Mitochondria magic: Exercise’s value soars with this news

 

Great Catch-22 here; you need exercise to recover, but you really need 100% recovery to do the required exercises. Have your competent? doctor EXACTLY EXPLAIN HOW TO GET AROUND THAT PROBLEM!

I can almost guarantee your doctor and hospital will KNOW NOTHING AND DO NOTHING! 

No human research will occur; nothing will be done! That is how fucking incompetent the whole stroke medical world is. Hopefully comeuppance will hit them all with a stroke. And they can regret their incompetence in not solving stroke to 100% recovery!

Al this incompetence is a result of NO leadership firing the incompetent persons!

Mitochondria magic: Exercise’s value soars with this news

Japanese researchers found that exercise triggers muscle cells to send mitochondria through the bloodstream to protect and repair brain tissue after stroke

• By David Kesiena
• Jan 26, 2026
• 7:00 am

Photo credit: Shutterstock.com / LightField-Studios-2

Scientists at Juntendo University School of Medicine have uncovered a remarkable process that explains how exercise protects the brain from stroke damage. The research team discovered that physical activity triggers muscle cells to produce mitochondria that travel through the bloodstream and deliver healing benefits directly to injured brain tissue.

The study, published in the journal MedComm on Jan. 15, reveals that blood platelets act as tiny transport vehicles, carrying these cellular powerhouses from muscles to the brain. Once they arrive, the mitochondria help damaged neurons survive oxygen deprivation and support the repair of critical brain structures. The findings could eventually lead to new treatments for stroke patients who are too frail to exercise on their own.(Slight problem here, the penumbra resolves itself into dead brain in the first week, so you need this exercise immediately! HOW THE FUCK WILL YOUR DOCTOR ACCOMPLISH THAT?)

 

✕

Powered By 

Research Assistant Professor Toshiki Inaba led the investigation alongside colleagues Nobukazu Miyamoto and Nobutaka Hattori at Juntendo’s Department of Neurology. The team conducted experiments using mouse models designed to replicate both stroke and dementia conditions, providing insights into how cellular communication might be harnessed for therapeutic purposes.

Watching mitochondria travel between cells

Miyamoto’s interest in mitochondrial migration began during a research fellowship at Massachusetts General Hospital and Harvard Medical School, where he first observed these cellular structures moving from one cell to another. That observation sparked the realization that mitochondrial transfer might offer treatment possibilities for various neurological conditions.

For the current study, researchers divided mice into groups and had some perform low-intensity treadmill exercise while others remained sedentary. The team then carefully tracked brain damage, movement abilities, memory function and changes in brain and muscle cells among both groups. They also measured mitochondrial levels and activity throughout the experiment.

The results showed clear advantages for the mice that exercised. These animals experienced less damage to white matter and myelin, the protective coating around nerve fibers. They also demonstrated better memory retention and movement capabilities compared to sedentary mice, while experiencing fewer complications following stroke events.

Researchers have demonstrated how mitochondria, which are abundant in muscle, could aid in stroke recovery through exercise-induced migration.(Photo courtesy of Dr. Toshiki Inaba from Juntendo University School of Medicine, Japan)

Platelets serve as cellular delivery system

The research revealed that exercise significantly increased mitochondrial production in both muscle tissue and the bloodstream. Blood platelets, typically known for their role in clotting, took on an unexpected function by capturing mitochondria from muscle cells and transporting them to the brain.

Once in the brain, these traveling mitochondria didn’t just reach neurons. They also made their way to support cells including oligodendrocytes, which produce protective myelin, and astrocytes, star-shaped cells that help form the blood-brain barrier. The mitochondria provided crucial support to cells in the damaged area and the surrounding region called the penumbra, where brain tissue remains vulnerable but potentially salvageable.

Inside these brain cells, the delivered mitochondria helped them endure low-oxygen conditions that typically cause widespread cell death after stroke. They supported the repair of white matter, the brain’s communication infrastructure, and reduced the cascade of complications that often follow stroke events.

Limited options drive search for new approaches

Current stroke treatment relies heavily on clot removal or dissolution, but these interventions only work within a narrow window after symptoms begin. Once that critical time frame passes, patients face limited therapeutic options. Physical rehabilitation and symptom management become the primary focus, yet many stroke survivors continue struggling with walking difficulties, speech problems and memory decline.

