Stroke drug shows potential MS benefits - myelin repair

 Ask your  competent? doctor EXAXTLY HOW MUCH MYELIN WAS DAMAGED IN YOUR STROKE! And the EXACT REPAIR PROTOCOLS!

No knowledge is a fireable offense all the way to the board of directors!

Stroke drug shows potential MS benefits

A stroke drug may help preserve and repair myelin damaged by multiple sclerosis, according to a review of animal studies.

Nimodipine was also linked to reduced inflammation, nerve damage and disease severity in several of the studies reviewed.

Myelin is the protective coating around nerve fibres that is damaged in multiple sclerosis, or MS, disrupting communication between the brain and the rest of the body.

Researchers in Iran reviewed five animal studies investigating whether nimodipine, a prescription medicine used to prevent blood vessel spasms after bleeding in the brain, could have potential as an MS treatment.

In MS, the immune system mistakenly attacks the myelin sheath, causing inflammation and nerve damage that can lead to a wide range of neurological symptoms.

Most current MS treatments work by modifying the immune system. While they can reduce relapses and slow disease progression, they generally do not directly repair myelin that has already been lost.

Nimodipine works by relaxing narrowed blood vessels to improve blood flow to injured brain tissue.

Previous research has suggested that the drug may also reduce inflammation and nerve damage while supporting myelin repair.

Four of the five studies involved rodents with experimental autoimmune encephalomyelitis, or EAE, a condition commonly used to model MS.

The fifth used cuprizone, a toxin that causes demyelination, meaning the loss of the protective myelin coating around nerves.

The studies differed substantially in the animals and disease models used, nimodipine doses, treatment methods and outcome measures, so researchers could not combine the results into a single statistical analysis.

Instead, they carried out a narrative review of the results.

Overall, nimodipine was linked to reduced disease severity in the EAE models.

One study found that the drug reduced the severity of relapsing-remitting EAE and lessened disease severity during the early active phase.

Other studies reported reduced relapse rates, fewer sensory and motor problems and effects suggesting protection of nerve cells.

Nimodipine was also linked to less myelin loss and fewer demyelinated nerve fibres.

In one study, treatment increased the number of nerve fibres showing signs of remyelination, the process through which damaged myelin is rebuilt.

The findings were accompanied by increased activity in genes linked to myelin and higher numbers of cells involved in myelin regeneration.

Animals treated with nimodipine also showed fewer signs of inflammation in the brain and spinal cord and lower blood levels of some inflammation-related proteins.

The drug was also linked to improved blood flow and oxygen levels in the spinal cord, while one study found reduced clinical scores and improved motor performance.

In the cuprizone model, nimodipine was linked to fewer reactive immune cells in the brain and faster, more complete myelin repair.

The researchers called for further studies to reproduce the findings and early-stage human trials to determine whether nimodipine can safely provide similar benefits for people with MS.

The researchers wrote: “These findings underscore the potential of drug repositioning to uncover novel clinical mechanisms for nimodipine and expand its therapeutic applications to other diseases, such as MS.

“Preclinical evidence suggests that nimodipine may attenuate disease severity and demyelination and may promote repair-related processes in rodent models relevant to MS.”

Lithium and Brain Health: Could a Deficiency Raise Alzheimer’s Risk?

 A big warning buried in here: Lithium Is NOT Benign! Read all of this and grill your doctor on it.

Lithium and Brain Health: Could a Deficiency Raise Alzheimer’s Risk?

Here's a fascinating question: could lithium deficiency contribute to cognitive impairment? Is there a link between lithium and brain health?

Most healthcare professionals think about lithium, if they think about it at all, as the stuff in rechargeable batteries or as a powerful prescription drug for bipolar disorder. They probably do not think about lithium and brain health or imagine that too little of this natural mineral might have anything to do with Alzheimer’s disease. New research suggests it may be time to reconsider that assumption.

That idea is especially surprising because lithium is not officially recognized as an essential nutrient. There is no Recommended Dietary Allowance for lithium. Doctors do not routinely measure lithium levels in healthy people. There is no recognized “lithium deficiency disease” comparable to iron-deficiency anemia or vitamin D deficiency.

And yet a remarkable study published in Nature (August 6, 2025), raised a provocative possibility: tiny amounts of naturally occurring lithium may play an important role in keeping the aging brain healthy.

The title alone should have attracted enormous attention:

“Lithium deficiency and the onset of Alzheimer’s disease“

This was not a casual experiment carried out by investigators in a small lab in a foreign country. The research involved investigators from Harvard Medical School, Boston Children’s Hospital and the Rush Alzheimer’s Disease Center. They examined human brains as well as sophisticated mouse models of Alzheimer’s disease.

Lithium and Brain Health: A Mineral Hiding in Plain Sight?

Lithium is a naturally occurring element. It is found in rocks and soil. As a result, lithium gets into groundwater, drinking water, food and us. Unlike calcium, magnesium, iron or zinc, however, lithium has never achieved membership in the official essential-nutrient club.

Perhaps that is because the amounts normally present in the body are extraordinarily small. The lithium concentrations used to treat bipolar disorder, on the other hand, are vastly greater than the trace amounts normally circulating in people. The dose of lithium found in the prescription drug LITHOBID® prescribed for “manic episodes of Bipolar Disorder” is:

“3 tabs (900 mg) Morning” and “3 tabs (900 mg) Nighttime”

That’s a whopping 1,800 mg of lithium carbonate (or roughly 340 mg of pure lithium). There is considerable toxicity associated with this high dose of lithium and the boxed warning that comes with LITHOBID® (lithium carbonate) states:

WARNING

“Lithium toxicity is closely related to serum lithium levels, and can occur at doses close to therapeutic levels. Facilities for prompt and accurate serum lithium determinations should be available before initiating therapy.”

