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, June 11, 2021

Moderate alcohol intake lowers stress-related brain activity, may reduce CVD risk

This can't be true, this earlier research says NO ALCOHOL.

Drinking any amount of alcohol causes damage to the brain, study finds

 There is no way you can justify consuming any alcohol even with the massive amount of stress you are undergoing because your doctor knows nothing and does nothing for your 100% recovery.

The latest here:

Moderate alcohol intake lowers stress-related brain activity, may reduce CVD risk

Among adults who underwent brain imaging, moderate alcohol intake reduced stress-related brain signals, which may in part explain the link between moderate alcohol intake and reduced risk for major adverse CV events, a speaker reported.

Kenechukwu Mezue

The researchers assessed whether alcohol intake was associated with lower risk for major adverse CV events after adjustment for lifestyle and socioeconomic confounders and whether the association was related to reduced activity of stress neurobiology. Kenechukwu Mezue, MD, MSc, clinical and research nuclear cardiology fellow at Massachusetts General Hospital and Harvard Medical School, presented the findings at the American College of Cardiology Scientific Session.

red wine
Source: Adobe Stock

“The benefit of how alcohol brings this [CV] benefit is quite uncertain,” Mezue said during a web briefing. “We do know that chronic stress is related to cardiovascular events. Studies have shown that certain brain regions trigger inflammation. Alcohol acutely reduces activity in these same brain regions. So we asked the question, could alcohol’s mechanism of benefit involve stress-related neurobiology?”

For the analysis of the relationship between alcohol consumption and major adverse CV events, the researchers included 53,064 participants from the Mass General Brigham Biobank who completed a health survey with information on alcohol consumption. For the analysis of the effect of stress neurobiology, the researchers included 752 participants who underwent fluorodeoxyglucose PET/CT brain imaging to assess the balance between pro-stress and regulatory signals.

Compared with no or little alcohol intake (< 1 drink per week), moderate alcohol intake (1 to 14 drinks per week) was associated with reduced risk for major adverse CV events in a univariate analysis (OR = 0.732; 95% CI, 0.696-0.769; P = 2.017 x 10-34) and after adjustment for demographic factors, CVD risk factors, health behaviors, socioeconomic factors and psychological factors (OR = 0.799; 95% CI, 0.752-0.847; P = 4.173 x 10-13), Mezue said, noting that moderate alcohol consumption was also linked to reduced risk for major adverse CV events compared with heavy alcohol consumption (> 14 drinks per week).

In the imaging cohort, after adjustment for age and sex, moderate alcohol consumption was associated with less stress-associated neural activity compared with little/no or heavy alcohol consumption (P = .018), he said.

When the researchers conducted a mediation analysis (indirect path from moderate alcohol consumption to amygdalar activity to major adverse CV events, log odds = –0.04; P < .05), “we did show that stress-associated neural activity significantly mediated the beneficial impact of alcohol on cardiovascular clinical events in our study cohort,” Mezue said.

“This study certainly tries to provide some mechanistic explanation for why alcohol may have a beneficial effect,” Eugene Yang, MD, chair of the ACC’s Cardiovascular Diseases Prevention Council and cardiologist at the University of Washington, Seattle, said during a discussion after the presentation. “[The results are] consistent with what we have seen in other studies. Other studies have shown that the amygdala plays a role in alcohol addiction. It would be interesting to know if ... binge drinking was associated with stress-related activity in the amygdala, and if it translated to clinical outcomes. A survey from several years ago indicated that binge alcohol consumption seemed to carry a higher cardiovascular event rate.”

 

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