Exercise has long been recognized as beneficial for both stroke prevention and recovery. However, many stroke patients are elderly and lack the physical stamina required to exercise intensively enough to gain those protective benefits. This reality makes the search for alternative approaches particularly urgent.

Inaba acknowledged that while the research team has identified several technical and biological challenges through additional experiments, the approach holds promise for reducing neurological problems after stroke. The applications might extend beyond stroke to include mitochondrial diseases and related neurodegenerative conditions where current treatment options remain limited.

From mice to potential human therapies

The pathway from laboratory findings to clinical treatments typically spans years and requires extensive testing for safety and effectiveness. If the mitochondrial transfer approach proves successful in human trials, it could potentially allow stroke patients to receive the benefits of exercise through transfusions of platelet preparations enriched with mitochondria.

Such a treatment would be particularly valuable for patients who cannot engage in physical rehabilitation due to age, frailty or the severity of their condition. The approach might also offer hope for preventing the progression of vascular dementia, a condition that currently has no established treatments.

The research team’s work builds on growing scientific understanding of how cells communicate and share resources. By revealing the specific mechanism through which exercise protects the brain, the scientists have opened a new avenue for developing therapies that could help millions of stroke survivors worldwide maintain better neurological function and quality of life.

SOURCE: juntendo

New study sheds light on stroke recovery via exercise-induced migration of mitochondria

 Great Catch-22 here; you need exercise to recover, but you really need 100% recovery to do the required exercises. Have your competent? doctor EXACTLY EXPLAIN HOW TO GET AROUND THAT PROBLEM!

I can almost guarantee your doctor and hospital will KNOW NOTHING AND DO NOTHING! 

No human research will occur; nothing will be done! That is how fucking incompetent the whole stroke medical world is. Hopefully comeuppance will hit them all with a stroke. And they can regret their incompetence in not solving stroke to 100% recovery!

Al this incompetence is a result of NO leadership firing the incompetent persons!

New study sheds light on stroke recovery via exercise-induced migration of mitochondria

Researchers show how exercise protects the brain against stroke by inducing migration of tiny powerhouses through the bloodstream

Peer-Reviewed Publication

Juntendo University Research Promotion CenterResearchers have demonstrated how mitochondria, which are abundant in muscle, could aid in stroke recovery through exercise-induced migration.

Physical rehabilitation and symptom management still remain the mainstay of treatment for stroke, as clot removal or dissolution is effective only within a narrow time frame after the stroke. After that, many patients are left with long-term problems like difficulty in walking, speaking, and memory decline. Exercise has been beneficial in preventing strokes and improving recovery. However, the majority of these patients, being elderly, are too frail to exercise enough to gain these benefits.In an innovative study published in the journal MedComm on January 15, 2026, a team of researchers led by Research Assistant Professor Toshiki Inaba from the Department of Neurology, Juntendo University School of Medicine, Japan, along with Dr. Nobukazu Miyamoto and Dr. Nobutaka Hattori from Juntendo University School of Medicine, Japan, explored how exercise protects the brain against stroke at a biological level through mitochondrial migration

“It was during my research fellowship with Assistant Professor Kazuhide Hayakawa at Massachusetts General Hospital/Harvard Medical School that I first observed that these mitochondria could travel from one cell to another, leading to the realization that mitochondrial transfer could be harnessed for a wide range of therapeutic applications. This motivated us to explore intercellular mitochondrial transfer as a novel treatment strategy,” explains Dr. Miyamoto.

 

The team used mouse models that mimic stroke as well as dementia. Some mice from both these groups were then made to perform low-intensity treadmill exercise. The researchers then compared brain damage, movement, memory, and changes in brain, muscle cells, and mitochondrial dosage and activity among the mice that exercised and those that did not. Mice that underwent treadmill exercise showed clear benefits, such as less damage to the white matter and myelin, better memory and movement, and mitigation of post-stroke complications.

