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:

Saturday, January 21, 2017

A meta-analysis of randomized controlled trials and prospective cohort studies of eicosapentaenoic and docosahexaenoic long-chain omega-3 fatty acids and coronary heart disease risk

I really hate these literature searches and meta-analysis, they always seem to need more followup to be useful rather than doing it right in the first place and doing some real research. Regardless, I bet your doctor does nothing with this information. I assume higher CHD risk pretty much correlates to higher stroke risk, to be confirmed with your doctor.
A. Because s/he never read it.
B. Because s/he could not be bothered to understand how to implement it in a protocol.
C. It is not my job. I am waiting for SOMEONE ELSE TO SOLVE THE PROBLEM.
Mayo Clinic Proceedings, 01/17/2017
The target of this study was to assess the impact of eicosapentaenoic and docosahexaenoic acid (EPA+DHA) on coronary heart disease (CHD), and to lead meta–analyses of prospective cohort studies to estimate the association between EPA+DHA consumption and CHD risk. Outcomes show that EPA+DHA might be connected with lessening CHD risk, with a greater benefit found among higher–risk populations in RCTs.


  • For this study they design a systematic literature search. From January 1, 1947, to November 2, 2015 they search Ovid/Medline, PubMed, Embase, and the Cochrane Library, 18 RCTs and 16 prospective cohort studies examining EPA+DHA from foods or supplements and CHD, including myocardial infarction, sudden cardiac death, coronary death, and angina, were recognized.
  • Random–effects meta–analysis models were utilized to generate summary relative risk estimates (SRREs) and 95% CIs.
  • Heterogeneity was analyzed in subgroup and sensitivity examinations and by meta–regression.
  • Dose–response was assessed in stratified dose or consumption investigations.
  • Publication bias evaluations were performed.


  • Among RCTs, there was a nonstatistically significant decrease in CHD risk with EPA+DHA provision (SRRE=0.94; 95% CI, 0.85–1.05).
  • Subgroup examinations of information from RCTs demonstrated a statistically significant CHD risk decrease with EPA+DHA provision among higher–risk populations, including participants with elevated triglyceride levels (SRRE=0.84; 95% CI, 0.72–0.98) and elevated low–density lipoprotein cholesterol (SRRE=0.86; 95% CI, 0.76–0.98).
  • Meta–analysis of information from prospective cohort studies resulted in a statistically significant SRRE of 0.82 (95% CI, 0.74–0.92) for higher consumptions of EPA+DHA and risk of any CHD event.
Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

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