Summary: Researchers found an association between low vitamin D levels and reduced brain volume. Lower vitamin D was also linked to an increased risk of stroke and dementia. Up to 17% of dementia cases could be prevented by increasing vitamin D.
Source: University of South Australia
Dementia is one of the major causes of disability and dependency among older people worldwide, affecting thinking and behaviors as you age. But what if you could stop this degenerative disease in its tracks?
A world-first study from the University of South Australia could make this a reality as new genetic research shows a direct link between dementia and a lack of vitamin D.
Investigating the association between vitamin D, neuroimaging features, and the risk of dementia and stroke, the study found:
low levels of vitamin D were associated with lower brain volumes and an increased risk of dementia and stroke
genetic analyses supported a causal effect of vitamin D deficiency and dementia.
in some populations as much as 17 percent of dementia cases might be prevented by increasing everyone to normal levels of vitamin D (50 nmol/L).
Dementia is a chronic or progressive syndrome that leads to deterioration in cognitive function. About 487,500 Australians live with dementia and it is the country’s second leading cause of death. Globally, more than 55 million people have dementia with 10 million new cases diagnosed every year.
Supported by the National Health and Medical Research Council, the genetic study analysed data from 294,514 participants from the UK Biobank, examining the impact of low levels of vitamin D (25 nmol/L) and the risk of dementia and stroke. Nonlinear Mendelian randomisation (MR) – a method of using measured variation in genes to examine the causal effect of a modifiable exposure on disease – were used to test for underlying causality for neuroimaging outcomes, dementia, and stroke.
Senior investigator and Director of UniSA’s Australian Centre for Precision Health, Professor Elina Hyppönen, says the findings are important for the prevention of dementia and appreciating the need to abolish vitamin D deficiency.
“Vitamin D is a hormone precursor that is increasingly recognised for widespread effects, including on brain health, but until now it has been very difficult to examine what would happen if we were able to prevent vitamin D deficiency,” Prof Hyppönen says.
“Our study is the first to examine the effect of very low levels of vitamin D on the risks of dementia and stroke, using robust genetic analyses among a large population.
“In some contexts, where vitamin D deficiency is relatively common, our findings have important implications for dementia risks. Indeed, in this UK population we observed that up to 17 per cent of dementia cases might have been avoided by boosting vitamin D levels to be within a normal range.”
The findings are incredibly significant given the high prevalence of dementia around the world.
“Dementia is a progressive and debilitating disease that can devastate individuals and families alike,” Prof Hyppönen says.
“If we’re able to change this reality through ensuring that none of us is severely vitamin D deficient, it would also have further benefits and we could change the health and wellbeing for thousands.”
“Most of us are likely to be ok, but for anyone who for whatever reason may not receive enough vitamin D from the sun, modifications to diet may not be enough, and supplementation may well be needed.”
Higher vitamin D status has been suggested to have beneficial effects on the brain.
To investigate the association between 25-hydroxyvitamin D [25(OH)D], neuroimaging features, and the risk of dementia and stroke.
We used prospective data from the UK Biobank (37–73 y at baseline) to examine the association between 25(OH)D concentrations with neuroimaging outcomes (N = 33,523) and the risk of dementia and stroke (N = 427,690; 3414 and 5339 incident cases, respectively). Observational analyses were adjusted for age, sex, ethnicity, month, center, and socioeconomic, lifestyle, sun behavior, and illness-related factors. Nonlinear Mendelian randomization (MR) analyses were used to test for underlying causality for neuroimaging outcomes (N = 23,901) and dementia and stroke (N = 294,514; 2399 and 3760 cases, respectively).
Associations between 25(OH)D and total, gray matter, white matter, and hippocampal volumes were nonlinear, with lower volumes both for low and high concentrations (adjusted P-nonlinear ≤ 0.04). 25(OH)D had an inverse association with white matter hyperintensity volume [per 10 nmol/L 25(OH)D; adjusted β: –6.1; 95% CI: –11.5, –7.0]. Vitamin D deficiency was associated with an increased risk of dementia and stroke, with the strongest associations for those with 25(OH)D <25 nmol/L (compared with 50–75.9 nmol/L; adjusted HR: 1.79; 95% CI: 1.57, 2.04 and HR: 1.40; 95% CI: 1.26, 1.56, respectively).
Nonlinear MR analyses confirmed the threshold effect of 25(OH)D on dementia, with the risk predicted to be 54% (95% CI: 1.21, 1.96) higher for participants at 25 nmol/L compared with 50 nmol/L. 25(OH)D was not associated with neuroimaging outcomes or the risk of stroke in MR analyses. Potential impact fraction suggests 17% (95% CI: 7.22, 30.58) of dementia could be prevented by increasing 25(OH)D to 50 nmol/L.
Low vitamin D status was associated with neuroimaging outcomes and the risks of dementia and stroke even after extensive covariate adjustment. MR analyses support a causal effect of vitamin D deficiency on dementia but not on stroke risk.