For decades, most medical interest in lithium has revolved around lithium the medication, not lithium the nutrient-like trace element.

If you would like to get a thorough background about the history of lithium dating back to the 19th century, you will want to read my prior article titled:

“Rediscovering Low-Dose Lithium for Mood Disorders“

You may be surprised to learn that the original soft drink “Seven Up” was once called 7UP Lithiated Lemon Soda. It has been estimated that the original formula contained 5 mg of lithium citrate. One marketing slogan was: “It takes the ouch out of the grouch.”

There is no lithium in the current 7UP!

Fast forward to Harvard researchers and their article a year ago in Nature (August 6, 2025).

What Did the Researchers Find in Human Brains?

The scientists measured 27 metals in the blood and brains of older people who had normal cognition, mild cognitive impairment (MCI) or Alzheimer’s disease. MCI is important because it can represent an early stage on the road toward dementia.

Of all the metals measured, lithium stood out. It was the only metal significantly reduced in the prefrontal cortex in both MCI and Alzheimer’s disease. That is intriguing enough. But there was another surprise.

Blood levels of lithium were not significantly lower in people with MCI or Alzheimer’s disease.

In other words, this was not simply a matter of people having less lithium circulating throughout their bodies. Something seemed to be happening specifically inside vulnerable parts of the brain. The investigators discovered a possible explanation: amyloid plaques appeared to trap lithium.

Amyloid beta is the sticky protein that accumulates in the brains of people with Alzheimer’s disease. The researchers found lithium concentrated in those deposits, leaving less lithium available to surrounding brain tissue. That raises the possibility of a nasty feedback loop:

Alzheimer’s pathology begins → amyloid traps lithium → less lithium remains available to brain cells → the shortage may make Alzheimer’s pathology worse → still more amyloid accumulates.

That is a hypothesis, not established medical fact. But it is a fascinating one.

Lithium and Brain Health: What Happens When the Brain Doesn’t Get Enough Lithium?

Here is where the research becomes quite intriguing. The investigators deliberately reduced lithium in the diets of mice. This lowered lithium levels in the cerebral cortex by roughly half. The consequences were dramatic.

Lithium depletion increased two hallmarks of Alzheimer’s disease:

• Amyloid beta, which forms plaques
• Phosphorylated tau, which contributes to the tangles found inside nerve cells

That was only part of the story. Lithium deficiency also activated inflammatory cells in the brain called microglia. I have to be honest with you. I am totally fascinated by microglia. Think of these cells as part of the brain’s housekeeping and immune system.

This is not a perfect analogy, but for our purposes you could imagine microglia as minute vacuum cleaners, sucking up debris, old cellular brain fragments and even infectious agents. In other words, they are part of the brain’s immune defense against pathogens. They also help dispose of the brain’s cellular debris, including amyloid.

When lithium became deficient, these cells shifted toward a more inflammatory state and became less effective at clearing amyloid. The lithium-depleted animals also lost synapses, axons and myelin. Synapses allow brain cells to communicate. Axons carry electrical messages. Myelin is the insulation surrounding many of those nerve fibers.

Here’s the key piece to the puzzle. The mice experienced accelerated memory and cognitive problems. That is a remarkable collection of results from reducing one trace element that most nutrition experts think is unimportant.

A Possible Culprit: GSK-3 Beta

Now we must take a brief foray into neuroscience. Please don’t let the alphabet soup scare you away. An enzyme called glycogen synthase kinase-3 beta, thankfully abbreviated GSK-3β, appears to play a key role in several processes associated with Alzheimer’s disease.

Among other things, excessive GSK-3β activity can contribute to abnormal phosphorylation of tau. Along with amyloid beta, phosphorylated tau is considered an important marker of Alzheimer’s disease. Consider this: The FDA has approved blood tests that measure phosphorylated tau. In its May 16, 2025 announcement the agency offered this headline:

“FDA Clears First Blood Test Used in Diagnosing Alzheimer’s Disease”

New Test Provides Less Invasive Option, Reduces Reliance on PET Scans and Increases Diagnosis Accessibility

Lithium and Brain Health

Lithium has been known to affect the enzyme GSK-3β. The Harvard investigators found that lithium deficiency increased GSK-3β activity in brain cells. When they blocked GSK-3β experimentally, they reversed many of the harmful effects produced by lithium deficiency. This included improvements in amyloid accumulation, tau abnormalities, inflammation and myelin problems.

That provides something scientists always want: a plausible biological mechanism. It does not, however, prove that taking lithium will prevent Alzheimer’s disease in human beings. That distinction is crucial.

Then Came Lithium Orotate

Perhaps the most intriguing part of the Nature experiment involved different forms of lithium.

The prescription form most people know is lithium carbonate. It is the form of lithium that is used by psychiatrists to treat people with bipolar disorder.

The Harvard scientists used lithium orotate.

Here is how they described their findings with regard to Alzheimer’s disease (AD):

“Replacement therapy with lithium orotate, which is a Li [lithium] salt with reduced amyloid binding, prevents pathological changes and memory loss in AD mouse models and ageing wild-type mice. These findings reveal physiological effects of endogenous Li in the brain and indicate that disruption of Li homeostasis may be an early event in the pathogenesis of AD. Li replacement with amyloid-evading salts is a potential approach to the prevention and treatment of AD.”

Their experiments suggested that lithium carbonate was more readily trapped by amyloid deposits. Lithium orotate appeared less likely to become sequestered in plaques and consequently delivered more lithium to the surrounding brain tissue.

