Each minute delay of IV thrombolysis worsens survival, functional outcomes in stroke

UNTIL YOU KNOW EXACTLY HOW FAST IT HAS TO BE TO GET 100% RECOVERY  JUST SHUT UP WITH THIS FEARMONGRING. This is a totally fucking useless piece of research, you all need to be fired. Tell me exactly why you should stay employed when you don't solve the problem in front of you?

Each minute delay of IV thrombolysis worsens survival, functional outcomes in stroke

For every 1-minute delay in delivery of IV thrombolysis for acute ischemic stroke, the chance of survival decreased by 0.6%, researchers reported.
As door-to-needle time increased, so too did the risk for intracerebral hemorrhage and worse 90-day functional outcomes.

Source: Adobe Stock.

“Our findings highlight that door-to-needle time is a key factor in achieving favorable outcomes after a stroke, emphasizing the importance of constant improvement of in-hospital treatment routines,” David Darehed, PhD, postdoctoral researcher in the department of public health and clinical medicine at Umeå University, Sweden, and colleagues wrote. “The odds of worse outcomes per minute may seem small but translates to large numbers considering greater decreases in door-to-needle time combined with the commonness of the disease.”
The nationwide registry-based study published in Stroke assessed adult patients in Sweden admitted for stroke who underwent IV thrombolysis between 2010 and 2017 (n = 14,132; median age, 74 years; median NIH Stroke Scale score, 8 points). Researchers compared survival, intracranial hemorrhage and functional outcomes with the door-to-needle times for each patient.
Researchers observed that from 2010 to 2017, door-to-needle time decreased from approximately 65 to 38 minutes. The median door-to-needle time during the study period was 47 minutes.
Per-minute delay in door-to-needle IV thrombolysis for stroke was associated with:

• lower odds of 90-day survival (OR = 0.994; 95% CI, 0.992-0.996);
• higher odds of intracranial hemorrhage within 36 hours (OR = 1.003; 95% CI, 1-1.006);
• worse functional outcomes for daily living (OR = 1.003; 95% CI, 1.001-1.005);
• worse functional outcomes for living conditions (OR = 1.004; 95% CI, 1.002-1.005); and
• worse mobility at 3 months (OR = 1.004; 95% CI, 1.003-1.006).

“The finding that higher age, higher NIH Stroke Scale, and longer onset-to-door time was related with shorter door-to-needle time, explain why the results showed only after adjustment for confounders,” the researchers wrote. “Before 2014, patients older than 80 years were not eligible for IV thrombolysis; hence, most of these patients were included in the later part of the study, which may explain the relationship for age. Delays related to NIH Stroke Scale and onset-to-door time should be possible to target in future quality improvement efforts aiming to achieve a quick and correct stroke diagnosis.”

Indirect measurement of anterior-posterior ground reaction forces using a minimal set of wearable inertial sensors: from healthy to hemiparetic walking

I got absolutely nothing out of this. NO SOLUTION  to the gait problems of stroke survivors, so useless. 

Indirect measurement of anterior-posterior ground reaction forces using a minimal set of wearable inertial sensors: from healthy to hemiparetic walking

• Dheepak Arumukhom Revi,
• Andre M. Alvarez,
• Conor J. Walsh,
• Stefano M.M. De Rossi &
• Louis N. Awad 

Journal of NeuroEngineering and Rehabilitation volume 17, Article number: 82 (2020) Cite this article

Abstract

Background

The anterior-posterior a (AP-GRF) and propulsion and braking point metrics derived from the AP-GRF time series are indicators of locomotor function across healthy and neurological diagnostic groups. In this paper, we describe the use of a minimal set of wearable inertial measurement units (IMUs) to indirectly measure the AP-GRFs generated during healthy and hemiparetic walking.

