Diabetes increases risk of poor cognition by 2X, 12 weeks of Vitamin D not help (but 18 weeks did) – RCT
Vitamin D Supplementation and Cognition in People with Type 2 Diabetes: A Randomized Control Trial
Journal of Diabetes Research, Volume 2019, Article ID 5696391, 13 pages. https://doi.org/10.1155/2019/5696391
Mary A. Byrn mbyrn@luc.edu, William Adams, Sue Penckofer, and Mary Ann Emanuele
Loyola University Chicago, Chicago, IL, USA
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Vitamin D levels did not even get to 30 ng in 3 months
Aim. Type 2 diabetes increases the risk of cognitive decline which adversely impacts self-management of the disease. Evidence also supports a relationship between low serum 25(OH)D levels and poor cognition. The purpose of this trial was to assess vitamin D supplementation on cognitive executive functioning in persons living with type 2 diabetes.
Methods. This was a double-blinded RCT where participants were randomized to receive either weekly vitamin D3 supplementation (50,000 IUs) or a matching comparator (5,000 IUs) for three months. The primary outcome was a battery of neuropsychological tests. Serum 25(OH)D was measured by liquid chromatography/tandem mass spectrometry. Repeated assessments of cognitive measures were collected over 12 weeks using alternative testing forms to minimize practice effects.
Results. Thirty participants were randomized to either the low-dose allocation () or the high-dose allocation (). Most participants were female (83%) and identified as Black (57%). For all cognition measures, there was no statistically significant finding between participants who received high-dose vitamin D supplementation and those who received low-dose supplementation. However, when assessing cognitive function in both groups over time, minimal improvement on the Symbol-Digits, the Stroop Interference Test, and the Trail Making Test Part B was observed.
Conclusions. To our knowledge, this is the first randomized control trial to examine the effects of vitamin D supplementation on cognitive function in people with type 2 diabetes. However, no significant differences in cognitive outcomes between participants who received high-dose therapy and those who received low dose were found.
Introduction
Diabetes increases the risk of cognitive dysfunction. The incidence of dementia is 1.5 to 2.5 times higher in persons with diabetes than the general population [1]. There is evidence that cognitive decline significantly impacts the ability to self-manage diabetes [2]. Strategies to prevent cognitive decline in persons with diabetes have not been well studied. Interestingly, there is recent research suggesting the potential role of vitamin D in cognition and Alzheimer’s disease [3]. One study reported that in persons who had vitamin D deficiency, the risk for all-cause dementia and Alzheimer’s was doubled [4]. Vitamin D deficiency has been reported to negatively affect neuronal vitamin D receptors and adversely affect both growth factor signaling and neural activity [5, 6]. Therefore, providing vitamin D supplementation to improve cognition in persons with diabetes who are at a greater risk for cognitive dysfunction merits investigation.
Among individuals without diabetes, there is a significant association between low serum 25(OH)D and poor cognition. In fact, seven systematic reviews (or meta-analyses) have reported an association between low serum 25(OH)D and impaired cognition [7–13]. The majority of these syntheses were completed using observational designs (both cross sectional and longitudinal). Although there is evidence of an association between low serum 25(OH)D effects and poor cognition, clinical intervention studies have failed to associate increased serum 25(OH)D levels with improved cognitive outcomes [14]. However, one recent randomized controlled trial examined supplementation (4,000 vs. 400 IU daily) of vitamin D for 18 weeks in 82 healthy adults [15]. These authors reported that nonverbal (visual) memory seemed to improve from higher doses of vitamin D supplementation, more so for individuals with insufficient vitamin D levels at baseline (<75 nmol/L), but verbal memory and other cognitive domains did not [15].