Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Friday, February 17, 2017

Vitamin D is not associated with incident dementia or cognitive impairment: An 18-y follow-up study in community-living old men

Whom the fuck is going to explain this in layperson terms along with the other 29 posts I have on vitamin D? I most certainly have no clue what this is saying.
Do you really expect the thousands of doctors out there that need to impart this evidence to their patients to all do it correctly? And your doctor is one of those that can do it correctly?
We need a fucking protocol, damn it all, our stroke medical leaders are so fucking incompetent that it is lucky if they even know what the word protocol means.
American Journal of Clinical Nutrition, 02/17/2017
Olsson E, et al. – In this cohort study, the researchers examined the connection between vitamin D, assessed in 3 different ways, and the risk of dementia. They demonstrate that there is no relationship between baseline vitamin D status and long–term risk of dementia or cognitive impairment over an 18–y period of time.


  • In this study, the researchers measured plasma 25-hydroxyvitamin D [25(OH)D] with the utilization of high-performance liquid chromatography–mass spectrometry, assessed dietary vitamin D intake with the use of 7-d dietary records, and created a vitamin D–synthesis genetic risk score (GRS) at baseline (1991–1995) in a cohort of 1182 Swedish men (mean age: 71 y).
  • In a maximum of 18 y (median: 12 y) of follow-up, 116 men developed Alzheimer disease, 64 men developed vascular dementia, and 250 men developed all-cause dementia.
  • An additional 80 men declined in cognitive function as evaluated with the utilization of the Mini-Mental State Examination.
  • Adjusted HRs and ORs were figured with the utilization of Cox and logistic regressions.


  • The results of this study showed that the mean ± SD plasma 25(OH)D concentration was 68.7 ± 19.1 nmol/L.
  • Plasma 25(OH)D, dietary vitamin D intake, and vitamin D–synthesis GRS were not related to any cognitive outcomes (crude and adjusted HRs and ORs were ∼1.0 for all continuous exposures).
  • It was observed in the findings that the adjusted HR for all-cause dementia was 0.88 (95% CI: 0.59, 1.31) in men with plasma 25(OH)D concentrations ≤50 compared with &
  • >75 nmol/L.
  • Findings revealed that the adjusted HR for all-cause dementia was 0.92 (95% CI: 0.63, 1.32) for the lowest compared with highest tertiles of vitamin D intake.
  • In addition, the adjusted HR for the continuous GRS for all-cause dementia was 1.04 (95% CI: 0.91, 1.19).
Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

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