 

Notably, exercise increased mitochondrial levels in muscle and blood, facilitating their migration between tissues via platelets. The platelets acted like delivery trucks, carrying mitochondria produced in the muscle cells to the brain cells, including neurons and their support cells, such as the protective myelin-forming cells (oligodendrocytes) and the star-shaped astrocytes, which form a protective barrier between the blood and the brain. Once in the brain, these mitochondria helped brain cells in the damaged area, as well as in the surrounding region, called the penumbra, survive under low-oxygen conditions, supported repair of white matter, and reduced post-stroke complications.(Slight problem here, the penumbra resolves itself into dead brain in the first week, so you need this exercise immediately! HOW THE FUCK WILL YOUR DOCTOR ACCOMPLISH THAT?)

 

“Currently, there are limited effective therapies for reducing post-stroke neurological sequelae, and no established treatments to prevent the progression of vascular dementia. Although additional experiments have revealed several technical and biological challenges, the proposed approach has the potential to contribute to a future in which neurological sequelae after cerebral infarction can be mitigated. Moreover, the therapeutic applications may extend beyond stroke to mitochondrial diseases and related neurodegenerative disorders,” says Dr. Inaba.

 

This pioneering study opens up exciting possibilities for new treatments for stroke recovery and prevention of vascular dementia, and possibly other debilitating diseases that cause brain cell degeneration. If found safe and successful in human trials, the benefits of exercise could be reaped through the transfusion of mitochondria-laden platelets.

 

Reference

Authors	Toshiki Inaba1, Nobukazu Miyamoto1, Kenichiro Hira1, Chikage  Kijima1, Yoshifumi Miyauchi1, Hai-Bin Xu1, Kazo Kanazawa1, Yuji Ueno1,2, and Nobutaka Hattori1,3
Title of original paper	Mitochondrial intercellular transfer via platelets after physical training exerts neuro-glial protection against cerebral ischemia
Journal	MedComm
DOI	10.1002/mco2.70590
Affiliations	1Department of Neurology, Juntendo University School of Medicine, Japan 2Department of Neurology, University of Yamanashi, Japan 3Neurodegenerative Disorders Collaborative Laboratory, RIKEN Center for Brain Science, Japan

 

About Assistant Professor Toshiki Inaba

Dr. Toshiki Inaba is a Research Assistant Professor at the Department of Neurology, Juntendo University School of Medicine, Japan. He has over 27 publications to his credit. His areas of research include neurology, systems neuroscience, cerebrovascular physiology, neuroprotection, neuroinflammation, glia, and endothelial dysfunction.

Risperidone Use in Dementia Linked to Increased Stroke Risk Regardless of CVD History

 Great Catch-22 here; if your doctor can't prevent your post stroke dementia, they could cause another stroke.  So, ask your competent? doctor FOR EXACT DEMENTIA PREVENTION PROTOCOLS! NO excuses allowed!

And your doctor knew of this last year, right?

Antipsychotics in Dementia Tied to Wider Range of 'Serious Harms' April 2024

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this!

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here: 

Risperidone Use in Dementia Linked to Increased Stroke Risk Regardless of CVD History

The antipsychotic risperidone is associated with increased stoke risk in older adults with dementia, even in those without cardiovascular disease (CVD), results of a large population-based study showed.

“We knew that risperidone increased risk of stroke; however, there were no major studies examining whether this risk differed according to the clinical history of the patient,” co-first author Byron Creese, PhD, Department of Psychology, Brunel University of London, Uxbridge, England, told Medscape Medical News.

“We found that the relative risk of stroke associated with risperidone was the same across all subgroups. In this respect, we could say there is no ‘safer’ group to give risperidone to, at least when it comes to clinical history,” Creese said.

The study was published online on October 9 in The British Journal of Psychiatry.

Similar Stroke Risk Across All Groups

Up to 50% of individuals living with dementia experience agitation or aggression during the course of the illness. While nondrug interventions are recommended as first-line treatment, antipsychotics such as risperidone are often used when symptoms are severe.

Until now, little was known about risperidone influenced stroke risk in patients with and without a history of CVD.

To find out, the researchers compared the incidence of stroke in adults living with dementia who were prescribed risperidone with that of a matched control group across subgroups of patients with and without a prior history of stroke and other types of CVD.

Using the UK Clinical Practice Research Datalink, they identified 28,403 older adults who initiated risperidone after dementia diagnosis. Patients who had received other antipsychotics within 90 days before being prescribed risperidone were excluded as these medications also increase stroke risk. Each risperidone user was propensity score-matched to up to five control individuals with dementia who were not prescribed antipsychotics (n = 136,324).