Methods

Ten healthy individuals and five individuals with chronic post-stroke hemiparesis completed a 6-minute walk test over a walking track instrumented with six forceplates while wearing three IMUs securely attached to the pelvis, thigh, and shank. Subject-specific models driven by IMU-measured thigh and shank angles and an estimate of body acceleration provided by the pelvis IMU were used to generate indirect estimates of the AP-GRF time series. Propulsion and braking point metrics (i.e., peaks, peak timings, and impulses) were extracted from the IMU-generated time series. Peaks and impulses were expressed as % bodyweight (%bw) and peak timing was expressed as % stance phase (%sp). A 75%-25% split of 6-minute walk test data was used to train and validate the models. Indirect estimates of the AP-GRF time series and point metrics were compared to direct measurements made by the forceplates.

Results

Indirect measurements of the AP-GRF time series approximated the direct measurements made by force plates, with low error and high consistency in both the healthy (RMSE= 4.5%bw; R²= 0.93) and post-stroke (RMSE= 2.64%bw; R²= 0.90) cohorts. In the healthy cohort, the average errors between indirect and direct measurements of the peak propulsion magnitude, peak propulsion timing, and propulsion impulse point estimates were 2.37%bw, 0.67%sp, and 0.43%bw. In the post-stroke cohort, the average errors for these point estimates were 1.07%bw, 1.27%sp, and 0.31%bw. Average errors for the braking estimates were higher, but comparable.

Conclusions

Accurate estimates of AP-GRF metrics can be generated using three strategically mounted IMUs and subject-specific calibrations. This study advances the development of point-of-care diagnostic systems that can catalyze the routine assessment and management of propulsion and braking locomotor deficits during rehabilitation.

The neuromechanical processes underlying healthy bipedal locomotion are multi-factorial [1–3] and converge on locomotor patterns that are characteristically fast, efficient, and stable [1, 4]. An impaired ability to transition from step to step is a locomotor deficit common across diagnostic groups [5–13]. During the step-to-step transition of each gait cycle, a braking force is generated by the leading limb as it makes contact with the ground in front of the body. To efficiently accelerate the body into the next step, coordination of the timing and magnitude of the forward propulsion force generated by the trailing limb is required [1, 14–16]. Moreover, to walk faster, healthy individuals symmetrically increase the magnitude of propulsion generated by each limb while maintaining the relative timing of the propulsion peak [15, 17, 18]. In individuals with impaired propulsion function, walking is often slow, metabolically expensive, and unstable [19–22].

Laboratory equipment such as instrumented treadmills and forceplates are the gold standard in characterizing propulsion and braking function during healthy [23, 24] and impaired [5, 6, 9, 10, 20, 25–27] walking by way of direct measurements of the anterior-posterior ground reaction forces (AP-GRFs) generated during walking and point metrics extracted from the AP-GRF time series (Fig. 1). For example, older adults are reported to generate up to 22% less peak propulsion (i.e., the peak of the anterior ground reaction force) compared to young adults [23, 24], and in people post-stroke, the propulsion generated by the paretic limb is up to 68% less than the non-paretic limb [9, 20, 26, 27]. Studies that have combined AP-GRF measurements with clinical evaluations have shown the clinical consequences of impaired propulsion function. Indeed, asymmetry in the propulsion impulses generated by the paretic and non-paretic limbs is correlated with hemiparetic severity [9, 28]. Moreover, deficits in propulsion function are highly related to walking speed [29] and long distance walking [30] after stroke—key determinants of community participation and perceived quality of life [19, 31, 32].

Fig. 1

Anterior-posterior ground reaction force (AP-GRF) time series and salient propulsion and braking metrics

Full size image

Despite the importance of propulsion to a functional bipedal gait, conventional rehabilitation efforts have, by and large, been unable to restore propulsion function after neurological injury or dysfunction. The development and study of interventions that target propulsion function is a highly active area of research [12, 33–41]; however, the clinical translation of these experimental approaches is hindered by the limited access that rehabilitation clinicians have to the sophisticated instrumentation (i.e., forceplates and instrumented treadmills) and personnel with advanced training required to collect, analyze, and interpret ground reaction force data. Moreover, even in settings with access to a motion analysis laboratory, locomotor differences inherent to treadmill walking and the small collection footprint of most overground forceplate walkways limit ecological validity. Together, these limitations of the current state-of-the-art motivate the development of point-of-care propulsion diagnostic systems. The clinical management of locomotor propulsion deficits will remain untenable if the measurement instruments used to assess limb propulsion remain inaccessible.

