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.

Friday, July 24, 2026

Association of low vitamin B12 status with incident dementia and stroke: an EHR database study

 

Until we able able to determine vitamin B12 deficiency on our own this really doesn't help us.  Would the blood testing for hemoglobin prior to donating blood be able to be modified to test for this? And no one is going to give themselves B12 injections so what are the protocols for taking supplements?

Association of low vitamin B12 status with incident dementia and stroke: an EHR database study


  • 1. Department of Anesthesiology, Chi Mei Hospital, Liouying, Tainan, Taiwan

  • 2. Department of Anesthesiology, E-Da Hospital, I-Shou University, Kaohsiung, Taiwan

Abstract

Background: 

Epidemiological evidence linking low vitamin B12 status to dementia risk remains inconsistent, partly reflecting differences in exposure definitions, study designs, and analytical approaches. This study evaluated the association between low vitamin B12 status and long-term risks of incident dementia, related neurocognitive, and cerebrovascular outcomes.

Methods: 

This propensity score–matched retrospective cohort study used de-identified electronic health record data from the TriNetX Global Collaborative Network. Adults aged ≥50 years with two vitamin B12 measurements <300 pg./mL within a 2-year window were matched 1:1 with patients who had two vitamin B12 measurements of 300–900 pg./mL using the same framework. A 1-year landmark period was applied, with outcome follow-up beginning on day 366 after the index date. The primary outcome was incident all-cause dementia over 10 years. Secondary outcomes included Alzheimer’s disease, vascular dementia, other dementia subtypes, mild cognitive impairment, stroke, and all-cause mortality. An exposure-gradient analysis was performed among patients with vitamin B12 deficiency, defined as two measurements <200 pg./mL.

Results: 

After matching, 129,159 patients remained in each group. Low vitamin B12 status was associated with a higher risk of all-cause dementia (Hazard ratio [HR] 1.33, 95% confidence interval [CI] 1.27–1.39, p < 0.001). Associations were also observed for Alzheimer’s disease, vascular dementia, and other dementia subtypes (HRs 1.31–1.34), mild cognitive impairment (HR 1.33), stroke (HR 1.31), and all-cause mortality (HR 1.23; all p < 0.001). Among patients with vitamin B12 deficiency, the association with all-cause dementia was stronger (HR 1.64, p < 0.001). Results were consistent across six prespecified sensitivity analyses and sex-stratified subgroup analyses.

Conclusion: 

Low vitamin B12 status was associated with an increased long-term risk of incident all-cause dementia, with a numerically stronger association among patients with vitamin B12 deficiency. Given the observational design and potential residual bias, these findings should be interpreted as hypothesis-generating rather than causal. Further prospective studies with serial biomarker monitoring and interventional studies of vitamin B12 correction are needed to clarify this association.


More at link.

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