When researchers gave extremely small amounts of lithium orotate to Alzheimer’s-prone mice, the results were impressive. In one model, lithium orotate nearly prevented the accumulation of amyloid and abnormal tau when given before substantial disease developed. In older animals that already had extensive pathology, treatment reduced amyloid deposits substantially.

In aging mice without genetically engineered Alzheimer’s disease, lithium orotate also helped preserve synapses and memory. Even more surprising, the doses were designed to keep lithium concentrations in the range naturally found in the body rather than the much higher blood concentrations used to treat bipolar disorder.

Long-term treatment at these tiny doses did not produce detectable changes in the kidney and thyroid laboratory tests the investigators monitored in the mice. Please notice the last three words in that sentence: “in the mice.”

We cannot automatically assume that the same dose, safety or brain benefits would apply to people. That is why clinical trials matter!

What About Human Evidence Re: Lithium and Brain Health?

Fortunately, the lithium story does not depend entirely upon laboratory animals. There have been some intriguing human clues for years. One of the largest comes from Denmark (JAMA Psychiatry, Oct. 1, 2017).

Investigators compared lithium concentrations in drinking water with dementia diagnoses in 73,731 people with dementia and 733,653 controls.

People exposed over the long term to the highest category of lithium in drinking water had a lower rate of dementia than people in the lowest category:

“Long-term increased lithium exposure in drinking water may be associated with a lower incidence of dementia in a nonlinear way…”

But there was a wrinkle. The relationship was not linear. An intermediate exposure group actually had a higher rate of dementia than the lowest group. The investigators therefore appropriately warned that geography, socioeconomic factors or other unmeasured differences might have influenced the results.

That study should prevent anyone from making the simplistic argument that “more lithium in the water equals less dementia.” It isn’t that straightforward.

Another observational study from England found that people exposed to prescription lithium had a lower incidence of dementia (PLoS Medicine, March 17, 2022).

The conclusions:

“We observed an association between lithium use and a decreased risk of developing dementia. This lends further support to the idea that lithium may be a disease-modifying treatment for dementia and that this is a promising treatment to take forwards to larger randomised controlled trials (RCTs) for this indication.”

A “systematic review” of “Trace lithium levels in drinking water and risk of dementia” published in the International Journal of Bipolar Disorders (Aug. 30, 2024) concluded:

“The reviewed evidence shows that trace-Li levels in the water are sufficient to lower the incidence or mortality from dementia. Considering the lack of options for the prevention or treatment of dementia, we should not ignore these findings. Future trials of Li should focus on long term use of low or even micro doses of Li in the prevention or treatment of dementia.”

Again, however, observational research can identify an association. It cannot prove cause and effect. It can encourage investigators to perform large-scale, long-term randomized clinical trials.

One relatively small “pilot” clinical trial produced disappointing results (JAMA Neurology, April 1, 2026). There were 41 people getting lithium carbonate (150 or 300 mg of lithium carbonate) and 39 getting placebo. There was no meaningful benefit for those getting lithium.

Were Researchers Studying the Wrong Dose…and the Wrong Lithium?

The Harvard 2025 Nature experiment was not testing conventional psychiatric doses of lithium carbonate. It was investigating something fundamentally different: restoration of lithium concentrations toward the extraordinarily low levels normally present in brain tissue. It also found that lithium orotate behaved differently from lithium carbonate in the presence of amyloid.

That raises a question worth answering:

Would truly tiny doses of lithium orotate protect the human brain without producing the adverse effects associated with much larger doses of lithium carbonate?

We don’t know. Nobody should pretend that we do. But in June 2026, a review in JAMA Psychiatry made almost exactly that point:

“The 25-Year Evolution of Lithium as a Disease-Modifying Agent in Dementia”

The authors introduce their review this way:

“Lithium, a long-established cornerstone therapy for bipolar disorder, is a biologically plausible disease-modifying agent for neurodegenerative disorders, including mild cognitive impairment (MCI) and Alzheimer disease (AD).”

The authors have pulled together a wealth of information in this article. We highly recommend that all neuroscientists interested in dementia and Alzheimer disease read this article in its entirety. If you know such researchers, please pass it along!

They conclude:

“Across molecular, cellular, imaging, epidemiologic, and early clinical domains, lithium displays remarkable convergence across translational domains. Yet compelling biology alone is insufficient. Definitive, adequately powered randomized clinical trials are required to determine whether lithium meaningfully slows cognitive decline.”

“If validated, lithium could represent a rare example of a low-cost, mechanistically grounded, disease-modifying therapy for neurodegeneration. In short, 75 years after transforming psychiatric care, lithium is now at the forefront of a new frontier: the fight against dementia.”

Why Hasn’t the Link Between Lithium and Brain Health Received More Attention?

Imagine if a pharmaceutical company announced a new molecular compound that:

• influenced amyloid and tau;
• calmed inflammatory brain cells;
• helped preserve synapses and myelin;
• affected an enzyme implicated in Alzheimer disease;
• restored memory in animal experiments;
• and might cost pennies rather than thousands of dollars.

We suspect Wall Street analysts, biotech investors and Alzheimer’s researchers would be paying very close attention. They might be competing to invest in the company developing such a drug.

Lithium presents an awkward economic problem. It is an element. You cannot patent lithium itself. Companies can potentially patent new formulations, delivery systems or particular uses, so saying there is no commercial opportunity would go too far. Nevertheless, the financial incentive for enormous clinical trials may be considerably weaker than it is for a proprietary new drug that could sell for tens of thousands of dollars a year.

That is precisely why public and philanthropic funding could be so important. A cheap treatment should not become scientifically uninteresting simply because it is cheap. We believe the Alzheimer’s research community should pursue this question aggressively, precisely because the answer might turn out to be either very important or completely disappointing. Both outcomes would be valuable.