Risperidone was associated with an increased risk for stroke in the overall cohort and in all subgroups over 1 year and in a 12-week sensitivity analysis.

“The principal new finding from this study was that relative risk of stroke was comparable across all subgroups,” the investigators wrote.

In the overall cohort, the unadjusted incidence rate of stroke (per 1000 person-years) was 53 in risperidone users vs 41 in control individuals. In multivariable adjusted Cox models, risperidone users had a 28% higher risk for stroke than matched control individuals (adjusted hazard ratio [aHR], 1.28).

For risperidone users and matched control individuals with a stroke history, the incidence rates for stroke were 222 and 177 per 1000 person-years, respectively (aHR, 1.23).

“Although the relative risk of 1.23 may appear modest, a baseline 1-year risk of 177 per 1000 person-years is significant, and clinicians should be mindful of prescribing a drug that increases stroke risk further in an already at-risk group,” the authors wrote.

For risperidone users and matched control individuals with no stroke history, stroke incidence rates were 29 and 22 per 1000 person-years, respectively, with an aHR of 1.34 — which was not statistically different to that of the stroke history subgroup (aHR, 1.23).

“Therefore, on average, a patient with stroke history has about the same relative risk of stroke if prescribed risperidone as a patient with no stroke history,” the authors noted.

Important New Evidence

Reached for comment, Raya Elfadel Kheirbek, MD, MPH, professor of medicine, and chief in the Division of Gerontology, Geriatrics, and Palliative Medicine, University of Maryland School of Medicine, Baltimore, said this large, real-world analysis provides “important new evidence to guide antipsychotic prescribing in dementia, particularly in relation to stroke risk.”

“While prior studies have established an association between risperidone and increased cerebrovascular events, this study offers novel insights by stratifying risk across subgroups with and without preexisting CVD or stroke,” Kheirbek told Medscape Medical News.

The findings, she said, “challenge the prevailing clinical assumption that heightened risk is largely confined to individuals with prior stroke or CVD, and emphasizes that even patients perceived as ‘low risk’ carry meaningful stroke risk with risperidone initiation,” she said.

For clinicians, Kheirbek said, the study provides “quantifiable, patient-relevant data to support more informed, individualized discussions around risk.”

The data can help “contextualize treatment decisions within each patient’s clinical narrative, particularly when considering use in populations already vulnerable to poor functional recovery after stroke,” Kheirbek said. The data also underscore the importance of short-term vigilance: risk was highest within the first 12 weeks of treatment, she noted.

“Overall, the findings support a cautious, guideline-concordant approach to risperidone prescribing — reserving it for severe symptoms that have not responded to nonpharmacological strategies, and centering decisions on both clinical evidence and patient/family priorities,” said Kheirbek.

Also commenting on the findings Badr Ratnakaran, MBBS, chair of the American Psychiatric Association Council on Geriatric Psychiatry said that the link between antipsychotic use and a higher risk of cerebrovascular events in older adults with dementia is already well recognized.

“Ideally, treatment for agitation and psychosis in dementia should begin with nonpharmacologic approaches,” said Ratnakaran, who was not involved in the study.

“These include identifying potential sources of distress, such as urinary infections, creating a calm environment, using gentle redirection, soothing music, massage, aromatherapy, and addressing sensory impairments.”

“However, if nonpharmacological measures fail to control these symptoms or in acute emergencies, antipsychotics can be used. Ideally, shared decision-making with an explanation of the black box warning of increased risk of mortality must be made with patients and/or their caregivers about the judicious use of antipsychotics for the management of behavioral and psychological symptoms of dementia,” Ratnakaran said.

“The American Psychiatric Association’s guidelines on the use of antipsychotics for the management of agitation in dementia also support a patient-centered plan in using nonpharmacological and pharmacological interventions, including antipsychotics,” Ratnakaran added.

This study had no commercial funding. Creese declared receiving consultancy fees from Milbotix Ltd and IGC Pharma. Kheirbek is an associate editor of the Journal of Gerontology Medical Sciences. Ratnakaran had no disclosures.

What Is The 2 Finger Test In Dementia?

 Most stroke survivors would fail this if they have a disability in one hand, so make sure you decline to take it. By declining it, you prove you don't have dementia.