Wearable sensors are a promising solution for this measurement gap. Indeed, wearable sensors have been used to extend gait measurements outside of the laboratory [42–47] and a wide range of methods and sensors have proven effective in providing indirect measurements of the ground reaction forces generated during walking [48–51]. These methods, however, have largely not been effective for the AP-GRFs and depend on assumptions of healthy, consistent walking patterns that may not translate to impaired locomotor patterns [51, 52]. Recent work has shown that inertial measurement units (IMUs) can be used to make measurements during healthy [44] and hemiparetic walking [53] that are highly correlated to key features of propulsion. The aims of this study were to extend this work by describing the use of a minimal set of IMUs to indirectly measure the AP-GRF generated during healthy and hemiparetic walking and provide estimates of: (i) the AP-GRF time series and (ii) salient propulsion and braking point metrics (i.e., peak magnitudes, peak timings, and impulses) extracted from the time series (see Fig. 1).

Antioxidant cocktail key to preventing Alzheimer's

Good luck trying to find the EXACT PROTOCOL on this. 

Antioxidant cocktail key to preventing Alzheimer's

MedicalXpress Breaking News-and-Events|June 29, 2020

Research from The University of Western Australia has found a diet rich in nutrients and antioxidants may prevent or even reverse the effects of Alzheimer's disease.

The study, published in Open Biology, found taking a combination of antioxidants at increasing doses was more beneficial at preventing the debilitating disease than any other treatment currently available. Chronic degenerative diseases such as Alzheimer's are attributed to more than 70 percent of deaths globally and oxidative stress, chronic metabolic acidosis and free radicals in the body play a key role in the aging process.

The results showed that antioxidants react with free radicals in the body to render them harmless. Dr. Gerald Veurink carried out the research while working at UWA's Medical School and examined a range of antioxidants to discover which ones were most effective at protecting the neurons in the body's nervous system. He found complex phenolic carotenoid, as well as antioxidants such as vitamin C and vitamin E in high concentrations, were most effective at reducing the risk of Alzheimer's disease. Dr. Veurink said while a nutrient-rich diet helped stabilize the pH levels in the body that caused oxidative stress, the simultaneous supplementation of an antioxidant combination cocktail was most effective at preventing and managing chronic disease. "The combination of antioxidants at sufficiently high, personalized doses and a nutrient-rich, low-carbohydrate diet appears to have the biggest impact on patients suffering with Alzheimer's," Dr. Veurink said. He also found a combination of antioxidants rather than a single antioxidant helped combat oxidative stress. Dr. Veurink said a holistic approach to healthcare that optimized individual dietary needs was needed to delay and prevent these chronic diseases. To read more, click here

Alzheimer's Changes Tied to Childhood Cognitive Experience

Big fucking whoopee.

Useless. We need to know what to do NOW to prevent Alzheimers.

How many cups of coffee should I be drinking?

 Coffee May Lower Your Risk of Dementia Feb. 2013 

 Or is your doctor using one of these to prevent dementia? 

1.  The End of Alzheimer's: The First Program to Prevent and Reverse Cognitive Decline by Dale Bredesen 

 

2.  A Real Alzheimer's Prevention Program from The University of California

 

3. I'm a Brain Doctor, and This Is What I Do to Prevent Alzheimer's December 2018 

 

4. Reversing the Alzheimer’s Catastrophe April 2007

The latest here:

