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, April 24, 2020

Study: Moderate lifetime drinking may lead to lower Alzheimer-related beta amyloid deposits in the brain

You do know your doctor will never approve so don't try this.

Your doctor will never tell you about this benefit, you'll get this instead. Of course you'll have to figure out the dose needed yourself. 

Safest level of alcohol consumption is none, worldwide study shows

  I however will be doing this because social engagement is also proven to prevent Alzheimers.

With this, however I have to substitute women friends.

Men must drink with male friends twice a week to stay healthy, study finds

December 2017

Study: Moderate lifetime drinking may lead to lower Alzheimer-related beta amyloid deposits in the brain


“Korean researchers studied 414 men and women, average age 71, who were free of dementia or alcohol-related disorders. All underwent physical exams, tests of mental acuity, and positron emission tomography (PET) and magnetic resonance imaging (MRI) scans. They were carefully interviewed about their drinking habits.
The study, in PLOS Medicine, measured drinking in “standard drinks” — 12 ounces of beer, five ounces of wine, or one-and-a-half ounces of hard liquor. Compared with abstainers, those who drank one to 13 standard drinks a week had a 66 per cent lower rate of beta amyloid deposits in their brains.
The results applied only to those who drank moderately for decades, and not to those who recently began drinking moderately or drank more than 13 drinks a week.”

The Study:

Association of moderate alcohol intake with in vivo amyloid-beta deposition in human brain: A cross-sectional study (PLOS Medicine). From the Abstract:

  • Background: An emerging body of literature has indicated that moderate alcohol intake may be protective against Alzheimer disease (AD) dementia. However, little information is available regarding whether moderate alcohol intake is related to reductions in amyloid-beta (AB) deposition, or is protective via amyloid-independent mechanisms in the living human brain. Here we examined the associations of moderate alcohol intake with in vivo AD pathologies, including cerebral A? deposition, neurodegeneration of AD-signature regions, and cerebral white matter hyperintensities (WMHs) in the living human brain.
  • Conclusions: In this study, we observed in middle- and old-aged individuals with neither dementia nor alcohol-related disorders that moderate lifetime alcohol intake was associated with lower cerebral AB deposition compared to a lifetime history of not drinking. Moderate lifetime alcohol intake may have a beneficial influence on AD by reducing pathological amyloid deposition rather than amyloid-independent neurodegeneration or cerebrovascular injury.

The Study in Context:

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