple sclerosis. If I understand you well, you are saying that the sun (UV) might have an impact but the vitamin D would be only a consequence and once again not the cause?
This is correct

Source: Press release of University of Adelaide. Interview carried out by Xavier Gruffat with Prof. Hutchinson by e-mail between July 10 and 11, 2018.

Informations sur la rédaction de cet article et la date de la dernière modification: 11.07.2018