Alzheimer's Changes Tied to Childhood Cognitive Experience

Slower rate of cognitive decline linked with early-life enrichment

by Judy George, Senior Staff Writer, MedPage Today June 29, 2020

A higher level of early-life cognitive enrichment -- such as learning a foreign language, reading and being read to, and playing games like checkers -- was tied to a slower rate of late-life cognitive decline, a clinical-pathological longitudinal cohort study showed.
This effect occurred partly through an association with lower levels of Alzheimer's pathology changes, reported Shahram Oveisgharan, MD, of Rush University in Chicago, and colleagues, in JAMA Neurology.
"The findings suggest that cognitive health in old age depends in part on cognitive development in early life," Oveisgharan told MedPage Today. "Intervention programs such as Head Start targeting disadvantaged youths can result not only in better school performance and better job opportunities, but also in healthier late-life cognition and cognitive resilience," he said.
"Notably, these effects were independent of late-life socioeconomic status and late-life reports of cognitive activity, suggesting the benefits of early-life cognitive enrichments go beyond long-term changes in lifestyle or behavior," observed Timothy Hohman, PhD, of Vanderbilt University Medical Center in Nashville, and Catherine Kaczorowski, PhD, of the Jackson Laboratory in Bar Harbor, Maine, in an accompanying editorial.
"These findings carry important public health implications, suggesting that late-life cognitive decline can be modified through thoughtful and intentional changes to public policy addressing early-life enrichment, defined herein by socioeconomic status in early life, availability of cognitive resources at 12 years of age, participation in cognitively stimulating activities at 6 years of age, and to a lesser extent, early-life foreign language instruction," they added.
Physical and cognitive activities in midlife have been tied to less late-life cognitive decline in earlier research. Previous studies also have shown that mentally-stimulating late-life activities may help slow brain aging.
In this analysis, Oveisgharan and colleagues evaluated 813 autopsied brains from the Rush Memory and Aging Project to explore whether early-life experiences were associated with Alzheimer's pathology. Study participants had enrolled from 1997 to 2019; they were followed for an average of 7 years before death and had cognitive and clinical assessments annually. Mean age at death was 90 and 69% were women.
At baseline, participants reported four indicators of early-life cognitive experience that researchers used to build a composite measure: early-life socioeconomic status including parents' education level; availability of cognitive resources at age 12 based on home environment features like a newspaper subscription, encyclopedia, globe, or atlas; frequency of participating in cognitively stimulating activities including being read to at age 6; and early-life foreign language instruction to age 18.
The researchers derived a continuous global Alzheimer's pathology score from counts of diffuse plaques, neuritic plaques, and neurofibrillary tangles and used 19 neuropsychological tests to create a cognitive assessment measure.
After controlling for age at death, sex, and educational level, a higher level of early-life cognitive enrichment was tied to a lower global Alzheimer's pathology score (estimate -0.057±0.022, P=0.01), but not with any other dementia-related pathological changes.
Early cognitive enrichment also was associated with less cognitive decline (mean -0.13 units per year, range -1.74 to 0.85). An indirect effect through Alzheimer's pathological changes accounted for 20% of the association between early-life enrichment and late-life cognitive decline; 80% was a direct association, the researchers reported.
"In addition to increasing cognitive reserve and promoting better cognitive performance in late life, early-life cognitive enrichment also promotes what has recently been termed resistance to Alzheimer's disease neuropathology, in that it reduces the risk of developing Alzheimer's disease neuropathology through an unidentified mechanism," Hohman and Kaczorowski noted.
"There may be a critical early-life period when cognitive enrichment has direct effects on future Alzheimer's disease neuropathology, in addition to the well-characterized cognitive benefits associated with a variety of similar measures of cognitive reserve," they added.
Participants in the study largely were women and white and results are not directly generalizable to the population, Oveisgharan and colleagues said. "Our childhood socioeconomic measure is unlikely to have fully captured the variability in early life socioeconomic circumstances," they acknowledged. Early-life data were captured retrospectively and subject to recall bias, and unmeasured confounders may have influenced results.

Last Updated June 30, 2020

• Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

The study was supported by the National Institute on Aging.
Researchers disclosed support from the NIH.
Editorialists disclosed support from the NIH and BrightFocus Foundation.

Primary Source

JAMA Neurology

Source Reference: Oveisgharan S, et al "Association of early-life cognitive enrichment with Alzheimer disease pathological changes and cognitive decline" JAMA Neurol 2020; DOI: 10.1001/jamaneurol.2020.1941.

Secondary Source

JAMA Neurology

Source Reference: Hohman TJ and Kaczorowski CC "Modifiable lifestyle factors in Alzheimer disease: An opportunity to transform the therapeutic landscape through transdisciplinary collaboration" JAMA Neurol 2020; DOI: 10.1001/jamaneurol.2020.1114.

