Thursday, September 19, 2024

When Are We Officially “Old”?

 For me it's only when my trochanteric bursitis kicks in on my left hip that I feel old.

At 68 now, I'm still middle aged since I'm going to get to 100.  My fellow travelers on the Iceland trip I just completed were mostly in their 70's and laughed heartily at my definition of middle-aged.

Seljalandsfoss, you can actually walk behind this waterfall, I didn't because of 5 yards of slippery slanted rocks

Spent a hour here, wonderfully relaxing, but expensive drinks.


 

 

 
Skagafoss, with Rockey, who was on my Bhutan trip also

 

 

 

 

 

 

 

 

 

 
Gullfoss

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

When Are We Officially “Old”?

Coach Maloney was my soccer coach in middle school and a mentor along the way. He’d been a former star high school athlete and practiced with our team, regularly dribbling past us with ease and outrunning us by several strides. Though he had thick muscular legs, he sported a rotund torso and a mostly bald head. At the time, I’d thought he was so old, which is why I marveled at his athleticism.

Yesterday, I looked back through my yearbook, and realized, “Oh my god. He was 38.”

I’m 40 now — and coach doesn’t look nearly as old as I remembered. It illustrates how our perception of age changes as we get a few years under our belt. There’s always an inner you that feels younger, and ready to conquer the world. Even if the person staring back in the mirror doesn’t match that feeling.

So when do we become old — officially? And how should we think and talk about our seniors? These questions go right to the heart of how we live and treat each other.

Our definition of age has quickly evolved over the past 100 years, as life expectancies have risen dramatically, even discounting for the impact of falling infant mortality rates. This is particularly true for wealthy people, who are getting especially healthy years in their final chapters. Everything is relative in life, and aging is no different. If we reach a point where people are routinely living to 120+ and maintaining good health, perhaps turning 70 will be seen as middle-aged.

In the realm of academia, researchers technically define old age as 65, as this is a common point of retirement. It’s also when you become eligible for Social Security and Medicare. Per Dr. Karl Pillemeer, “For policy-planning purposes, ‘over 75’ is a much more meaningful demographic than ‘over 65’.” He adds that it is because people past 75 are much more likely to develop chronic disease. People between 65 and 75 are far more similar to those in middle age. So perhaps we shall respectfully dub old age as 75?

But is this even the right way to think about age? What words should we even use to describe it?

The word “old” feels inherently derogatory, and is associated with deterioration and obsolescence. It fails to account for the complexity and heterogeneity of aging. Some 40-year-olds are bedridden with diseases. Conversely, my dad is 70, swims over a mile a day, and still doesn’t need blood pressure meds.

It’s all relative.

Another option is “elderly”, but that also carries tons of baggage. It evokes feelings of someone needing extensive help just living, of them being unable to do the basics, like cleaning up after themselves and getting groceries.

The term was more common decades ago but has simply warped and become problematic. One simple test of language perceptions is to poll people in a retirement home on how much they identify with these terms. Per Dr. Clara Berridge, you’d be lucky to get one or two people in a crowded room to raise their hand when you use the term “elderly”.

Meanwhile, “geriatric” has too strong of a medical connotation, and evokes feelings of extended family trying to find the appropriate care for a high-maintenance loved one.

The term “senior” is confusing because it invites the question, “Senior to whom?” The term is also used with universities and high schools, and in job titles, such as “Senior Vice President”.

“Senior citizen” has readily apparent flaws, as many people aren’t actually citizens in the United States. The term also feels very 1990s, and paired with baggage as well.

The term “older” tends to have a less negative connotation, though it still feels like a label, though less so than “old”.

One recommended option is: “older adults”. This label is shown to reduce negative perceptions and stereotyping more than other terms. This might feel persnickety and unnecessary. But remember that language can very much evoke quick conclusions and discriminatory thinking.

Older adults isn’t a perfect solution. It implies there is a group of younger adults, which isn’t properly defined. But the ambiguity itself helps reduce categorical thinking.

And to be clear, we can’t erase the societal bias that goes against older adults. More than 93% of people between the ages of 50 and 80 will experience ageism at some point. Sadly, it’s a form of bigotry that most of us will both experience and unintentionally perpetrate. Which is why we should think more clearly about how we describe age, to help account for this bias.

This is particularly true as we witnessed a full-scale attack on President Biden for his age, with mean-spirited memes showing him falling downstairs and stammering over his words. And while I get that he’s the president, and open to criticism as any other, I worry that the ageist floodgates have been opened to take shots at everyday people.

And the problem is — this bias is even common with older adults against each other. Dr. Clara W. Martinson observed a 55+ condo where residents didn’t want other residents in wheelchairs playing games in the display window. Why? Because they worried it would lower their property value. One resident even wanted a separate dining hall for those in wheelchairs, saying that, “I don’t like the intermingling of the well and the sick.”

And this is the challenge: we draw conclusions about older adults based on their physical status. Healthy older adults get more of a hall pass for being old, while the others are placed into a lower tier as if they have somehow failed in life.

This is why it’s problematic to use phrases like, “80 is the new 50.” It plays pretend with what aging actually is, and creates a meritocratic psychology around an unfair process. It’s the framework of “successful aging” which is ableist. It causes harm and mental health issues in those dealing with chronic disease.