Lithium Is NOT Benign!

Before anyone rushes to the Internet to order lithium orotate, we need to wave a large red flag.

Lithium can be toxic.

Prescription lithium carries a boxed warning because toxic blood concentrations can occur surprisingly close to therapeutic concentrations. Kidney function, thyroid function, electrolytes and lithium blood concentrations require monitoring when conventional lithium therapy is prescribed.

Lithium as a drug for bipolar disorder can cause:

• tremor
• nausea and diarrhea
• thirst and excessive urination
• fatigue and muscle weakness
• thyroid problems
• kidney problems
• neurological toxicity at excessive blood concentrations

Dehydration and changes in salt intake can alter lithium concentrations.

Drug interactions are another concern. Diuretics, ACE inhibitors and NSAID-type pain relievers can increase the risk of lithium accumulation and toxicity.

That is why experimenting on your own with prescription lithium is a terrible idea.

And we would not recommend taking even a low-dose, over-the-counter lithium supplement for the prevention or treatment of dementia without discussing it with a very knowledgeable health professional.

“Natural” and “low dose” do not automatically mean “risk free.”

Don’t Confuse Milligrams of a Salt With Milligrams of Lithium

Here is another source of enormous confusion.

A bottle may list the weight of lithium orotate, while another product or prescription lists lithium carbonate. Those numbers do not necessarily represent the same amount of elemental lithium.

It is rather like comparing the weight of sodium chloride with the amount of sodium it contains.

Anyone designing a clinical trial—or contemplating supplementation—needs to distinguish carefully between:

1. the weight of the lithium compound,
2. the amount of elemental lithium it supplies,
3. and the blood or tissue lithium concentration it ultimately produces.

This is one more reason amateur home compounding is a bad idea.

What We Know and What We Don’t

Here is what the science suggests today.

• Naturally occurring lithium is present in the human brain.
• The Harvard-led investigators found significantly less available lithium in vulnerable brain tissue from people with mild cognitive impairment (MCI) and Alzheimer’s disease.
• Reducing lithium in mice aggravated amyloid, tau, inflammation, structural brain damage and memory loss.
• Very-low-dose lithium orotate prevented or reversed many of those abnormalities in mouse models.
• Several epidemiological studies and some small human trials have produced intriguing signals suggesting that lithium exposure might be associated with less dementia or slower cognitive decline.

But…

• We do not know whether lithium deficiency causes Alzheimer disease in humans.
• It is not clear that low-dose lithium orotate can prevent MCI or Alzheimer disease.
• The ideal dose remains a mystery.
• We do not know whether long-term, very-low-dose lithium would be safe.
• And we do not know if measuring lithium in blood tells us anything useful about lithium availability inside the human brain. The Nature study suggests it may not.

Those are not minor unanswered questions. They are precisely the questions a well-designed randomized clinical trial should answer.

Our Bottom Line on Lithium and Brain Health

For over 75 years, medicine has viewed lithium primarily as a psychiatric drug for bipolar disorder. Perhaps that focus has been too narrow. The 2025 Nature study raises the startling possibility that lithium also has a normal physiological role in the aging brain and that disruption of lithium balance could contribute to the processes that eventually produce Alzheimer disease. The finding that lithium orotate protected aging and Alzheimer-prone mice is provocative.

But mice are not people! We are not recommending lithium orotate to prevent or treat Alzheimer’s disease. The human evidence is nowhere near strong enough to justify such a recommendation.

What we are recommending is research. Lots of it.

The appropriate response to this research is neither breathless enthusiasm nor a dismissive shrug. It is a large, carefully designed, long-term randomized trial testing very-low-dose lithium orotate against placebo, with careful monitoring of cognition, Alzheimer biomarkers, kidney function, thyroid function and adverse effects.

If lithium fails, we need to know that. If an inexpensive trace element can help preserve the aging human brain, we desperately need to know that too.

For a disease as devastating as Alzheimer’s, this is one stone that should not be left unturned.

Final Words:

We know there were a lot of technical terms in this article and we are grateful that you hung in there with us for this complicated story. We sincerely hope you found the research we described intriguing. There are a number of references at the bottom of this post that you could share with healthcare providers who are interested. We hope you will pass this article on to friends, family members, physicians and neuroscientists.

Should you wish to learn more about lithium and Alzheimer disease, you might want to listen to our podcast on this topic:

Show 1451: Rethinking Dementia: Is What We Believed about Alzheimer’s Wrong?
Instead of focusing only on amyloid plaque in the brain, should we be rethinking dementia? Multiple interventions could protect cognition.

Here are links to the podcast on Apple podcasts and Spotify.

These long analyses take many hours to create and your support is invaluable. Should you wish to support our work, here is a link.

Citations

• Moore, G.J., et al, "The 25-Year Evolution of Lithium as a Disease-Modifying Agent in Dementia: A Narrative Review," JAMA Psychiatry, June 10, 2026, doi: 10.1001/jamapsychiatry.2026.1296
• Aron, L., et al, "Lithium deficiency and the onset of Alzheimer’s disease," Nature, Aug. 6, 2025, doi: 10.1038/s41586-025-09335-x
• Kessing, L.V., et al, "Association of Lithium in Drinking Water With the Incidence of Dementia," JAMA Psychiatry, Oct. 1, 2017, doi: 10.1001/jamapsychiatry.2017.2362
• Chen, S., et al, "Association between lithium use and the incidence of dementia and its subtypes: A retrospective cohort study," PLoS Medicine, March 17, 2022, doi: 10.1371/journal.pmed.1003941
• Fraiha-Pegado, J., et al, "Trace lithium levels in drinking water and risk of dementia: a systematic review," International Journal of Bipolar Disorders, Aug. 30, 2024, doi: 10.1186/s40345-024-00348-5
• Gildengers, A.G., et al, "Low-Dose Lithium for Mild Cognitive Impairment: A Pilot Randomized Clinical Trial," JAMA Neurology, April 1, 2026, doi: 10.1001/jamaneurol.2026.0072

The Shifting Landscape of Secondary Stroke Prevention

 But you haven't even solved the problem of 100% recovery, you should solve the most pressing problem first.

