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, May 16, 2020

Alcohol Consumption and Risk of Parkinson's Disease: Data from a Large Prospective European Cohort

Well good,  hopefully my coffee habit will prevent Parkinsons'. Hopefully your doctor has a more exact Parkinson's prevention since I don't know how much coffee I should be drinking. To make sure I'm not falling short I drink 12 cups a day.

Parkinson’s Disease May Have Link to Stroke March 2017

 The latest here:

Alcohol Consumption and Risk of Parkinson's Disease: Data from a Large Prospective European Cohort

First published: 01 May 2020
Funding agency: The European Prospective Investigation into Cancer and Nutrition study is funded by a number of grants; however, no funding source had any role in the preparation of this article.
Relevant conflicts of interests/financial disclosures: Nothing to report.


Abstract


Background

Parkinson's disease (PD) etiology is not well understood. Reported inverse associations with smoking and coffee consumption prompted the investigation of alcohol consumption as a risk factor, for which evidence is inconclusive.

Objective

To assess the associations between alcohol consumption and PD risk.

Methods

Within NeuroEPIC4PD, a prospective European population‐based cohort, 694 incident PD cases were ascertained from 209,998 PD‐free participants. Average alcohol consumption at different time points was self‐reported at recruitment. Cox regression hazard ratios were estimated for alcohol consumption and PD occurrence.

Results

No associations between baseline or lifetime total alcohol consumption and PD risk were observed. Men with moderate lifetime consumption (5–29.9 g/day) were at ~50% higher risk compared with light consumption (0.1–4.9 g/day), but no linear exposure–response trend was observed. Analyses by beverage type also revealed no associations with PD.

Conclusion

Our data reinforce previous findings from prospective studies showing no association between alcohol consumption and PD risk. © 2020 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
The etiology of Parkinson's disease (PD) is complex and likely involves both genetic and environmental factors.1 There are strong and consistent observations that cigarette smoking2-4 and coffee drinking4, 5 are associated with a decreased risk of PD. Although the specific mechanisms are still poorly understood, these observed associations are probably not explained by reverse causation or confounding.3-5
In addition to smoking and coffee consumption, alcohol consumption is another possible factor involved in the development of PD. Several meta‐analyses on the association between alcohol consumption and the risk of PD have been conducted, all suggesting an inverse association.6, 7 The results, however, are as yet inconclusive: the inverse association was mainly observed in retrospective case‐control studies, but was not as clear in studies based on prospective cohorts.
By design, case‐control studies have some limitations. First, these studies are prone to recall bias, as the disease status and disease characteristics may affect the retrospective assessment of alcohol consumption habits. Another risk is selection bias because controls may not well reflect the source population. Finally, associations observed in case‐control studies may be the result of reverse causality, for example, when premorbid changes led to reduced alcohol consumption.
Few large prospective studies, largely avoiding these biases, have been published on alcohol consumption and PD risk. Three large‐scale cohort studies, all conducted in the United States, concluded that there is no or only weak evidence for a decreased risk of PD in association with total alcohol consumption.8-10 Specific types of alcoholic beverages, however, were suggested to have different effects: a lower PD risk was reported for moderate beer drinkers,8, 9 whereas liquor consumption was associated with higher risk.8
Our objective was to assess the association between alcohol consumption and the risk of PD in a large European prospective cohort study. We present risk estimates for average alcohol consumption 12 months prior to the recruitment (short term) and during lifetime, that is, since the age of 20 years (long term), as well as the PD risks associated with different types of alcoholic beverages.

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