It’s an unconscious bias that comes naturally and without notice, namely because our heavy focus on chronological age is a modern construct and not a great measure of actual aging. Some 65-year-olds are running companies. Others are at the mercy of early-onset dementia.

The challenge is that we are proven to define a successful older adult, in this case, aged 65 and older, as having completed three criteria:

  1. Having avoided major diseases.

  2. Having no disabilities.

  3. Having maintained full physical and cognitive function.

I fail at all of these due to my stroke, but I do have full cognitive function

This is not only a narrow criteria, but deceptively hard to attain, with only 12% of older adults fitting into this category. So we implicitly categorize the remainder in a “less than” category, without actually saying it.

I urge you to live healthy, treat your body kindly, and turn to others with an empathetic heart. Remember that we are all on this shared journey of getting older, and will all succumb to the wear and tear life inevitably brings.

Think carefully about how you describe, think about, and treat older adults. You will one day be one of them. And remember that ill health visits many otherwise disciplined, health-oriented people. Do not judge someone for a disease or disability beyond their control.

Remember that aging is a gift, and the mere act of being alive alongside another is an exceedingly rare, and special coincidence.




Stormont Vail earns national award for providing prestigious stroke care

 

I wouldn't go there if all they are offering is 'care'; NOT RECOVERY!

Anytime I see 'care' in any stroke press release I know the stroke medical world is not willing to disclose actual results because they are so fucking bad, it wouldn't look good, so misdirection is used. Don't fall for that misdirection! By touting 'care' they are not telling you about results or recovery which survivors want! Survivors don't care about your 'care'; you FUCKING BLITHERING IDIOTS; they want 100% recovery! Why aren't you providing that?

Big fucking whoopee.

 

 But you tell us NOTHING ABOUT RESULTS. They remind us they 'care' about us multiple times but never tell us how many 100% recovered.  You have to ask yourself why they are hiding their incompetency by not disclosing recovery results.  ARE THEY THAT FUCKING BAD?


Three measurements will tell me if the stroke medical world is possibly not completely incompetent; DO YOU MEASURE ANYTHING?  I would start cleaning the hospitals by firing the board of directors, you can't let incompetency continue for years at a time.

There is no quality here if you don't measure the right things.

  1. tPA full recovery? Better than 12%?
  2. 30 day deaths? Better than competitors?
  3. rehab full recovery? Better than 10%?

 

You'll want to know results so call that hospital president(whomever that is) RESULTS are; tPA efficacy, 30 day deaths, 100% recovery. Because there is no point in going to that hospital if they are not willing to publish results.

In my opinion this partnership allows stroke hospitals to continue with their tyranny of low expectations and justify their complete failure to get survivors 100% recovered. Prove me wrong, I dare you in my stroke addled mind. If your stroke hospital goal is not 100% recovery you don't have a functioning stroke hospital.

 

All you ever get from hospitals are that they are following guidelines; these are way too static to be of any use. With thousands of pieces of stroke research yearly it would take a Ph.D. level research analyst to keep up, create protocols, and train the doctors and therapists in their use. 

If your stroke hospital doesn't have that, you don't have a well functioning stroke hospital, you have a dinosaur. 

Read up on the 'care' guidelines yourself. Survivors want RECOVERY not 'care'

“What's measured, improves.” So said management legend and author Peter F. Drucker 

The latest invalid chest thumping here:

Stormont Vail earns national award for providing prestigious stroke care

TOPEKA, Kan. (WIBW) - Stormont Vail Health was awarded the Get With The Guidelines-Stroke Gold Plus quality achievement from the American Heart Association.

According to a press release from Stormont Vail, the award recognizes the health center’s dedication to providing stroke patients with its treatment. The award is based on national guidelines.

The criteria for the award include:

  • Fulfilling specific quality benchmarks for diagnosing and treating stroke patients
  • Ensuring that medications and other treatments adhere to the latest evidence-based guidelines
  • Educating patients on managing their health and recovery at home

In addition, Stormont Vail earned the Target: StrokeSM Honor Roll Elite award for providing prompt and efficient care(NOT RECOVERY!) that enhances stroke patients’ chances of survival and recovery.

Stormont Vail also received the Target: Type 2 Diabetes™ Honor Roll award for ensuring access to evidence-based care(NOT RECOVERY!) for hospitalized stroke patients with Type 2 diabetes.

The Lancet Neurology: Air pollution, high temperatures, and metabolic risk factors driving global increases in stroke, with latest figures estimating 12 million cases and over 7 million deaths from stroke each year

In the business world you would be immediately fired for excuses like this and DOING NOTHING TO SOLVE STROKE! 

WRONG! PREVENTION SHOULD NOT BE THE TOP PRIORITY! With all the research out there to stop the 5 causes of the neuronal cascade of death in the first week thus saving millions to billions of neurons.We can and should work on 100% recovery.  If we had any leadership at all in stroke we would create a strategy to solve stroke to 100% recovery! If you don't believe it can be done; GET THE HELL OUT OF STROKE!