I refused to allow my Mom at 95 to take a cognitive test, she only has an 8th grade education and thus would get labeled incorrectly.

Similar to Catch-22; The term "catch-22" comes from the 1961 novel by Joseph Heller, where it describes a situation in the military where a pilot could avoid flying combat missions by claiming insanity, but the very act of claiming insanity would prove his sanity and thus he would have to continue flying.

Other sources claim this is it since the video completely failed at telling us about it! 

The "2-finger test" for dementia, often called the Interlocking Finger Test, assesses coordination, memory, and motor skills by having someone replicate a specific finger gesture, like interlocking fingers or touching thumb to index finger repeatedly, to spot early signs of cognitive decline, though it's a screening tool, not a definitive diagnosis, revealing issues with processing, memory, or motor control often seen in dementia. Difficulty performing these simple tasks (slowness, hesitation, errors) can signal underlying neurological changes.

What Is The 2 Finger Test In Dementia?

Cannabis could help alleviate depression and suicidality among people with PTSD

How is your doctor treating you if you are among the 23% ?

23% chance of stroke survivors getting PTSD

Don't worry, your doctor will never write you a prescription for marijuana or CBD and your state legislature won't update their stupid medical marijuana laws to allow this as an approved option. So, legal state or Canada, but you can't do either, you can't treat yourself unless you are medically trained. And if you are medically trained you can't prescribe marijuana to yourself if you won't prescribe it to others.  Good Catch-22 there,  so you are screwed.  

Cannabis could help alleviate depression and suicidality among people with PTSD

Nov 5, 2019    |   For more information, contact Thandi Fletcher

Cannabis may be helping Canadians cope with the effects of post-traumatic stress disorder (PTSD), new research suggests.
In an analysis of health survey data collected by Statistics Canada from more than 24,000 Canadians, researchers from the BC Centre on Substance Use (BCCSU) and University of British Columbia (UBC) found that people who have PTSD but do not medicate with cannabis are far more likely to suffer from severe depression and have suicidal thoughts than those who reported cannabis use over the past year.
The study, published today in the Journal of Psychopharmacology, is the first to document the relationships between PTSD, cannabis use, and severe mental health outcomes in a sample representative of the population.

Stephanie Lake

“We know that with limited treatment options for PTSD, many patients have taken to medicating with cannabis to alleviate their symptoms,” says lead author Stephanie Lake, a research assistant at the BCCSU and PhD candidate at UBC’s school of population and public health. “However, this is the first time that results from a nationally representative survey have shown the potential benefits of treating the disorder with cannabis.”
Data was obtained from Statistics Canada’s 2012 Canadian Community Health Survey – Mental Health (CCHS-MH), which covers Canadians aged 15 and older. Among 24,089 eligible respondents, 420 reported a current clinical diagnosis of PTSD. In total, 106 people with PTSD, or 28.2 per cent, reported past-year cannabis use, compared to 11.2 per cent of those without PTSD.
The researchers found that PTSD was significantly associated with a recent major depressive episode and suicidal ideation among people who don’t use cannabis. Specifically, cannabis non-users with PTSD were about seven times more likely to have experienced a recent major depressive episode and 4.7 times more likely to have thoughts of suicide compared to cannabis non-users without PTSD, the researchers found.
Among cannabis-using respondents, PTSD was not associated with a recent depressive episode or suicide ideation. Over one-quarter of Canadians with PTSD reported past-year cannabis use, which is remarkably high compared to the prevalence of recent use in the general Canadian population (estimated at 11.4 per cent in the present study).

M-J Milloy

People exposed to trauma, including survivors of acute injury, conflict, violence and disaster, suffer from depression, suicide, and substance use disorders at disproportionately high rates compared to the general population. Canada is estimated to have one of the highest prevalence rates of PTSD worldwide, affecting an estimated 9.2 per cent of the population.
“We’re only just beginning to understand what the therapeutic potential of cannabis may be for a variety of health conditions,” says senior author Dr. M-J Milloy, research scientist at BCCSU and Canopy Growth Professor of Cannabis Science at UBC. “These findings are promising, and merit further study in order to fully understand the benefits of cannabis for people living with PTSD.”

Find other stories about: BC Centre on Substance Use, Cannabis, M-J Milloy, Posttraumatic stress disorder (PTSD), PTSD, Stephanie Lake

Cannabis assists the endocannabinoid system in supporting the process of neurogenesis.