The Shifting Landscape of Secondary Stroke Prevention

Ischemic stroke remains a leading cause of mortality and long-term disability worldwide(Yeah and the solution is 100% recovery protocols! Or are you too blitheringly stupid to see that?), with recurrent cerebrovascular events contributing substantially to cumulative neurologic injury, functional decline, and health care burden. Although major advances in acute stroke management have significantly improved survival, secondary prevention following an index ischemic stroke continues to represent a critical challenge in contemporary cerebrovascular care. 

Of the more than 800,000 strokes in the US every year, 1 in 4 are recurrent events.1 The risk for recurrent stroke varies widely across patient populations and stroke phenotypes, ranging from 10% to 15% within 12 months among patients with advanced microvascular disease or large artery atherosclerosis.2 

This risk persists despite advances in risk factor modification and the widespread availability of evidence-based guidelines and online resources, highlighting gaps between recommended care and real-world implementation. Barriers including health care access, treatment adherence, economic burden, patient engagement, and uncertainty in individualized risk assessment continue to limit the effectiveness of secondary prevention strategies. 

 

Closing the gap between clinical evidence and real-world implementation remains essential to reducing recurrent stroke burden and improving functional outcomes among stroke survivors.

Despite these challenges, most funding in cerebrovascular research continues to emphasize innovative technologies and pharmacotherapies, with comparatively less emphasis on translational research and implementation gaps.

Present Day Stroke Care

Persistent Risk After Index Stroke

The risk for recurrent ischemic stroke remains substantial throughout both early and late periods following the index event. After the acute period — when recurrent stroke risk is highest, typically within the first few weeks after stroke — the underlying mechanism (eg atrial fibrillation or an unstable atherosclerotic plaque) is often identified, and individualized treatment is initiated. However, long-term risk persists well beyond the immediate post-stroke period. 

Longitudinal cohort studies consistently demonstrate sustained elevation in recurrent stroke risk over subsequent years, driven by persistent and uncontrolled vascular risk factors, including hypertension, dyslipidemia, obesity, diabetes mellitus, atrial fibrillation, obstructive sleep apnea, substance use (including tobacco and alcohol), and systemic vascular dysfunction.3 Without effective risk factor modification, the likelihood of recurrent stroke or other vascular events remains considerable. 

Perhaps more importantly, recurrent cerebrovascular events often result in greater cumulative disability than the initial stroke, contributing to progressive neurologic impairment, reduced functional independence, dementia, and diminished quality of life. These events also have substantial downstream consequences, including increased caregiver burden and higher health care costs for patients and health systems. 

Barriers to Effective Secondary Prevention

Among the many limitations in successful secondary stroke prevention strategies is fragmentation of post-discharge care delivery. Stroke survivors frequently transition from hospitalization to outpatient care characterized by delayed or unscheduled stroke specialist follow-up, inadequate coordination between inpatient and ambulatory care teams, and limited access to multidisciplinary prevention services. These structural barriers are particularly pronounced in geographically underserved and rural populations, where access to vascular neurology, cardiology, rehabilitation medicine, and comprehensive stroke centers remains limited. 

Follow-up care is essential for reinforcing the benefits of antithrombotic therapy, lipid-lowering treatments, dietary and lifestyle modifications, and recognition of stroke warning signs and symptoms. Because many stroke risk factors are clinically silent, particularly hypertension, dyslipidemia, and diabetes, ongoing follow-up with primary and subspecialty care providers is necessary to ensure patients achieve target blood pressure, cholesterol, and glycemic goals. 

Economic and Structural Challenges in Long-Term Care

The whole fucking problem here is you're referring to 'care' NOT RECOVERY!

The economic burden of long-term stroke management represents another important challenge to successful secondary prevention. Effective post-stroke care often requires prolonged pharmacotherapy, outpatient specialist visits, repeat diagnostic testing, rehabilitation services, and management of multiple chronic conditions. Out-of-pocket costs, insurance limitations, prescription drug costs, transportation challenges, geographic barriers to subspecialty care, and restricted access to rehabilitation services can all impair adherence to recommended care.  

Although strategies such as out-of-network exemptions, teleneurology appointments, and partially subsidized pharmacy coverage may help address some barriers, they do not fully resolve challenges to effective secondary prevention. These financial and structural barriers disproportionately affect socioeconomically vulnerable populations and contribute to persistent disparities in recurrent stroke outcomes.

We asked doctors the one supplement you should be taking to support healthy aging—they all said the same one

 Really? What about this?  I guess doctors don't bother keeping up with research, they learned it all in medical school.

Are Omega-3 Supplements Actually Good for Your Brain? And why the fuck doesn't your doctor know anything EXACT about this. Weasel words do not count!

We asked doctors the one supplement you should be taking to support healthy aging—they all said the same one

Doctors resoundingly recommend omega-3 fatty acids—here’s why.

Reviewed by Dietitian Katey Davidson, M.Sc.FN, RD, CPT

Key Points

• Doctors recommend omega-3s as the top supplement to support healthy aging.
• Omega-3s support heart, brain and inflammatory health as you age.
• While omega-3s can help, overall lifestyle habits remain the foundation of healthy aging.