Stroke Survivors – reduce your risk of having another stroke - research trial from Hunter Medical Research Institute, Australia

Have at it.  

Stroke Survivors – reduce your risk of having another stroke - research trial from Hunter Medical Research Institute, Australia

How will the success of the research programs be measured?

So we can measure if the program works, we will ask you to do the following before you start the program, and again every 3 months while you are involved in the study (for 12 months all together):

1. Answer some questions about your stroke, your medications, your health, how much exercise you do and your diet
2. Take regular blood pressure measures for 1 week at home (we will send you a monitor and show you how to use it)
3. Wear an activity monitor on your thigh for 1 week to measure how active you are (we will send the monitor to you)
4. We might also ask you to do an interview with one of our research team about your experience in being involved in the study.

Who can participate?

You are suitable to participate if you:

• are aged over 18 years
• have had a stroke or TIA in the last 10 years
• are able to walk at least short distances without someone helping you
• have an internet connection and either a laptop computer or tablet device at home (we may be able to provide one if you don’t)
• have medical clearance from your doctor to exercise (we will help arrange this)
• are living in Australia

Register your interest

To find out more or to register your interest please contact the Stroke Research Register, Hunter on (02) 4042 0093 (strokeregister@hmri.org.au)

Association of pre-stroke metformin use, stroke severity, and thrombolysis outcome

So that brings up an immediate question. 'Should metformin be immediately given to stroke patients as part of their hyperacute therapy?'  WHOM will answer that question? Specific names needed. You can see the fucking incompetence of all the stroke medical world in that nothing seems to have been done with this in the past 4.5 years.

You could stay forever young (or young for a long time) with this diabetes drug 

Dec. 2015

In this one is this line:The drug, which is cheaply available for just $0.16 a day, works by boosting the number of oxygen molecules released into a cell, which in turn seems to benefit the robustness and longevity of the body’s basic building blocks. (This would seem to be much easier and faster than HBOT. I'm requesting this at my next stroke, my doctor won't know what hit her when I tell her how to treat me.)

My list of 31 things I was going to demand after my next stroke. I guess metformin isn't in there.

 The latest here:

Association of pre-stroke metformin use, stroke severity, and thrombolysis outcome

Laura P Westphal, Roni Widmer, Ulrike Held, Klaus Steigmiller, View ORCID ProfileChristian Hametner, Peter Ringleb, Sami Curtze, Nicolas Martinez-Majander, Marjaana Tiainen, Christian H Nolte, Jan F Scheitz, Hebun Erdur, Alexandros A Polymeris, Christopher Traenka, Ashraf Eskandari, Patrik Michel, View ORCID ProfileMirjam R Heldner, Marcel Arnold, View ORCID ProfileAndrea Zini, Laura Vandelli, Jonathan M Coutinho, Adrien E Groot, Visnja Padjen, Dejana R Jovanovic, Yannick Bejot, Céline Brenière, Guillaume Turc, Pierre Seners, Alessandro Pezzini, Mauro Magoni, Didier Leys, Sixtine Gilliot, Michael J Scherrer, Georg Kägi, Andreas R Luft, Henrik Gensicke, Paul Nederkoorn, Turgut Tatlisumak, Stefan T Engelter, Susanne Wegener

First published June 29, 2020, DOI: https://doi.org/10.1212/WNL.0000000000009951

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Abstract

Objective: To evaluate whether pretreatment with metformin (MET) is associated with less stroke severity and better outcome after intravenous thrombolysis (IVT), we analyzed a cohort of 1919 stroke patients with type-2 diabetes in a multicenter exploratory analysis.

Methods: Data from patients with diabetes affected by ischemic stroke treated with IVT were collected within the European Thrombolysis in Ischemic Stroke Patients (TRISP) collaboration. We applied propensity score matching (PSM) to obtain balanced baseline characteristics of patients treated with and without MET.