Don't worry, your doctor will never write you a prescription for marijuana or CBD and your state legislature won't update their stupid medical marijuana laws to allow this as an approved option. So, legal state or Canada, but you can't do either, you can't treat yourself unless you are medically trained. And if you are medically trained you can't prescribe marijuana to yourself if you won't prescribe it to others.  Good Catch-22 there.

Cannabis assists the endocannabinoid system in supporting the process of neurogenesis.

Neurogenesis (growing new brain cells), in adults, is critical to learning, mood regulation and maintaining brain health; the endocannabinoid system plays an active role in this process. Interestingly, many psychiatric disorders, like depression and schizophrenia, are accompanied by impaired neurogenesis.

The brain begins the neurogenesis process immediately following injury. It does so by increasing its proliferation of neural progenitor cells (NPCs). In this way, the brain attempts to heal the injury and prevent further damage.

What Role Does the Endocannabinoid System Play in Neurogenesis?

The endocannabinoid system is the body’s own system of cannabinoid molecules and cannabinoid receptors that are predominantly found in the brain and throughout the immune system, although these receptors are also found throughout the organs and tissues of your body.  When the brain is injured, as in a stroke or force related traumatic injury, the endocannabinoid system ramps up production of endocannabinoid molecules and receptors. Scientists believe this is evidence that the endocannabinoid system is involved in neural regeneration.

In animal studies, the participation of the endocannabinoid system in neurogenesis has been confirmed. In an animal model of brain injury, mice bred to lack cannabinoid receptor CB₁ or mice with the activity of the CB₁ receptor blocked, had reduced neurogenesis. In in vitro studies on neural cells, growth and division of NPCs were inhibited when the activity of the CB₁ and CB₂ receptors were blocked.

Cannabidiol (CBD) has been shown to increase neurogenesis in animals. For example, one study on an animal model of chronic stress found that CBD could undo the reduced neurogenesis and the anxiety. Animal studies have also shown that neurogenesis only occurs after long term administration of cannabinoids, so it doesn’t have an immediate effect.

Further evidence for the role of the endocannabinoid system in neurogenesis was found by looking more closely at the brain. High levels of CB₁ and CB₂ receptors were found in the part of the brain that is known to be responsible for containing NPCs and promoting neuron growth and differentiation, the subventricular zone (SVZ). The two kinds of diacylglycerol lipases (DAGLs), enzymes that help synthesize the endocannabinoid 2-arachidonoylglycerol (2-AG), were also found in this part of the brain. Their presence also points to an active role of the endocannabinoid system in neurogenesis.

The mechanism seems to involve both cannabinoid receptors, CB₁ and CB₂. A variety of protein signalling cascades have been found to result in neural regeneration in both animals and brain cells studied in vitro. These signaling pathways, once activated by cannabinoid molecules binding to the cannabinoid receptors, first encourage NPCs to grow and divide, a process called proliferation.

After the population of NPCs has grown, they then begin to migrate to different parts of the brain and undergo a transformation into the type of brain cell that is needed. This is called differentiation, and it is also mediated by cannabinoids. After differentiation, cannabinoid receptors remain on the cells and are thought to play a part in the signalling pathways that decide whether the cell should continue to live or should undergo programmed cell death, or cell maintenance.

However, the practical use of cannabis for encouraging neural regeneration is going to be limited by the psychoactive side effects of activating the CB₁ receptor by THC. Some researchers are examining other ways of manipulating the endocannabinoid system to encourage neurogenesis by administering drugs that prevent endocannabinoids from being broken down in the brain. This would increase the numbers of endocannabinoids present in the brain and exert proliferative effects while limiting any undesirable psychoactive effects.

Unemployment may increase risk for stroke

So you have a great Catch-22 here. Your doctor didn't get you to 100% recovery so you likely lost your job and now you are at a greater risk for getting a stroke. 
http://www.healio.com/cardiology/stroke/news/online/%7B73dd5bf7-6ec3-4178-bf12-7aeec6aca689%7D/unemployment-may-increase-risk-for-stroke 
 

Eshak ES, et al. Stroke. 2017;doi:10.1161/STROKEAHA.117.016967.

April 13, 2017

Periods of unemployment increased the risk for stroke in men and women in Japan, according to findings published in Stroke.