Healthy aging isn’t just about living longer—it’s about staying active, sharp and independent as you get older. While no supplement can replace the healthy lifestyle habits that matter most, such as eating a well-balanced diet and staying active, some may help fill common nutrient gaps and offer additional support as you age.

To find out which supplement doctors recommend most for aging well, we asked physicians to name the single supplement they’d prioritize. Their answer was unanimous: omega-3 fatty acids, specifically docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). 

“There is no magic pill (or supplement), but if I had to choose one with the best balance of evidence, safety and multisystem benefit, omega-3 fatty acids would be the clear winner,” says Sejal Desai, M.D. 

Here’s why this supplement can support healthy aging and what doctors want you to know before taking it.

Why Omega-3s Support Healthy Aging

They Help Reduce Chronic Inflammation

One reason doctors consistently recommend omega-3s is their effect on chronic inflammation. While temporary inflammation is a normal part of the body’s immune response—such as healing a cut—low-grade inflammation that lingers over time can be harmful and contribute to premature aging.

Sometimes called “inflammaging,” this persistent inflammation can become more common with age, especially when lifestyle habits also play a role. Marked by higher levels of inflammatory compounds in the body, it's thought to be a major driver of age-related decline. Over time, it can quietly wear on tissues and organs throughout the body, affecting everything from blood vessels to brain cells.

“Omega-3s help reduce chronic, low-grade inflammation by producing anti-inflammatory signaling molecules,” says Alex Jabourian, D.O. A recent study found that omega-3 supplementation may help reduce several inflammatory markers, including C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α)—all of which are associated with chronic inflammation and age-related disease. Benefits were especially noted for individuals with chronic inflammation, such as type 2 diabetes, heart disease and autoimmune conditions.

They Support Heart Health as You Age

As you get older, heart health becomes increasingly important, as the risk of cardiovascular disease tends to rise with age. Supplementing with omega-3s may help mitigate that risk. “Patients who already have a high risk of heart disease can benefit greatly from it,” says Nneoma Oparaji, M.D., M.H.S., ABOM, DipABLM.

“Omega-3s support cardiovascular health by lowering triglycerides, improving blood vessel function and reducing the risk of major cardiac events,” explains Jabourian. Triglycerides are a type of fat in the blood, and elevated levels are associated with a greater risk of heart disease and stroke. Omega-3s may help lower those levels.

For instance, a 2021 review in 149,051 participants found that omega-3 supplementation was associated with a reduced risk of death from heart disease, heart attacks and other major cardiovascular events. Taking a combination of EPA and DHA was linked to the greatest improvements in heart health.

Another 2025 analysis found that omega-3 supplementation was associated with improved markers of vascular health in people with heart disease, including arterial wave reflection and endothelial function—two measures tied to how well blood vessels respond to changes in blood flow. Researchers saw the strongest benefits with EPA and DHA, the same forms of omega-3s found in fish oil.

That said, more research is needed to better understand which populations may benefit the most and the appropriate dosing. 

They May Help Protect Brain Function

Forgetfulness, slower processing speed and difficulty concentrating can become more common with age, which is why keeping your brain healthy is so important. While occasional memory lapses are normal, significant changes in cognitive function can affect everything from decision-making and focus to how independently you’re able to move through daily life.

DHA, one of the main omega-3 fatty acids, is a key structural part of brain cell membranes, says Zergabachew Asfaw M.D., FACP. In fact, it makes up around 40% of fatty acids in the brain. Getting enough may help maintain the structure and flexibility of those membranes, which supports efficient communication between brain cells.

Omega-3 supplements may be especially beneficial for older adults who don’t get enough EPA and DHA in their diet. These omega-3s are mostly found in fatty fish.

Other Tips for Healthy Aging

“Supplements work best alongside consistent lifestyle habits,” says Jabourian. In other words, omega-3s can help, but the routines you practice every day still matter most.

• Stay Active. Cardiovascular exercise and resistance training can help support heart health, preserve muscle mass and maintain metabolic health as you age. Jabourian recommends regular exercise, aiming for at least 150 minutes of moderate activity and two days of strength training per week.   
• Prioritize Protein and a Whole-Food Diet. A diet built around minimally processed foods, adequate protein, fiber-rich carbohydrates and healthy fats can help support muscle maintenance, as well as metabolic and cardiovascular health. Asfaw recommends a Mediterranean-style eating pattern, which has been linked to lower inflammation, better physical function and a lower risk of frailty in older adults.
• Eat Anti-Inflammatory Foods. Fruits, vegetables, legumes, nuts, olive oil and fatty fish are all staples of an anti-inflammatory eating pattern.
• Protect Your Sleep. Sleep is when much of your body’s repair and recovery happens, helping your cells stay healthy. “Aiming for seven to eight hours of sleep a night supports metabolic and heart health,” says Oparaji.
• Be Social. Higher social engagement is linked with healthier aging and a lower risk of premature death. This could mean joining a walking group, having family dinners, hosting neighborhood potlucks or signing up for a book club.
• Avoid Smoking and Limit Alcohol. Smoking and excess alcohol intake can accelerate many of the processes tied to age-related decline, including inflammation, cardiovascular strain and cognitive changes. Avoiding both can help support long-term health.

Our Expert Take

If there’s one supplement doctors agree is worth considering for aging well, it’s omega-3s. Between their anti-inflammatory effects and benefits for heart and brain health, this supplement may help support several of the systems that tend to become more vulnerable with age. 

That said, they’re not a substitute for healthy habits. Think of omega-3s as one piece of the puzzle, not the whole picture. For the biggest payoff, combine it with regular movement, quality sleep, a nutrient-dense diet and strong social connections.

