Written by Susan Sweeny Johnson, PhD. Those who were Vitamin D deficient were 60% more likely than those who were Vitamin D sufficient to experience cognitive decline.
The active form of vitamin D in the blood stream is calcitrol (1,25dihydroxycholecalciferol). It plays an important role in regulating calcium absorption, bone deposition and circulating calcium levels in the body. It also plays a role in promoting a healthily immune response (1). Since receptor for vitamin D have been found in nerve cells, and calcium levels regulate nerve signals, vitamin D may play a significant role in promoting healthy brain function (1-2). One study suggested a link between calcitrol and curcuminoids and the ability to clear beta-amyloid structures associated with Alzheimer’s disease (3).
In this large study of 865 adults aged 65+, low levels of circulating levels of 25(OH)D (vitamin D) were correlated with brain function decline over the six years of follow-up. This study analyzed the data collected from the In CHIANTI population–based study conducted in Italy between 1998 and 2006 which was established to look for risk factors for late-life disability (4).
The study participants were divided into four groups based on baseline blood 25(OH)D levels as follows:
- Group 1 – severely vitamin D deficient, 25(OH)D < 25nmol/l
- Group 2 – deficient, 25(OH)D 25nmol/l to 50nmol/l
- Group 3 – insufficient, 25(OH)D 50nmol/l to 75nmol/l
- Group 4 – sufficient, >75nmol/l
At 3 years and 6 years, they were given the Mini-Mental State Examination (MMSE), a standard mental assessment test for cognitive function, together with Trail-Making Test A which measures attention and Trail-Making Test B which measures execution.
Overall those who were severely 25(OH)D deficient (Group 1) were approximately 60% more likely than those who were 25(OH)D sufficient (Group 4) to experience substantial cognitive decline on the MMSE score (p for linear trend < 0.001)* and 31% more likely to have substantial decline on the Trails B score (p for linear trend = 0.04). There were no significant associations between 25(OH)D levels and performance on Trails A. The same pattern of associations was observed when the sample was restricted to participants who did not exhibit dementia at baseline.
One strength of this study is that the data could be analyzed to look for other variables that might also affect cognitive decline. There was no significant change in the above trends when the data was corrected for age, sex, education, baseline cognitive score, season tested, alcohol consumption, current smoking status, depressive symptoms, body mass index (BMI), total energy intake, serum vitamin E level (alpha tocopherol), and impaired mobility. Note, though, that all participants were of Italian descent.
Further studies should address the role of vitamin D in cognitive function and neuroprotection.
In a study designed to estimate health care costs for elderly dementia patients, it was found that the annual cost of providing informal care to elderly community-dwelling veterans with dementia was estimated to be $18,385 per patient in 1998. The larger components of this cost are care giving time ($6,295) and caregiver’s lost earnings ($10,709). All aspects of costs increase with disease severity and problem behavior. Most of this cost increase derives from the increased care giving time required for the provision of physical care (5).
According to recent estimates, as many as 2.4 million to 5.1 million Americans have Alzheimer’s disease (AD), an extreme dementia. The number of people age 65 and older is expected to grow from 39 million in 2008 to 72 million in 2030, and the number of people with AD doubles for every 5-year interval beyond age 65 (6). This implies a significant rise in dementia care costs in the near future.
* p is a measure of the significance of the data, p < 0.05 is considered significant
Source: Llewellyn, David J., et al. “Vitamin D and risk of cognitive decline in elderly persons.” Archives of internal medicine 170.13 (2010): 1135-1141.
© 2010 American Medical Association. All rights reserved.
Posted July 23, 2010.
References:
- Buell JS, Dawson-Hughes B. Vitamin D and neurocognitive dysfunction: preventing
“D”ecline? Mol Aspects Med. 2008;29(6):415-422. - McCann JC, Ames BN. Is there convincing biological or behavioral evidence linking
vitamin D deficiency to brain dysfunction? FASEB J. 2008;22(4):982-1001. - Masoumi A, Goldenson B, Ghirmai S, et al. 1alpha,25-dihydroxyvitamin D3 interacts
with curcuminoids to stimulate amyloid-beta clearance by macrophages of Alzheimer’s disease patients. J Alzheimers Dis. 2009;17(3):703-717. - Ferrucci L, Bandinelli S, Benvenuti E, et al. Subsystems contributing to the decline in ability to walk: bridging the gap between epidemiology and geriatric practice in the InCHIANTI study. J Am Geriatr Soc. 2000;48(12):1618-1625.
- J Gerontol B Psychol Sci Soc Sci. 2001 Jul;56(4):S219-28 from the PubMed website.
- From the National Institute on Aging.