Japan’s employment system is different than in the United States, as employees are part of a “lifetime employment system” who will dedicate themselves to a steady job, Ehab S. Eshak, MD, MSc, PhD, visiting associate professor at Osaka University in Japan, said in a press release. If they happen to lose the position, it is possible that they will be re-employed into substandard or lower positions, he said.
Eshak and colleagues reviewed data from men (n = 21,902) and women (n = 19,826) aged 40 to 59 years in Japan. Those with a history of CVD or cancer at baseline were excluded from the study. Participants were categorized by employment status, which was determined through pre-baseline and baseline surveys: continuously employed, job loss, re-employed and continuously unemployed. Participants were followed until incidence of first stroke, death, relocation from the study area or the end of the study.
Throughout the follow-up period (mean, 15 years), men experienced 973 cases (577 ischemic, 396 hemorrhagic) of newly diagnosed stroke, and women experienced 460 cases (219 ischemic, 133 hemorrhagic).
The multivariable HR for stroke incidence in men who lost their jobs was 1.58 (95% CI, 1.18-2.13) and 1.51 (95% CI, 1.08-2.29) in women. The HR for mortality in women who lost their jobs was 2.48 (95% CI, 1.26-4.77) vs. 2.22 (95% CI, 1.34-3.68) in men.
Re-employed men experienced an increase in stroke incidence (multivariable HR = 2.96; 95% CI, 1.89-4.62) and mortality (multivariable HR = 4.21; 95% CI, 1.97-8.9), but re-employed women did not (multivariable HR for mortality = 1.28; 95% CI, 0.76-2.17; multivariable HR for incidence = 1.3; 95% CI, 0.98-1.69).
“For re-employed women, it is plausible not seeing an increased risk as that in men because the pattern of Japanese women’s participation in the labor force by age group is represented by an M shape, reflecting their tendency to have a career break during their 30s, in response to their family responsibilities, and then return to the labor force in their 40s, which is different from men in whom to proportion of working age men without job is relatively low in Japan,” Eshak and colleagues wrote.
Higher risks for stroke mortality was seen in men (multivariable HR = 5.24; 95% CI, 2.66-10.31) and women (multivariable HR = 5.35; 95% CI, 2.44-7.76) who were continuously unemployed.

Is Marijuana Dangerous? These New Stats Suggest So A poorly understood illness in long-term marijuana users appears to be on the rise.

So fucking what? The uses for stroke rehabilitation would likely be short-term. But our stupid federal legislators will glom onto anything negative about marijuana and not even approve research proving the positives. With this mindset aspirin, alcohol and warfarin would have never been approved.  I would suggest moving to one of the legal states or countries.

My 13 reasons for marijuana use post-stroke.  

But don't listen to me, I have absolutely no medical training, you don't need medical training to read and understand research on its' good points.

Your Mom and Grandmother need to be screaming in their faces that marijuana is useful for stroke rehab, so get the fuck out of the way. http://www.fool.com/investing/2017/01/07/is-marijuana-dangerous-these-new-stats-suggest-so.aspx?source=yahoo-2&
Last year was, unquestionably, marijuana's breakout year if there ever was one.
You could certainly argue that 1996, the first year that California approved medical cannabis, or 2012, the first year that Colorado and Washington approved recreational weed, were marijuana's breakout years. But 2016 saw five states approve medical cannabis (two of which did so by entirely legislative means), while four additional states legalized recreational pot, doubling the number of adult-use states to eight. Furthermore, Gallup's poll showed that nationwide approval for pot is now at an all-time high of 60%, and sales of legal weed continue to grow by a double-digit annual percentage.
Marijuana also enters 2017 with a lot of momentum. President-elect Donald Trump placed his support behind the legalization of medical cannabis during his campaign, and he's maintained that the federal "hands-off" approach to regulating pot is probably the best method for now. In other words, marijuana would appear to be on track to grow sales and add more legal states to the medical cannabis and recreational pot columns in the years to come.

Nationwide legalization remains elusive

However, a rescheduling of marijuana at the federal level remains elusive. Republicans in charge of Congress have demonstrated little desire to change its current illicit status, and the U.S. Drug Enforcement Agency passed on its opportunity to reschedule the substance this past August. The DEA suggested in its ruling that marijuana has a high potential for abuse, currently has no accepted medical use, and that it lacks accepted safety measures of use, even under medical supervision.