Read the original article on EatingWell

Reorganization of motor unit discharge-state space during ischemia-assisted fatigue: an energy landscape analysis

 I'm sure your competent? doctor can apply this research to resolve your post stroke fatigue! NO? You then don't have a functioning stroke doctor, do you?

Reorganization of motor unit discharge-state space during ischemia-assisted fatigue: an energy landscape analysis

• Yi-Ching Chen,
• Yen-Ting Lin &
• Ing-Shiou Hwang 

We’re sharing this article early to provide faster access to peer-reviewed, accepted research. It is citable and carries a permanent DOI. This version is subject to further edits and will be replaced automatically by the final Version of Record. All legal disclaimers apply.

Abstract

Background

Neuromuscular fatigue increases variability in motor-unit (MU) discharge and force output, yet how it reorganizes population-level MU discharge dynamics remains poorly understood. Conventional analytical approaches primarily quantify discharge magnitude, variability, and common synaptic input, providing limited information regarding the organization of discharge-state space. Hence, we applied a time-resolved energy landscape framework that preserves a joint representation of the mean and variability of pooled MU discharge to characterize fatigue-related reorganization of population-level MU discharge-state space. This approach was motivated by the premise that force steadiness depends on the joint organization of neural drive level and neural drive variability.

Methods

Force output and decomposed surface electromyographic signals were recorded during submaximal isometric wrist extension before and after an ischemia-assisted fatigue protocol in forty healthy adults(I'm sure your doctor can extrapolate results to stroke subjects, right?). Thirty-five participants exhibiting post-fatigue reductions in maximal voluntary contraction force were included in subsequent analyses. Pooled MU discharge activity was represented by the instantaneous mean firing rate and analyzed using a sliding-window approach. Energy landscapes were constructed in a two-dimensional discharge-state space defined by the mean and variability of pooled MU discharge activity, enabling quantification of landscape structure (basin number, basin area, and basin depth) and state-space occupancy (centroid location and centroid dispersion).

Results

Fatigue significantly increased force fluctuation magnitude (P < 0.001) and altered the organization of MU discharge-state space. Specifically, fatigue increased the number (P = 0.017) and area (P = 0.012) of attractor basins, indicating a broader distribution of preferred discharge configurations. Fatigue also induced significant shifts in centroid location (P ≤ 0.008) and increased centroid dispersion (P = 0.004), reflecting broader occupancy of discharge states. Furthermore, fatigue-related increases in force fluctuation magnitude were positively associated with basin area expansion (r = 0.368, P = 0.030) and centroid dispersion (r = 0.468, P = 0.005).

Conclusion

Ischemia-assisted fatigue reorganized the state-space architecture of pooled MU discharge activity, resulting in broader discharge-state occupancy and reduced force steadiness. Energy landscape analysis provides a complementary time-resolved framework that preserves the joint evolution of the mean and variability of pooled MU discharge, offering a novel state-space perspective on fatigue-related decline in force stability.

'The Good Life'; Lessons From the World's Longest Scientific Study of Happiness by Robert Waldinger, MD and Marc Schulz, PhD

 The short answer is relationships. 

I'm very good at this, My best friend from first grade on, thru high school and college is whom I bought the cabin with in northern Minnesota, second one is a college roommate from senior year(1978) The three of us get together at the cabin for boys weekend yearly. I thought I was an introvert until I realized that in order to make friends after moving to Michigan I had to interact and found I'm very good at that, now can crack jokes at my expense at the parties I'm invited to.  My stroke at 50 galvanized restoring my old college friendships after dumping the ex.

Why my stroke was the best thing to ever happen to me

All leading to moving to Michigan and finding lots of new friendships.

When every second counts in a stroke, Norwalk Hospital is ready

 

 No, they are not! They refer to 'care'; NOT RECOVERY!

Talking about 'care' rather than recovery PROVES THEY ARE A FAILED HOSPITAL!

YOU are going to have to run it instead! 

When every second counts in a stroke, Norwalk Hospital is ready

Norwalk Hospital's nationally recognized stroke team provides lifesaving care(NOT RECOVERY!) and urges the community to know the signs of stroke.

When someone is having a stroke, every second matters. A fast, accurate response can make all the difference in saving a life and recovering well after a stroke. If you or someone you love has stroke symptoms, Northwell Health’s Norwalk Hospital is prepared — 24/7 — to provide timely, expert 

care(NOT RECOVERY!)

.

Norwalk Hospital has again earned national recognition from the American Heart Association for delivering timely, evidence-based stroke 

care(NOT RECOVERY!)

. For patients and families in Greater Norwalk, the award means you can feel confident that a highly trained team is ready to diagnose stroke quickly, provide advanced treatment and support you through recovery.

“This is our fourth consecutive year achieving Gold PLUS status with Stroke Honor Roll Elite Plus and Type 2 Diabetes Honor Roll,” says Michele Lecardo, DNP, neuroscience coordinator at Norwalk Hospital. “This is a true testament to the sustainability of our stroke program. This year, we also received the ‘advanced therapy’ recognition for our endovascular 

care(NOT RECOVERY!)

, or clot-removing through mechanical thrombectomy. This is such an amazing achievement and I’m so proud to be a part of this team.”

Norwalk Hospital also received a Commitment to Quality award from the American Heart Association for its stroke program.

“Only 222 hospitals nationwide have been given this award,” Lecardo says.

“Stroke care depends on speed, accuracy and teamwork,” says Daryl Story, MD, director of the Norwalk Hospital stroke program. “When patients arrive quickly, our team evaluates them, determines the right treatment and acts fast to help protect brain function and improve outcomes.”

Stroke care(NOT RECOVERY!)

 is a team effort. At Norwalk Hospital, that team includes emergency medical services, emergency department staff, neurologists, neurosurgeons, radiologists, nurses, pharmacists, rehabilitation specialists and many others. Each role matters, from the first 911 call to diagnosis, treatment, recovery planning and rehabilitation.