Results: Of 1919 stroke patients with type-2 diabetes who underwent IVT, 757 (39%) had received MET before stroke (MET+), whereas 1162 (61%) had not (MET-). MET+ patients were younger with a male preponderance. Hypercholesterolemia and pretreatment with statins, antiplatelets or antihypertensives were more common in the MET+ group. After PSM, the two groups were well balanced with respect to demographic and clinical aspects. Stroke severity on admission (NIHSS 10.0 ± 6.7 vs. 11.3 ± 6.5), 3-months degree of independence on modified Rankin Scale (mRS): 2 [IQR 1.0, 4.0] vs. 3 [IQR 1.0, 4.0] as well as mortality (12.5% vs. 18%) were significantly lower in the MET+ group. The frequency of symptomatic intracerebral hemorrhages did not differ between groups. HbA1c levels were well balanced between both groups.

Conclusions: Stroke patients with diabetes on treatment with MET receiving IVT had less severe strokes on admission and a better functional outcome at 3 months. This suggests a protective effect of MET resulting in less severe strokes as well as beneficial thrombolysis outcome.

• Received April 19, 2019.
• Accepted in final form January 6, 2020.

• © 2020 American Academy of Neurology

Medical management with interventional therapy versus medical management alone for unruptured brain arteriovenous malformations (ARUBA): final follow-up of a multicentre, non-blinded, randomised controlled trial

If you have one of these you should have a long discussion with your doctor. 

Lots of controversy.

Unruptured cerebral arteriovenous malformations are better off treated medically: the ARUBA trial

September 2017 

Leading Cause of Stroke in Young Going Untreated – and It Shouldn’t, Study Finds - AVMs  March 2016

The latest here:

Medical management with interventional therapy versus medical management alone for unruptured brain arteriovenous malformations (ARUBA): final follow-up of a multicentre, non-blinded, randomised controlled trial

• Prof Jay P Mohr, MD
• Jessica R Overbey, DrPH
• Prof Andreas Hartmann, MD
• Prof Rüdiger von Kummer, DrMed
• Prof Rustam Al-Shahi Salman, FRCP
• Prof Helen Kim, PhD
• et al.
• Show all authors

Published:July, 2020DOI:https://doi.org/10.1016/S1474-4422(20)30181-2

Summary

Background

In A Randomized trial of Unruptured Brain Arteriovenous malformations (ARUBA), randomisation was halted at a mean follow-up of 33·3 months after a prespecified interim analysis showed that medical management alone was superior to the combination of medical management and interventional therapy in preventing symptomatic stroke or death. We aimed to study whether these differences persisted through 5-years' follow-up.

Methods

ARUBA was a non-blinded, randomised trial done at 39 clinical centres in nine countries. Adults (age ≥18 years) diagnosed with an unruptured brain arteriovenous malformation, who had never undergone interventional therapy, and were considered by participating clinical centres to be suitable for intervention to eradicate the lesion, were eligible for inclusion. Patients were randomly assigned (1:1) by a web-based data collection system, stratified by clinical centre in a random permuted block design with block sizes of two, four, and six, to medical management alone or with interventional therapy (neurosurgery, embolisation, or stereotactic radiotherapy, alone or in any combination, sequence, or number). Although patients and investigators at a given centre were not masked to treatment assignment, investigators at other centres and those in the clinical coordinating centre were not informed of assignment or outcomes at any of the centres. The primary outcome was time to death or symptomatic stroke confirmed by imaging, assessed by a neurologist at each centre not involved in the management of participants' care, and monitored by an independent committee using an adaptive approach with interim analyses. Enrolment began on April 4, 2007, and was halted on April 15, 2013, after which follow-up continued until July 15, 2015. All analyses were by intention to treat. This trial is registered with ClinicalTrials.gov, NCT00389181.

Findings

Of 1740 patients screened, 226 were randomly assigned to medical management alone (n=110) or medical management plus interventional therapy (n=116). During a mean follow-up of 50·4 months (SD 22·9), the incidence of death or symptomatic stroke was lower with medical management alone (15 of 110, 3·39 per 100 patient-years) than with medical management with interventional therapy (41 of 116, 12·32 per 100 patient-years; hazard ratio 0·31, 95% CI 0·17 to 0·56). Two patients in the medical management group and four in the interventional therapy group (two attributed to intervention) died during follow-up. Adverse events were observed less often in patients allocated to medical management compared with interventional therapy (283 vs 369; 58·97 vs 78·73 per 100 patient-years; risk difference −19·76, 95% CI −30·33 to −9·19).