The Lancet Neurology: Air pollution, high temperatures, and metabolic risk factors driving global increases in stroke, with latest figures estimating 12 million cases and over 7 million deaths from stroke each year

  • Between 1990 and 2021, the number of people who had a new stroke (up by 70%), died from a stroke (up by 44%), and stroke-related health loss (up by 32%), has risen substantially worldwide. 
  • Stroke is highly preventable, with 84% of the stroke burden in 2021 attributable to 23 modifiable risk factors, including air pollution, excess body weight, high blood pressure, smoking, and physical inactivity—presenting a public health challenge and an opportunity for action.
  • Notably, the contribution of high temperatures to poor health and early death due to stroke has risen 72% since 1990, a trend likely to increase in the future—underscoring the impact of environmental factors on the growing stroke burden. 
  • For the first time, the study reveals the high contribution (on a par with smoking) of particulate matter air pollution to subarachnoid haemorrhage (fatal brain bleed). 
  • Effective, accessible, and affordable measures to improve stroke surveillance, prevention (with the emphasis on managing blood pressure, lifestyle, and environmental factors), acute care, and rehabilitation need to be urgently implemented across all countries to reduce the stroke burden. 

Originally posted by The Lancet Neurology

Although stroke is highly preventable and treatable, there has been a rapid rise in the global stroke burden between 1990 and 2021, due to both population growth and the rise of aging populations worldwide, as well as a substantial increase in people’s exposure to environmental and behavioural risk factors. The findings of this major new analysis from the Global Burden of Disease, Injuries, and Risk Factors Study (GBD) are published in The Lancet Neurology(link is external)

journal and being presented at the World Stroke Congress in Abu Dhabi in October 2024 [1].

Globally, the number of people having a new stroke rose to 11.9 million in 2021 (up by 70% since 1990), stroke survivors rose to 93.8 million (up by 86%), and stroke-related deaths rose to 7.3 million (up by 44%), making the condition the third leading cause of death worldwide (after ischaemic heart disease and COVID-19). More than three-quarters of those affected by strokes live in low- and middle-income countries (LMICs).

Additionally, estimates suggest that worldwide, the overall amount of disability, illness, and early death—a measurement known as disability-adjusted life years (DALYs)—lost to stroke increased by 32% between 1990 and 2021, rising from around 121.4 million years of healthy life lost in 1990 to 160.5 million years in 2021, making stroke the fourth leading cause of health loss worldwide after COVID-19, ischaemic heart disease, and neonatal disorders.  

The burden of stroke is increasing in large part due to both population growth and the rise of aging populations worldwide, but also due to increasing contributions from preventable environmental, metabolic, and behavioural risk factors. Between 1990 and 2021, the global stroke burden linked to high body mass index (BMI; up by 88%), high temperatures (up 72%), high blood sugar (up 32%), diet high in sugar-sweetened drinks (up 23%), low physical activity (up 11%), high systolic blood pressure (up 7%), and diet low in omega-6 polyunsaturated fatty acids (up 5%) increased substantially.

However, if the impact of demographics is removed through age-standardisation (to allow comparisons between countries and over time), there has been a trend towards lower rates (age-standardised per 100,000 population) of incidence (down by 22%), prevalence (down 8%), deaths (down 39%), and DALYs (down 39%) worldwide, and across virtually all country income levels, since 1990.  But since 2015, improvements in global incidence rates have stagnated, while age-standardised rates of stroke incidence, death, prevalence and DALYs have got worse in Southeast Asia, East Asia, Oceania, and in people younger than 70 years.

"The global growth of the number of people who develop stroke, and died from or remain disabled by stroke is growing fast, strongly suggesting that currently used stroke prevention strategies are not sufficiently effective."

Lead author Professor Valery L Feigin from Auckland University of Technology, New Zealand, an affiliate professor at the Institute for Health Metrics and Evaluation (IHME) at the University of Washington, USA, said: “The global growth of the number of people who develop stroke, and died from or remain disabled by stroke is growing fast, strongly suggesting that currently used stroke prevention strategies are not sufficiently effective. New, proven effective population-wide and motivational individual prevention strategies that could be applied to all people at risk of having a stroke, regardless of the level of risk, as recommended in the recent Lancet Neurology Commission on Stroke [4] should be implemented across the globe urgently.”

The current study builds on previous GBD analyses [2] to provide the most up-to-date and comprehensive analysis of stroke burden and risk factor estimates in countries on a global scale between 1990 and 2021, to help guide health-planning, prevention, and resource allocation

Fast-growing burden of uncontrolled risk factors, mostly affecting LMICs

The study reveals striking differences in the overall stroke burden (as measured by age-standardised incidence, prevalence, death and DALY rates) between world regions and national income levels in 2021. In high-income North America and Australasia, and middle-income Latin America—regions with the lowest stroke burden—the age-standardised rates of incidence and prevalence were lowest in New Zealand (67.8 and 707.4 per 100,000 people respectively), death rates lowest in Canada (20.4 per 100,000 people), and DALY rates lowest in Australia (435.0 per 100,000) in 2021.

"Stroke-related health loss disproportionately impacts many of the most disadvantaged countries in Asia and sub-Saharan Africa." 

In contrast, in the regions of low- and middle-income East and Central Asia and sub-Saharan Africa, the rates of incidence, prevalence, death and DALYs were up to 2 to 10 times higher (over 248, 1458, 190, and 4320 per 100,000 people, respectively) in 2021.