Norwalk Hospital is certified by The Joint Commission as a Thrombectomy-Capable Stroke Center, meaning the hospital has advanced technology and expertise to treat complex strokes. Specially trained endovascular neurosurgeons use a biplane angiography system to treat ischemic strokes by removing blockages in blood vessels and restoring blood flow to the brain. They also use this technology to treat conditions that can cause hemorrhagic stroke or bleeding in the brain, like an aneurysm. They perform these lifesaving procedures through tiny incisions in the wrist or thigh, helping patients recover quickly.

The American Heart Association award reflect dependable, quality 

care(NOT RECOVERY!)

 as well as stroke education. Norwalk Hospital helps people in Greater Norwalk lower their risk for stroke by maintaining healthy blood pressure and cholesterol levels, preventing or managing diabetes, smoking cessations, eating well and exercising.

If stroke does happen, it’s important for everyone to understand the signs of stroke using the acronym B.E.F.A.S.T.:

• Balance: Sudden loss of balance or coordination
• Eyes: Sudden vision changes in one or both eyes
• Face: Facial drooping on one side
• Arms: Arm weakness or numbness
• Speech: Slurred speech or difficulty speaking
• Time: Time to call 911 immediately. Do not drive yourself to the hospital. Emergency medical services can begin the stroke evaluation and help expedite 

  care(NOT RECOVERY!)

   at the emergency department.

Every day, Norwalk Hospital’s stroke team sees the importance of recognizing stroke symptoms quickly and getting patients to the right 

care(NOT RECOVERY!)

 without delay. Fast treatment can lead to better outcomes: It can help save a life — and preserve the quality of that life.

“Our goal is to help people in Greater Norwalk understand that stroke is an emergency, and that experienced, compassionate and advanced 

care(NOT RECOVERY!)

 is available close to home,” says Lecardo.

Adults lose muscle with age—researchers found an unexpected health risk

 More reasons for your doctor to get you 100% recovered! 

DOES YOUR DOCTOR HAVE THE EXACT PROTOCOLS TO DO THAT?

Adults lose muscle with age—researchers found an unexpected health risk

The gradual loss of muscle that often comes with aging may do more than make everyday tasks harder.  

Known as sarcopenia, the condition is already linked to frailty and a higher risk of death. 

Now, a new study suggests it could also leave people more vulnerable to serious infections. 

people with sarcopenia faced a significantly higher long-term risk of infections than those with healthy muscle function. 

The elevated risk extended to respiratory infections, urinary tract infections, skin and soft tissue infections, and sepsis.  

The study, published in MedScience, followed participants for a median of more than 12 years, making it one of the largest investigations yet into the relationship between muscle health and infection risk.  

Researchers found a graded pattern: people with low muscle mass were at increased risk of infection, while those with more advanced sarcopenia faced an even greater risk. 

Professor Arshad Rather, a consultant geriatrician at Medical Express Clinic who was not involved in the research, said many people mistakenly assume significant muscle loss is simply an unavoidable part of getting older. 

“Losing some muscle with age is common, but becoming weak enough to affect daily life is not inevitable,” Rather told Newsweek. 

He said the earliest warning signs are often subtle. 

“Getting out of a chair without using your arms becomes harder,” Rather said. “Stairs take longer. You struggle with jars, luggage or heavy shopping bags. You may walk more slowly, feel more tired, or notice clothes fitting differently even though your weight has not changed much.” 

According to Rather, sarcopenia can affect people who appear to have a healthy weight, as muscle tissue can gradually be replaced by fat. 

The study’s findings add weight to a growing body of evidence suggesting that muscle plays an important role in immune health.  

While muscles are best known for movement, they also function as an endocrine organ, releasing signaling molecules called myokines that help regulate immune responses and inflammation.  

Muscle also acts as a reserve of amino acids that the body can draw upon during periods of illness or physiological stress. 

Researchers proposed several mechanisms that might explain the association.  

Reduced muscle mass could impair the production of immune-regulating myokines, limit the availability of amino acids needed by immune cells, and contribute to chronic low-grade inflammation that weakens the body’s defenses. 

Rather said the biological explanation is plausible.  

“Muscle is not just for movement,” he said. “It helps regulate inflammation and acts as a reserve of amino acids the body uses when fighting infection. When muscle mass and strength fall, that reserve shrinks.” 

He noted that the new findings showed people with sarcopenia faced a substantially higher risk of infections over time, including respiratory infections and sepsis. 

However, he cautioned that the research demonstrates an association rather than proving that muscle loss directly causes infections. 

Still, experts said there are good reasons to protect muscle health as people age.  

Rather pointed to resistance training and adequate protein intake as the most effective evidence-based strategies. 

“The best evidence for slowing it is still practical: regular resistance exercise two to three times a week, using weights, bands or supervised strength training, plus enough protein spread across the day,” he said. 

He added that maintaining strength earlier in life may provide a valuable buffer against future illness. 

“The key message is to start before a crisis,” Rather said. “Maintaining strength in your 50s and 60s gives you more reserve for illness, surgery, and recovery later in life.” 

Reference  

Meng Gao, Bolong Liu, Hequn Chen, Zewu Zhu, Juliet Matsika, Minghui Liu, Jiao Hu, Xiaogen Kuang, Jinbo Chen. Association of sarcopenia with the long-term risk of overall infections and infectious diseases: a prospective cohort study of 458 332 participants. MedScience, 2026, 20 (2) : 345-357 DOI:10.1007/s11684-026-1224-0. 

Contact Newsweek editors on this story: Kara Dolman and Emma Lee-Sang

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