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.

Saturday, June 24, 2017

Fluidity of the dietary fatty acid profile and risk of coronary heart disease and ischemic stroke: results from the EPIC-Netherlands cohort study

No clue how to use this, insider and big words were used to confuse the layperson.
http://www.nmcd-journal.com/article/S0939-4753(17)30129-1/fulltext?rss=yes

Highlights

  • This is the first study that investigated whether diets high in fluid fatty acids, either in relative terms (i.e. diets with a low lipophilic index, LI), or in combination with the quantity of fatty acids consumed (lipophilic load, LL), relate to the risk of cardiovascular disease among a European population.
  • In a Dutch population that typically consumes diets high in saturated fatty acids and low in polyunsaturated fatty acids, neither the overall fluidity of the dietary fatty acids consumed (LI), nor the combination of overall fluidity and amount of the dietary fatty acids consumed (LL) related to future risk of CHD or ischemic stroke.
  • Dietary LI and LL calculated in observational studies may have limited added value above original fatty acid classes and food sources in establishing the relation of fatty acid consumption with CVD.

Abstract


Background and aims

The fluidity of dietary fatty acids consumed has been suggested to inversely affect coronary heart disease (CHD) risk. Lipophilic index (LI) represents overall fluidity of the dietary fatty acid profile. Lipophilic load (LL) represents a combination of overall fluidity and absolute intake of dietary fatty acids. We investigated the relations of dietary LI and LL with risk of CHD and ischemic stroke (iStroke).

Methods and results

We used data from the prospective EPIC-NL study, including 36,520 participants aged 20-70 years. LI and LL were calculated using dietary intake data estimated with a validated FFQ. Incident CHD (n=2348) and iStroke (n=479) cases were obtained through linkage to national registers during 15 years follow-up. LI and LL were not associated with CHD risk (HRshighest-versus-lowest-quartiles : 0.93 [95%CI: 0.83, 1.04], and 0.92 [95%CI: 0.79, 1.07], respectively), and neither with iStroke risk (HRs 1.15 (95%CI: 0.89, 1.48), and 0.98 (95%CI: 0.70, 1.38), respectively). Original fatty acid classes (SFA, MUFA and PUFA), and LI and LL stratified by these fatty acid classes, were overall not related to CHD and ischemic stroke either.

Conclusions

In this Dutch population, neither the overall fluidity of the dietary fatty acid profile (LI), nor the combined fluidity and amount of fatty acids consumed (LL) were related to CHD or iStroke risk. Dietary LI and LL may have limited added value above original fatty acid classes and food sources in establishing the relation of fatty acid consumption with CVD.

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