Strikingly, half of all the disability and the lives lost to stroke globally (81 million healthy years of life lost) in 2021 were the result of haemorrhagic strokes—the deadliest form, mainly due to high blood pressure—despite being around half as common as ischaemic strokes (4.1 million new haemorrhagic strokes vs 7.8 million new ischaemic strokes). Most affected were people aged 70 and younger and those living in low-income countries, where the proportion of strokes that are intracerebral haemorrhage is double that of high-income countries (37% vs 18%).

“Stroke-related health loss disproportionately impacts many of the most disadvantaged countries in Asia and sub-Saharan Africa due to the growing burden of uncontrolled risk factors, especially poorly controlled high blood pressure, and rising levels of obesity and type 2 diabetes in young adults, as well as the lack of stroke prevention and care services in these regions,” explained co-author Dr Catherine O. Johnson, Lead Research Scientist at IHME. “The shift in stroke burden towards younger populations is likely to continue unless effective preventive strategies are implemented urgently.”

Increasing impact of environmental risk factors  

The study estimates that the total number of stroke-related DALYs attributable to 23 risk factors [3] globally has risen from 100 million years of healthy life lost in 1990 to 135 million in 2021—presenting a public health challenge and an opportunity for action. The largest proportions of these risk factors are found in Eastern Europe, Asia, and sub-Saharan Africa. 

Metabolic risk factors—especially high BMI, high systolic blood pressure, and high LDL cholesterol—contributed to the most stroke burden across all country income levels (ranging from 66-70%) in 2021, followed by environmental risk factors collectively (i.e., air pollution, low/high ambient temperature, lead exposure) in LMICs (35-53%).

“With 84% of the stroke burden linked to 23 modifiable risk factors there are tremendous opportunities to alter the trajectory of stroke risk for the next generation.”

In 2021, the five leading global risk factors for stroke were high systolic blood pressure, particulate matter air pollution, smoking, high LDL cholesterol, and household air pollution, with considerable variation by age, sex, and location (see figure 2).

For the first time, the study suggests that ambient particulate matter air pollution is a top risk factor for subarachnoid haemorrhage, contributing to 14% of the death and disability caused by this serious stroke subtype, on a par with smoking (see figure 2).

In contrast, substantial progress has been made in reducing the global stroke burden from risk factors linked to poor diet, air pollution, and smoking, with health loss due to diets high in processed meat and low in vegetables declining by 40% and 30%, respectively, particulate matter air pollution by 20%, and smoking by 13%. This suggests that strategies to reduce exposure to these risk factors over the past three decades, such as clean air zones and public smoking bans, have been successful.

“With 84% of the stroke burden linked to 23 modifiable risk factors there are tremendous opportunities to alter the trajectory of stroke risk for the next generation,” said Dr Johnson. “Given that ambient air pollution is reciprocally linked with ambient temperature and climate change, the importance of urgent climate actions and measures to reduce air pollution cannot be overestimated. And with increasing exposure to risk factors such as high blood sugar and diet high in sugar-sweetened drinks, there is a critical need for interventions focused on obesity and metabolic syndromes. Identifying sustainable ways to work with communities to take action to prevent and control modifiable risk factors for stroke is essential to address this growing crisis.”

Prevention must be top priority(WRONG! 100% RECOVERY IS!)

The authors say that by implementing and monitoring the evidence-based recommendations set out in the 2023 World Stroke Organization-Lancet Neurology Commission on stroke [4], there is an opportunity to drastically reduce the global burden of stroke in this decade and beyond, as well as improve brain health and the overall wellbeing of millions of people around the world.  

As Professor Feigin explained: “Additional and more effective stroke prevention strategies, with an emphasis on population-wide measures, such as task-shifting from doctors to nurses and health volunteers, and the wider use of evidence-based mobile and telehealth platforms, along with pragmatic solutions to address the critical gaps in stroke service delivery, workforce capacity building, and epidemiological surveillance systems must be urgently implemented across all countries.”

Writing in a linked Comment(link is external)

, Professor Ming Liu and Associate Professor Simiao Wu from West China Hospital, Sichuan University in China (who were not involved in the study) say: “Pragmatic solutions to the enormous and increasing stroke burden include surveillance, prevention, acute care, and rehabilitation. Surveillance strategies include establishing a national-level framework for regular monitoring of stroke burden, risk factors, and health-care services via community-based surveys and health records. Artificial intelligence and mobile technologies might not only facilitate the dissemination of evidence-based health services, but also increase the number of data sources and encourage participation of multidisciplinary collaborators, potentially improving the validity and accuracy of future GBD estimates. We hope that GBD analyses will continue to provide timely health data and inform action in the battle against stroke at the global, regional, and national levels.” 

Notes to editors

The study was funded by the Bill and Melinda Gates Foundation. The paper was conducted by the GBD 2021 Stroke Collaborators and researchers at the University of Washington, Seattle, USA.