Interpretation

After extended follow-up, ARUBA showed that medical management alone remained superior to interventional therapy for the prevention of death or symptomatic stroke in patients with an unruptured brain arteriovenous malformation. The data concerning the disparity in outcomes should affect standard specialist practice and the information presented to patients. The even longer-term risks and differences between the two therapeutic approaches remains uncertain.

Funding

National Institute of Neurological Disorders and Stroke for the randomisation phase and Vital Projects Fund for the follow-up phase.

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Association of Low to Moderate Alcohol Drinking With Cognitive Functions From Middle to Older Age Among US Adults

Say it isn't so. If you can afford that many drinks a week you probably also have good health care. Your doctor will use these other ones instead:

Safest level of alcohol consumption is none, worldwide study shows

 

Alcohol consumption increases risk for PAD, stroke

 

Even 'low-risk' drinking can be harmful

I can easily see social drinking having a lower cognitive decline, lots of social interactions means lesser chances of dementia. 

Or do you have cause and effect backwards per this research?

Smarter People Tend To Drink More Alcohol.

The latest here:

Association of Low to Moderate Alcohol Drinking With Cognitive Functions From Middle to Older Age Among US Adults

Ruiyuan Zhang, MD, MS¹; Luqi Shen, MS¹; Toni Miles, MD, PhD¹; et al Ye Shen, PhD¹; Jose Cordero, MD, MPH¹; Yanling Qi, PhD²; Lirong Liang, PhD³; Changwei Li, MD, PhD, MPH¹

Author Affiliations Article Information

JAMA Netw Open. 2020;3(6):e207922. doi:10.1001/jamanetworkopen.2020.7922

Key Points español 中文 (chinese) Question  Does an association exist between current low to moderate alcohol drinking and cognitive function trajectories or rates of cognitive decline from middle to older age among US adults?
Findings  In this cohort study of 19 887 participants from the Health and Retirement Study, with a mean follow-up of 9.1 years, when compared with never drinking, low to moderate drinking was associated with significantly better trajectories of higher cognition scores for mental status, word recall, and vocabulary and with lower rates of decline in each of these cognition domains.
Meaning  Current low to moderate alcohol consumption among middle-aged or older adults may be associated with better total cognitive function.

Abstract

Importance  Studies examining the association of low to moderate drinking with various cognitive functions have yielded mixed findings.
Objective  To investigate whether associations exist between low to moderate alcohol drinking and cognitive function trajectories or rates of change in cognitive function from middle age to older age among US adults.
Design, Setting, and Participants  A prospective cohort study of participants drawn from the Health and Retirement Study (HRS), a nationally representative sample of US adults, with mean (SD) follow-up of 9.1 (3.1) years. In total, 19 887 participants who had their cognitive functions measured in the HRS starting in 1996 through 2008 and who had participated in at least 3 biennial surveys were included. The data analysis was conducted from June to November 2019.
Exposures  Alcohol consumption and aging.
Main Outcomes and Measures  Trajectories and annual rates of change for the cognitive domains of mental status, word recall, and vocabulary and for the total cognitive score, which was the sum of the mental status and word recall scores. Participants were clustered into 2 cognitive function trajectories for each cognition measure assessed based on their scores at baseline and through at least 3 biennial surveys: a consistently low trajectory (representing low cognitive scores throughout the study period) and a consistently high trajectory (representing high cognitive scores throughout the study period).
Results  The mean (SD) age of 19 887 participants was 61.8 (10.2) years, and the majority of the HRS participants were women (11 943 [60.1%]) and of white race/ethnicity (16 950 [85.2%]). Low to moderate drinking (<8 drinks per week for women and <15 drinks per week for men) was significantly associated with a consistently high cognitive function trajectory and a lower rate of cognitive decline. Compared with never drinkers, low to moderate drinkers were less likely to have a consistently low trajectory for total cognitive function (odds ratio [OR], 0.66; 95% CI, 0.59-0.74), mental status (OR, 0.71; 95% CI, 0.63-0.81), word recall (OR, 0.74; 95% CI, 0.69-0.80), and vocabulary (OR, 0.64; 95% CI, 0.56-0.74) (all P < .001). In addition, low to moderate drinking was associated with decreased annual rates of total cognitive function decline (β coefficient, 0.04; 95% CI, 0.02-0.07; P = .002), mental status (β coefficient, 0.02; 95% CI, 0.01-0.03; P = .002), word recall (β coefficient, 0.02; 95% CI, 0.01-0.04; P = .01), and vocabulary (β coefficient, 0.01; 95% CI, 0.00-0.03; P = .08). A significant racial/ethnic difference was observed for trajectories of mental status (P = .02 for interaction), in which low to moderate drinking was associated with lower odds of having a consistently low trajectory for white participants (OR, 0.65; 95% CI, 0.56-0.75) but not for black participants (OR, 1.02; 95% CI, 0.74-1.39). Finally, the dosage of alcohol consumed had a U-shaped association with all cognitive function domains for all participants, with an optimal dose of 10 to 14 drinks per week.
Conclusions and relevance  These findings suggested that low to moderate alcohol drinking was associated with better global cognition scores, and these associations appeared stronger for white participants than for black participants. Studies examining the mechanisms underlying the association between alcohol drinking and cognition in middle-aged or older adults are needed.