Pro-legalization advocates, especially those who support the legalization of medical cannabis, have been particularly critical of the stance the DEA has taken with regard to labeling marijuana as having no medical benefits and not being safe. Various clinical studies run by universities and researchers have demonstrated clinical benefits for marijuana and/or its cannabinoids in treating diseases such as glaucoma, epilepsy, type 2 diabetes, chronic pain, and even cancer. What's more, pro-legalization advocates will point to the fact that no one has died from an overdose of marijuana as proof of its safety compared to prescription opioids, which claimed about 15,000 lives in 2015 from overdoses.

Is long-term marijuana use actually dangerous?

But marijuana's safety profile isn't perfect. In fact, according to recent data in the post-legalization environment in select states, marijuana could prove dangerous to some users.
As reported by CBS News last week, the number of incidences of a somewhat rare and mysterious illness characterized by nausea, vomiting, and abdominal pain in long-term marijuana users has been on the rise. The disease, known as cannabinoid hyperemesis syndrome, or CHS, tends to go largely undiagnosed by physicians, especially emergency room physicians, because a patient often has to present with similar symptoms on numerous occasions, and have standard imaging tests done, to rule out other possible causes of their symptoms(So it is impossible to diagnose in the emergency room). It's known to cause dehydration and kidney failure in patients, but resolve with IV fluids and the termination of marijuana use within a few days. Users also note that taking hot showers or baths tended to resolve the symptoms.

According to a study co-authored by Dr. Kennon Heard, an emergency room physician at the University of Colorado Hospital in Aurora, Co., emergency room visits with a CHS diagnosis(impossible to diagnose this quickly) nearly doubled in two Colorado hospitals since 2009, when medical cannabis became widely available within the state. "It is certainly something that, before legalization, we almost never saw. Now we are seeing it quite frequently," said Dr. Heard in his interview with CBS News.
However, Forbes contributor Robert Glatter, MD, also brings up an excellent point. Dr. Heard's study suggests that the propensity of long-term marijuana users to admit their use to a physician in a post-legalization environment may have led to an increase in diagnoses compared to the pre-legalization setting where admitting marijuana use to a physician was viewed as taboo. In other words, the near-doubling in CHS incidences since medical cannabis became widely available may be overstated.
What's also not well understood is what's caused a complete bifurcation from the norm when it comes to marijuana use. Normally, cannabis acts as an antiemetic that keeps people from being nauseous. In this instance, cannabis became the source of nausea in select long-term users. One theory, as pointed out by Glatter, is that a buildup of cannabidiol (CBD), the non-psychoactive component of pot, could be the cause. In animal models, low doses of CBD led to an antiemetic effect, whereas large CBD doses had the opposite effect.

Only time will tell

This recently released data suggests that there are still quite a lot of unknowns with regard to long-term marijuana use. It doesn't necessarily suggest that marijuana is dangerous; but it's not exactly a glowing endorsement for safety, either.
The only way the pot industry is going to sway Congress or the DEA is if there's clear-cut evidence from a Food and Drug Administration-approved clinical trial that the benefits of cannabis outweigh the apparent risks. Of course, getting the FDA's approval to run well-designed and controlled trials has been essentially nonexistent. This is one of the many Catch-22 loops pot is stuck in. Researchers can't offer acceptable evidence to the FDA that marijuana may have medically beneficial properties because of its schedule 1 status, but the DEA won't reschedule marijuana until it has this evidence in hand.
The other Catch-22 for pot is that even if Trump and Congress do wind up legalizing medical marijuana at the federal level, things aren't necessarily going to get easier for the industry. Rescheduling cannabis to schedule 2, the most logical step if it were legalized, would admit that the substance has medically beneficial properties, but it would also place medical cannabis under the strict regulation of the FDA. The FDA could dictate how pot businesses market and package their product, it would likely oversee the manufacturing and processing of pot, and it could require medical marijuana companies to run FDA-approved clinical studies to demonstrate the effectiveness of pot in treating certain ailments. In other words, we're talking about a wave of new regulations that could wind up bankrupting a number of smaller industry players.
2016 was unmistakably a great year for marijuana, but the future for pot isn't nearly as clear.