The labels have been added to this press release as part of a project run by the Academy of Medical Sciences seeking to improve the communication of evidence. For more information, please see: http://www.sciencemediacentre.org/wp-content/uploads/2018/01/AMS-press-release-labelling-system-GUIDANCE.pdf if you have any questions or feedback, please contact The Lancet press office pressoffice@lancet.com

[1] The Articles’ findings will be presented during the 16th World Stroke Congress in Abu Dabi, UAE to be held on October 23-26, 2024, Abstract Number 1482. The conference is open to registered delegates and media. Full program details are available here: https://worldstrokecongress.org/scientific-program/

[2] Global, regional, and national burden of stroke and its risk factors, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019 - The Lancet Neurology

[3] The risks included in the analysis were: (1) ambient particulate matter pollution; (2) household air pollution from solid fuels; (3) low temperature (daily temperatures below the TMREL); (4) high temperature (daily temperatures above the TMREL); (5) lead exposure; (6) diet high in sodium; (7) diet high in red meat; (8) diet high in processed meat; (9) diet low in fruits; (10) diet low in vegetables; (11) diet low in whole grains; (12) alcohol use (any alcohol dosage consumption); (13) diet high in sugar sweetened beverages; (14) diet low in fibre; (15) diet low in polyunsaturated fatty acids; (16) low physical activity (only for ischaemic stroke burden); (17) smoking; (18) second-hand smoke; (19) high BMI; (20) high fasting plasma glucose; (21) high systolic blood pressure; (22) high LDL cholesterol (only for ischaemic stroke burden); and (23) kidney dysfunction, as measured by low glomerular filtration rate (GFR; not assessed for subarachnoid haemorrhage burden).

[4] Pragmatic solutions to reduce the global burden of stroke: a World Stroke Organization–Lancet Neurology Commission - The Lancet Neurology

Additional key findings include: 

  • Age-standardised stroke incidence was lowest in Luxemburg (58 per 100,000 population) and highest in the Solomon Islands (355 per 100,000).
  • Age-standardised stroke prevalence was lowest in Cyprus (522 per 100,000 population) and highest in Ghana (2,046 per 100,000).  
  • The rate of people who die from stroke (age-standardised per 100,000 population) was lowest in Singapore (14 per 100,000) and highest in North Macedonia (277 per 100,000).
  • Age-standardised DALY rates were lowest in Switzerland (333 per 100,000 population) and highest in Nauru (6,100 per 100,000).

For interviews with the Article authors, please contact the media team at IHME: E) ihmemedia@uw.edu

Coffee could be more than a morning pick-me-up, according to new research

 Don't these researchers follow research at all? 

Not mentioning either Parkinsons or dementia prevention and is it really the caffeine?

Coffee May Lower Your Risk of Dementia Feb. 2013 

And this: Coffee's Phenylindanes Fight Alzheimer's Plaque December 2018

How coffee protects against Parkinson’s Aug. 2014 

Benefits Aren't Just From Caffeine December 2018

The latest here:

Coffee could be more than a morning pick-me-up, according to new research

A morning cup of coffee may do more than just perk you up, according to new research.

Moderate amounts of caffeine intake — defined as about three cups of coffee or tea a day — were associated with a lower risk of developing cardiometabolic multimorbidity, said the study’s lead author, Dr. Chaofu Ke, associate professor of epidemiology and biostatistics at Soochow University in Suzhou, China.

Cardiometabolic multimorbidity, or CM, is the coexistence of at least two cardiometabolic diseases such as coronary heart disease, stroke and type 2 diabetes.

“Coffee and caffeine consumption may play an important protective role in almost all phases of CM development,” Ke said.

Researchers analyzed data from about 180,000 people in the UK Biobank, a large biomedical database and research resource that follows people long-term. Those involved did not have cardiometabolic diseases at the outset.

The information included the participants’ self-reported caffeine consumption through coffee or black or greentea and the cardiometabolic diseases they developed through their primary care data, hospital records and death certificates, according to the study published Tuesday in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.

Moderate caffeine consumers had a reduced risk of new onset cardiometabolic multimorbidity. The risk was reduced by 48.1% if they had three cups a day, or 40.7% if they had 200 to 300 milligrams of caffeine daily, compared with people who didn’t drink or drank less than one cup, Ke said.

What do you think? Join 114 others in the comments

The study had a large sample size and used multiple biomarkers to support the findings, making it a strong look at how caffeine affects heart health, said Dr. Gregory Marcus, associate chief of cardiology for research and professor of medicine at the University of California, San Francisco. He was not involved in the research.

“These observations add to the growing body of evidence that caffeine, and commonly consumed natural substances that contain caffeine such as tea and coffee, may enhance cardiovascular health,” Marcus said in an email.

What researchers don’t know

The methodology is strong and the results line up with existing data about caffeine and heart health, but there are still questions about the extent of the connection between caffeine and heart health, Marcus said.

“It is important to emphasize that, while these data suggest a relationship between caffeine, tea, and coffee and a reduced risk of a combination of cardiovascular diseases, we need to be careful before we infer true causal effects,” Marcus said.

Because the study is observational, it can only show a connection between caffeine and heart health, he said. Other factors may actually be the cause of the improved heart health, he added.

“It remains possible that the apparent protective effects do not truly exist at all and that the positive associations are all explained by some as yet unknown or unmeasured true determining factor,” Marcus added.

“For example, perhaps those more likely to consume these substances also tend to have a healthier diet or to be more physically active.”

