Deans' stroke musings: Vitamin D status and rates of cognitive decline in a multiethnic cohort of older adults

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, November 1, 2016

Vitamin D status and rates of cognitive decline in a multiethnic cohort of older adults

More discussions with your doctor. You will need to bring it up otherwise your doctor will never research this.
https://www.mdlinx.com/internal-medicine/medical-news-article/2015/10/05/vitamin-d-cognitive-decline/6328661/?

JAMA Neurology, 10/05/2015Miller JW, et al.

The authors aim to assess associations between vitamin D (VitD) status and trajectories of change in subdomains of cognitive function in a cohort of ethnically diverse older adults. Low VitD status was associated with accelerated decline in cognitive function domains in ethnically diverse older adults, including African American and Hispanic individuals who exhibited a high prevalence of VitD insufficiency or deficiency. It remains to be determined whether VitD supplementation slows cognitive decline.

Methods

Longitudinal multiethnic cohort study of 382 participants in an outpatient clinic enrolled between February 2002 and August 2010 with baseline assessment and yearly follow-up visits.
Serum 25-hydroxyvitamin D (25-OHD) was measured, with VitD status defined as the following: deficient, less than 12 ng/mL (to convert to nanomoles per liter, multiply by 2.496); insufficient, 12 to less than 20 ng/mL; adequate, 20 to less than 50 ng/mL; or high, 50 ng/mL or higher.
Subdomains of cognitive function were assessed using the Spanish and English Neuropsychological Assessment Scales.
Associations were evaluated between 25-OHD levels (as continuous and categorical [deficient, insufficient, or adequate]) and trajectories of cognitive decline.
Serum 25-OHD levels, cognitive function, and associations between 25-OHD levels and trajectories of cognitive decline.

Results

Participants (N=382 at baseline) had a mean (SD) age of 75.5 (7.0) years; 61.8% were women; and 41.4% were white, 29.6% African American, 25.1% Hispanic, and 3.9% other race/ethnicity.
Diagnosis at enrollment included 17.5% with dementia, 32.7% with mild cognitive impairment, and 49.5% cognitively normal.
The mean (SD) 25-OHD level was 19.2 (11.7) ng/mL, with 26.2% of participants being VitD deficient and 35.1% insufficient.
The mean (SD) 25-OHD levels were significantly lower for African American and Hispanic participants compared with white participants (17.9 [15.8] and 17.2 [8.4] vs 21.7 [10.0] ng/mL, respectively; P<.001 for both).
The mean (SD) 25-OHD levels were similarly lower in the dementia group compared with the mild cognitive impairment and cognitively normal groups (16.2 [9.4] vs 20.0 [10.3] and 19.7 [13.1] ng/mL, respectively; P=.006).
The mean (SD) follow-up was 4.8 (2.5) years.
Rates of decline in episodic memory and executive function among VitD-deficient (episodic memory: β=-0.04 [SE=0.02], P=.049; executive function: β=-0.05 [SE=0.02], P=.01) and VitD-insufficient (episodic memory: β=-0.06 [SE=0.02], P<.001; executive function: β=-0.04 [SE=0.02], P=.008) participants were greater than those with adequate status after controlling for age, sex, education, ethnicity, body mass index, season of blood draw, vascular risk, and apolipoprotein E4 genotype.
Vitamin D status was not significantly associated with decline in semantic memory or visuospatial ability.
Exclusion of participants with dementia did not substantially affect the associations between VitD status and rates of cognitive decline.