Dementia, also known as senility, is a broad category of brain diseases that cause a long term, usually gradual decrease in the ability to think and remember, affecting a person’s daily functioning. Other common symptoms include emotional problems, difficulties with language and a decrease in motivation. A person’s consciousness is not believed to be affected. For the diagnosis to be present there must be a change from a person’s usual mental functioning and a greater decline than one would expect due to aging.
About 10% of people develop the disease at some point in their lives, with an increased incidence as an individual ages. As far as prevalence, about 3% of all people between the ages of 65–74 have dementia, 19% between ages 75 and 84 and nearly half of those over 85 years of age.
Studies examining the effect of low vitamin D levels on the onset of dementia are important, because 50% of the elderly have 25(OH)D levels less than 20 ng/ml and that increases to 70% – 90% among those with dementia.
Moreover, epidemiological evidence indicates that low 25(OH)D levels are associated with an increased risk of the onset of dementia. For example, in the Cardiovascular Health Study, low 25(OH)D was associated with hazard ratios for incident Alzheimer’s disease (AD) and all-cause dementia of more than two, meaning your risk of getting dementia was double if you were vitamin D deficient.
Evidence also shows that the risk for developing dementia is proportional to baseline vitamin D levels. Consistent with increased dementia risk, levels are also inversely associated with cognitive performance. This means that the lower your 25(OH)D level, the worse your brain functions.
Recently, Dr. Joshua Miller of Rutgers University and colleagues at UC Davis followed 382 subjects, for an average of 5 years after measuring the participants 25(OH)D levels and neuropsychological ability.
Miller JW, Harvey DJ, Beckett LA, Green R, Farias ST, Reed BR, Olichney JM, Mungas DM, DeCarli C. Vitamin D Status and Rates of Cognitive Decline in a Multiethnic Cohort of Older Adults. JAMA Neurol. 2015 Sep 14. doi: 10.1001/jamaneurol.2015.2115.
They associated baseline 25(OH)D levels to repeated neuropsychological tests of episodic memory, semantic memory, visuospatial ability and executive function.
Baseline 25(OH)D levels were around 19 ng/ml. The researchers found 70% of both African Americans and Hispanics had 25(OH)D levels < 20 ng/ml.
At baseline, a cross sectional analysis found all four functions were more impaired in those with 25(OH)D levels < 20 ng/ml compared to those ≥ 20 ng/ml, but only associations with episodic memory (P < .001) and executive function (P=.008) were statistically significant.
The authors found significant differences in the course of cognitive performance in association with 25(OH)D (whether treated as a continuous or categorical variable). Moreover, the rate of cognitive decline associated with 25(OH)D < 20 ng/ml was greatest for the 2 cognitive domains most strongly associated with Alzheimer’s Disease. This preventative effect of vitamin D was still present when participants with dementia were removed from the analysis.
The magnitude of the effect of vitamin D deficiency on brain function was considerable. For example, cognitive ability of individuals with low 25(OH)D declined 3 times greater than that of healthy subjects with 25(OH)D above 20 ng/ml.
The authors concluded:
“Our data support the common occurrence of VitD insufficiency among older individuals. In addition, these data show that African American and Hispanic individuals are more likely to have VitD insufficiency or deficiency. Independent of race or ethnicity, baseline cognitive ability, and a host of other risk factors, vitamin D insufficiency was associated with significantly faster declines in both episodic memory and executive function performance, which may correspond to elevated risk for incident AD dementia. Given that vitamin D insufficiency is medically correctable, well-designed clinical trials that emphasize enrollment of individuals of nonwhite race/ethnicity with hypovitaminosis D could be useful for testing the effect of vitamin D replacement on dementia prevention.”
The authors made no recommendation as to what aging people should do while we await randomized controlled trials (RCT). It is quite likely that a useful RCT will never be conducted, as it is unethical to identify a vitamin D deficient placebo group and not treat them.
The authors did not have enough subjects with 25(OH)D > 30 ng/ml to see if it was even more protective of brain function than levels above 20 ng/ml. Interestingly, they had 5 subjects with 25(OH)D above 50 ng/ml, which they excluded from the study. Three of those five were cognitively normal, one had mild dementia and the other severe dementia
Also, although it is not intuitively obvious, remember that serum 25(OH)D is also a marker of sun exposure, meaning there might be beneficial effects of sunlight above and beyond vitamin D. Furthermore, this study does not mean you will not get dementia if you have optimal vitamin D levels (whatever that optimal level is), it only means your risk is lower if your vitamin D level is ideal.
We stick with our long-standing recommendations: obtain natural vitamin D levels of around 40 – 80 ng/ml. The best way to do this is safe, sensible sun bathing whenever possible (when your shadow is shorter than you are) and supplementing with 5,000 IU/day of vitamin D3 on the days you can’t sunbathe.