The study also didn’t take into consideration the impact of caffeine from carbonated beverages or energy drinks, meaning that researchers can’t say whether those substances would also have a positive effect, Ke said.

Should you start drinking coffee?

Plenty of literature shows a benefit from caffeine consumption.

Several studies have suggested a lower risk of diabetes, Marcus said. And contrary to popular wisdom, drinking caffeine in coffee is associated with experiencing a lower risk of abnormal heart rhythms, he added, pointing to his and others’ research.

But much of that research is observational, and one study showed a mixed result, with more caffeine linked to additional daily step counts but less sleep, Marcus said.

Although the new study should provide comfort to those who already have a coffee or tea habit, it isn’t necessarily a sign to start a regular caffeine routine, Marcus said.

“It is also important to mention that more is not necessarily better,” he said.

“Even if caffeine, coffee, and tea in the amounts described in this study … are indeed healthy, there is also strong evidence that high-dose caffeine, particularly when included in artificial concoctions like energy drinks, may actually cause harmful and even dangerous heart rhythm problems.”

Clarification: A previous version of this story listed high blood pressure as a cardiometabolic disease. It has been removed from the list of such diseases to reflect the scope of the study.

Correction: A previous version of this story misstated the sample size of data collected from the UK Biobank and how many cups of coffee reduced risk.

Time to Say Goodbye to the B.M.I.?

 Now try the body roundness index.

Body Roundness Index (BRI) Calculator here

I'm from 3.8 (out of healthy zone) to 4.5 (out of healthy zone)

Mohammad with his hand rehabilitation device in the race for national prize

 Couldn't find anything in ether Google or Google Scholar on this, so no clue on how it works or efficacy. Does it open fingers with spasticity?

Mohammad with his rehabilitation device in the race for national prize

Mohammad with his rehabilitation device in the race for national prize
Photo credit: VGZ/Studio040

The company Osind Medi Tech of Nuenen citizen Mohammad Samheel has been nominated by health insurer VGZ as ”healthcare innovator of the future’. Specifically, it concerns the Hand in Motion, a rehabilitation device designed by Samheel to help people try to regain their hand function.

Biomedical engineer Samheel talks about the Hand in Motion: “This device was developed for use in arm and hand rehabilitation, for example after a stroke, and is based on intensive, task-oriented training. Patients can do their exercises while the therapist watches remotely. The Hand in Motion makes the rehabilitation process accessible and affordable”.

Samheel was born in India, but now lives with his Dutch wife and their son in Nuenen. “After graduating, I specifically focused on the rehabilitation of hand function, which is crucial for the independence of someone who is rehabilitating. In India, I founded my company Osind Medi Tech, which then moved to the Netherlands. When I approached institutions with my invention, the reactions were immediately enthusiastic. Rehabilitation clinics throughout the Netherlands were interested”.

Helping

For Samheel, it was a kind of ‘return to the past’. During his studies, orthopedists from the hospital he was in contact with asked if he wanted to help them with the rehabilitation of patients who had undergone surgery for a nerve disorder of the hand or tendon or because of a bone fracture. “There are devices for sale that help the patient make the hand movements that are necessary for rehabilitation. But these devices are unaffordable for most hospitals in India”.

And if they are available and break, they often cannot be repaired. Samheel: “So healthcare professionals (occupational therapists and physiotherapists) and interns are deployed to practice the necessary hand movements with the patient for an hour a day. Stretching and bending fingers: a simple exercise that requires a lot of valuable time from these healthcare professionals. There are simply many patients in India who need the help of an occupational therapist or physiotherapist”.

Prototype

The orthopedists asked Samheel if he could design a device that could take over the work of these healthcare professionals and that was accessible to many people. “So something had to be affordable and easy to use. It also had to be suitable for home use, because these patients cannot stay in hospital for a long time”. In collaboration with students from other studies, Samheel succeeded in making a prototype of the Hand in Motion in a short time.

With the acquisition of an international subsidy, the development of the rehabilitation device gained momentum. The Hand in Motion was further improved and made suitable for more applications. “The device now helps with bending, stretching, pinching and grasping(NO extension) and can be fully customised”, Samheel, who now runs his company from the Netherlands, says.

Cash prize

Health insurer VGZ, which organises annual elections for innovative healthcare inventions, got wind of Samheel’s invention. And now he has been nominated in the category ‘Zorgvernieuwer van de toekomst’. He has a chance to win a cash prize of €5,000 to further develop his product and further distribute Hand In Motion throughout healthcare in the Netherlands.

Until 26 September, everyone in the Netherlands can vote online via the VGZ website. The result is determined half by the votes and half by a professional jury. The award ceremony will take place during a final evening on 1 October at the VGZ head office in Arnhem.

For more information : Over Samen Voorop Awards | Coƶperatie VGZ | VGZ Zorgverzekering

Source: Studio040 

Brain Vasculature Changes Important for Predicting Cognitive Impairment

Once your doctor has predicted this problem, WHAT EXACT PROTOCOLS ARE GIVEN YOU TO PREVENT IT FROM HAPPENING? Don't have any do you? 

Your competent? doctor started working on neurovascular coupling 8 years ago, RIGHT?