Stroke Recovery After 2 Years: Making Sense of Milestones from Flint Rehab

My NIH stroke scale would have been a 10 - moderate. 

Stroke Recovery After 2 Years: Making Sense of Milestones from Flint Rehab

This line from there is damming: In our article on stroke recovery after 5 years, we highlighted how the severe lack of quality therapy after discharge from inpatient therapy has impeded recovery for many stroke patients.  

So NO PROTOCOLS, so you are screwed. 

Potential therapeutic use of ebselen for COVID-19 and other respiratory viral infections

Maybe you want to get familiar with ebselen?

Ebselen, an anti-inflammatory antioxidant, was originally developed by Daiichi Sankyo, in Japan, to treat patients who had suffered a stroke. But the compound was never marketed and has since come off patent. It’s also part of the National Institutes of Health Clinical Collection—several hundred small molecules that have, to some extent, gone through the gamut of human clinical trials and have been found to be safe, but never reached final FDA approval.

• ebselen (10 posts to December 2012)

 

Potential therapeutic use of ebselen for COVID-19 and other respiratory viral infections

Author links open overlay panelHelmutSies^ab

Michael J.Parnham^cd

https://doi.org/10.1016/j.freeradbiomed.2020.06.032Get rights and content

Highlights

•

Ebselen, an organoselenium compound, exhibits anti-inflammatory and antiviral activity.

•

Ebselen is a glutathione peroxidase and peroxiredoxin mimetic.

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Ebselen reacts with a multitude of protein thiols, resulting in pleiotropic effects.

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Ebselen is an effective inhibitor of Mpro, the main protease of SARS-CoV-2.

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Ebselen may serve as lead compound for drugs targeting COVID-19.

Abstract

Ebselen is an organoselenium compound exhibiting hydroperoxide- and peroxynitrite-reducing activity, acting as a glutathione peroxidase and peroxiredoxin enzyme mimetic. Ebselen reacts with a multitude of protein thiols, forming a selenosulfide bond, which results in pleiotropic effects of antiviral, antibacterial and anti-inflammatory nature. The main protease (M^pro) of the corona virus SARS-CoV-2 is a potential drug target, and a screen with over 10,000 compounds identified ebselen as a particularly promising inhibitor of M^pro (Jin, Z. et al (2020) Nature 582, 289-293). We discuss here the reaction of ebselen with cysteine proteases, the role of ebselen in infections with viruses and with other microorganisms. We also discuss effects of ebselen in lung inflammation. In further research on the inhibition of M^pro in SARS-CoV-2, ebselen can serve as a promising lead compound, if the inhibitory effect is confirmed in intact cells in vivo. Independently of this action, potential beneficial effects of ebselen in COVID-19 are ascribed to a number of targets critical to pathogenesis, such as attenuation of inflammatory oxidants and cytokines.

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