Neurovascular coupling in humans: Physiology, methodological advances and clinical implications April 2016

The latest here:

Brain Vasculature Changes Important for Predicting Cognitive Impairment

Several measurements of the brain, including blood flow and the brain’s ability to compensate for the lack of it, are better predictors of mild cognitive impairment (MCI) than risk factors like hypertension and high cholesterol.

The findings, published in the journal Alzheimer’s & Dementia, further the prospects of preventing or treating memory problems early before they progress to dementia. 

“People with mild cognitive impairment are at highest risk for the next step, which is dementia,” said Calin Prodan, MD, Oklahoma University College of Medicine, Oklahoma City, Oklahoma. “We’re trying to decipher the ‘fingerprints’ of mild cognitive impairment. What happens to the brain when a person moves from healthy ageing to mild cognitive impairment, and is there something we can do to intervene and prevent the decline to dementia?”

The researchers team took several types of brain measurements in people at 3 stages of life: young adults, older adults with ageing but healthy brains, and older adults with MCI. Each group played a short memory challenge game during functional near-infrared spectroscopy recording, and changes in plasma levels of extracellular vesicles (EVs) were assessed using small-particle flow cytometry. The game consisted of trying to memorise increasingly larger sequences of letters.

In the brains of young adults, blood flow increased, giving their brains the energy they needed to meet the demands of the game, a process called neurovascular coupling. In people with healthy ageing brains, the blood flow did not increase as much, but to compensate, their brains engaged other regions of the brain to help with the challenge, a process known as functional connectivity. In the brains of older adults with MCI, the blood flow was greatly reduced, and they lost the ability to compensate by recruiting other parts of the brain to help.

“People with mild cognitive impairment have lost that compensation mechanism,” said lead author Cameron Owens, PhD, Oklahoma University College of Medicine. “There is a drastic change in brain activity in those with mild cognitive impairment.”

Another type of assessment using a blood test gave researchers an additional window into the brains of people with cognitive impairment. This blood analysis measured the amount of cerebrovascular endothelial extracellular vesicles (CEEVs), which are tiny particles released from the cells lining the brain’s blood vessels. Existing research shows that when the inner lining of blood vessels is damaged, it secretes CEEVs. People with MCI  had more CEEVs in their brains than those with healthy ageing brains. Furthermore, MRI images confirmed that people with higher levels of CEEVs also had more ischaemic damage. The researchers believe this is the first time that CEEVs have been measured in a cognitive condition.

“Every brain is different, and there may be differing reasons for cognitive impairment, but having these predictors -- measuring neurovascular coupling, functional connectivity, and CEEVs -- potentially opens opportunities to develop individualised interventions, whether it’s a pharmacological therapy or non-invasive brain stimulation, or something as simple as cognitive behavioural therapy,” said coauthor Andriy Yabluchanskiy, PhD, Oklahoma University College of Medicine.

Reference: https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.14072

SOURCE: University of Oklahoma


CCL5 is essential for axonogenesis and neuronal restoration after brain injury

 Does your competent? doctor and hospital have enough functioning brain cells to see that this might help in stroke and get further research done in humans? Oh, you don't have a functioning stroke doctor or hospital, do you?

CCL5 is essential for axonogenesis and neuronal restoration after brain injury

Abstract

Background

Traumatic brain injury (TBI) causes axon tearing and synapse degradation, resulting in multiple neurological dysfunctions and exacerbation of early neurodegeneration; the repair of axonal and synaptic structures is critical for restoring neuronal function(Sounds exactly like the needs in stroke). C-C Motif Chemokine Ligand 5 (CCL5) shows many neuroprotective activities.

Method

A close-head weight-drop system was used to induce mild brain trauma in C57BL/6 (wild-type, WT) and CCL5 knockout (CCL5-KO) mice. The mNSS score, rotarod, beam walking, and sticker removal tests were used to assay neurological function after mTBI in different groups of mice. The restoration of motor and sensory functions was impaired in CCL5-KO mice after one month of injury, with swelling of axons and synapses from Golgi staining and reduced synaptic proteins-synaptophysin and PSD95. Administration of recombinant CCL5 (Pre-treatment: 300 pg/g once before injury; or post-treatment: 30 pg/g every 2 days, since 3 days after injury for 1 month) through intranasal delivery into mouse brain improved the motor and sensory neurological dysfunctions in CCL5-KO TBI mice.

Results

Proteomic analysis using LC-MS/MS identified that the “Nervous system development and function”-related proteins, including axonogenesis, synaptogenesis, and myelination signaling pathways, were reduced in injured cortex of CCL5-KO mice; both pre-treatment and post-treatment with CCL5 augmented those pathways. Immunostaining and western blot analysis confirmed axonogenesis and synaptogenesis related Semaphorin, Ephrin, p70S6/mTOR signaling, and myelination-related Neuregulin/ErbB and FGF/FAK signaling pathways were up-regulated in the cortical tissue by CCL5 after brain injury. We also noticed cortex redevelopment after long-term administration of CCL5 after brain injury with increased Reelin positive Cajal-Rerzius Cells and CXCR4 expression. CCL5 enhanced the growth of cone filopodia in a primary neuron culture system; blocking CCL5’s receptor CCR5 by Maraviroc reduced the intensity of filopodia in growth cone and also CCL5 mediated mTOR and Rho signalling activation. Inhibiting mTOR and Rho signaling abolished CCL5 induced growth cone formation.

Conclusions

CCL5 plays a critical role in starting the intrinsic neuronal regeneration system following TBI, which includes growth cone formation, axonogenesis and synaptogensis, remyelination, and the subsequent proper wiring of cortical circuits. Our study underscores the potential of CCL5 as a robust therapeutic stratagem in treating axonal injury and degeneration during the chronic phase after mild brain injury.

Graphical Abstract

Introduction

Traumatic brain injury (TBI) is a complex disorder caused by external forces and is also the most significant cause of death and disability for people under the age of 40 [23, 31]. According to the Glasgow Coma Scale (GCS), TBI can be clinically divided into mild (GCS:14–15), moderate (GCS:9–13) and severe (GCS:3–8). Mild TBI is the most common brain injury caused by contact sports (i.e., hockey, football), motor vehicle accidents, and falls. Evidence from long-term studies on soldiers and athletes suggest that mild and repeated mild brain injuries are associated with the development of Chronic Traumatic Encephalopathy (CTE) [19, 37, 44], and also increase the risk of early onset Parkinsonism [18], dementia, and Alzheimer’s disease (AD) [25, 48].

Axonal shredding and tearing upon the impact, also called traumatic axonal injury (TAI) or diffuse axonal idiopathic injury (DAI), are the initial direct damages from mechanical impact on brain tissue. TAI is characterized by impaired axoplasmic transport, axonal swelling, disconnection with small hemorrhagic and/or non-hemorrhagic lesions, and brain swelling [7]. Unfortunately, much evidence suggests that neurons within the adult mammalian CNS cannot regenerate their axons after injury [13, 43]. Several deleterious cascades will be activated, leading to axon degeneration after injury. First, damaged glial cells/oligodendrocytes may not be able to provide sufficient energy to support neurons and cause neuron degeneration after injury [33, 49]. Second, increased calcium (Ca2+) influx leads to neuron apoptosis and degeneration [33, 49]. Third, glia scar and myelin-associated inhibitory proteins, such as Nogo, myelin-associated glycoprotein (Mag), and oligodendrocyte myelin glycoprotein (OMgp), can inhibit axonal regeneration after injury [15].

Recent evidence suggests that CNS neurons can revert to an embryonic-like growth state in the chronic/remodeling phase of injury to facilitate axon regeneration [46]. This “redevelopment” state provides a permissive microenvironment and the intracellular machinery for axon regrowth [9]. The endogenous repair systems activate and repair damaged axons within the chronic phase after axonal injury. The molecular machinery underlying axon regeneration is very similar to axon growth, such as Rho-GTPases Cdc42, Rac-1, and RhoA, phosphoinositide 3-kinase (PI3K)/AKT signaling pathways, and mitogen-activated protein kinase (MAPK) signaling [38]. Importantly, Rho is also the target molecule for myelin-associated inhibitory proteins [15]. PI3K/Akt activates its downstream molecules - the mammalian target of rapamycin (mTOR) and promotes axonal regeneration, synaptic plasticity, and neuronal survival after injury [35, 45]. Modulating the mTOR pathway is a novel strategy to promote axon regeneration [10]. Among three types of MAP kinases, the Erk cascade is a major pro-survival intracellular signaling pathway that can be activated by GDNF (glial cell-line derived neurotrophic factor) to promote neurite outgrowth in the spinal cord [29].

Chemokine CCL5; C-C motif ligand 5, also known as RANTES (regulated on activation, normal T cell expressed and secreted), shows many protective roles after neuronal damage, such as in stroke [51] and AD [24, 28, 32, 53]. In brain trauma, the plasma level of CCL5 increases in both human patients and animals after injury [2, 20]. Interestingly, CCL5 was found to be raised around the axonal transection site in mice immediately after injury [3]. The increased CCL5 around the axon transection site induces leukocyte infiltration to the injury site, but its function on neurons is still unclear. Our previous study identified that CCL5 is an essential factor in activating glutathione peroxidase 1 (GPX1) after brain injury, consequently reducing oxidative stress and protecting hippocampal neurons from oxidative stress-induced death; this effect facilitated memory-cognition recovery in mice after mild brain injury [22]. We also showed that CCL5 contributes to hippocampal neurons’ ATP generation and synaptic complex formation [1]. In addition, CCL5 expression after spinal cord injury is associated with axon regeneration and immune suppression [57]. The plasma level of CCL5 is highly correlated with BDNF, EGF (epidermal growth factor), and VEGF (vascular endothelial growth factor) after stroke [51]; those trophic factors contribute to neuron growth and proper brain function. Taken together, these findings suggest that CCL5 can help neurons survive from energy shortage and promote axon and synapse regrowth after injury.

In the present study, we identified that this chemokine has a robust and attractive effect on neuron growth cone formation, axon growth and myelination during post-injury repair. We specifically demonstrate for the first time that these effects are related to the ability of neuronal CCL5 to promote axon growth cone formation, axonogenesis and myelination through P70S6/mTOR signaling and the NRG1/ErbB and FGF pathways, ultimately augmenting neuronal axon and synapse regrowth after injury. Together, CCL5 promotes recovery of axogenesis and neurogenesis after brain injury.