Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,922 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
My doctor and therapists were complete fucking failures at getting my left hand recovered, so grip strength there is poor, mainly because they never cured my spasticity!
While 10 percent may not sound like much, participants in the highest quintile (top 20 percent) enjoy nearly 25 percent less risk than those in the lowest quintile.
But there is a catch. The researchers focused on participants’ genetic predisposition to greater muscle strength. Some people are born stronger. Some respond more quickly, and dramatically, to muscle-building activities. (Neither of which describes me: When I worked on my grandfather’s farm in high school, he often told me I was “weak as a cat.”)
So, yeah: Where muscle strength is concerned, genetics can make a significant difference.
Even so, genetics are a predisposition, not an outcome. I lift weights five to six days a week and am stronger, and have greater endurance, than the average person of my age and size. Sure, I like being relatively trim. And I like feeling relatively fit.
Related video: How much weight should you be able to lift at your age?
(unbranded - Lifestyle)
At this point, though, I mostly care about longevity. Plenty of studies (here’s one, published in British Journal of Sports Medicine) show a link between strength training and increased longevity. The same is true for cardio workouts: According to a study published in PLOS Medicine, brisk walking for an hour can give you 3.2 hours of extra life, while an hour spent jumping rope can give you 11 hours of extra life.
When my time seems to be drawing near, I don’t want to look back and wish I had worked out more; at that point, too late will truly be too late. I also worry about dementia. I haven’t gone all Chris Hemsworth and taken a DNA test to find out if I have Alzheimer’s or dementia biomarkers, but my family history definitely indicates a predisposition.
I can’t change my genes, but I can change what I do. A 2020 study published in Neurology found that adopting four out of five of the basic healthy habits — don’t smoke, drink in moderation, exercise an average of 30 minutes a day, eat healthy, and maintain a healthy bodyweight — decreases the risk of developing Alzheimer’s by 60 percent compared with people who adopt none or one. A Harvard study found that even light exercise is associated with reduced risk.
I figure if a little is good, a lot is better.
If you’re interested in the underlying science, muscles release myokines, chemicals that produce a number of health benefits, including altering brain chemistry. (In simple terms, resistance training stimulates myokine production.)
That’s why I work out. I want to do the best I can with what my genetics allow. I want to live longer, and I want to increase my health span.
Alive is good, alive and healthy is better.
That’s also why I push myself: A study published in BMJ Open Sport & Exercise Medicine found that people in their 60s and 70s who do heavy resistance training — somewhere between six to 12 reps at 70 to 85 percent of your one-rep max — reported no loss of muscle strength or size, while those who did moderate to light resistance training continued to lose muscle strength and size.
I’ve seen the effects of cognitive decline, both on the person and on the people who care for them, and want to stay as sharp as I can for as long as possible.
And I’m guessing you do too.
So start picking up heavy things. You’ll be glad you did.
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
Immersive virtual reality therapy (VRT) is emerging as a promising tool for stroke rehabilitation, with evidence suggesting benefits for motor recovery. However, its specific impact on balance and gait, particularly in the subacute phase of stroke in clinical setting, remains insufficiently explored.
Objective
The primary objective was to determine whether integrating a VRT program into conventional therapy improves balance more effectively than conventional therapy alone in persons with subacute stroke. Balance was assessed using the Berg Balance Scale, complemented by the Sensory Organization Test to explore changes in sensory contributions to postural control. Secondary objectives were to evaluate the effects of VRT on gait performance and to assess usability, patient satisfaction, and potential adverse effects, such as cybersickness, associated with VRT.
Methods
This pilot pragmatic randomized controlled trial included thirty-four participants who were equally randomized to a CT-only group and to a group in which 20% of daily CT was replaced by VRT. Both groups received the same total therapy time over a 2-weeks intervention. Functional ambulation classification, 2-min walking test, 10-m walking test, Berg Balance Scale (BBS) were assessed at baseline (T0) and post-intervention (T1). Sensory reweighting in the VRT group was evaluated with the Sensory Organization Test (SOT) at T0 and T1. Group, time and interaction effects were analyzed using ANOVA with post-hoc tests when appropriate. Spearman correlations were performed to assess relationships between improvements in gait and balance and sensory scores.
Results
Both groups improved significantly over time on all outcomes (p < 0.001), with no main group effect (p > 0.05). A significant group × time interaction was found for the BBS (p = 0.023), with greater improvement in VRT than in CT group. In VRT group, BBS improvement significantly correlated with the visual score of the SOT (r = 0.544, p = 0.030).
Conclusion
Adding VRT to CT in the subacute phase after stroke appears as an adjuvant to CT for improving functional balance, as reflected by greater gains in the Berg Balance Scale, and inducing changes in sensory integration processes.
Trail registration: ClinicalTrials.gov, TRN: NCT07409116, Registration date: 06 February 2026.
Ask your competent? doctor; DOES THIS IMPROVE STROKE RECOVERY? Not nebulous excitability which means nothing to survivors! Oh NO, your doctor doesn't know about this and doesn't care to find out! Get that doctor fired for incompetence, not following research!
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
Transcranial near-infrared stimulation (tNIRS) is an emerging, light-based, non-invasive neuromodulation technique with great potential to improve functions like cognition and motor performance. Cortical excitability and hemodynamic changes represent key neurophysiological mechanisms of tNIRS effects. The selection of tNIRS parameters is closely associated with their functional effects, and the neurophysiological alterations induced in the human cerebral cortex by different parameter combinations warrant further exploration.
Methods
Twenty-two healthy participants received four types of active tNIRS and a Sham condition of tNIRS over the left motor cortex in a randomized order, which included five stimulus conditions: Sham, 810-nm continuous wave (CW), 810-nm 40-Hz pulsed wave (PW), 1064-nm CW, and 1064-nm 40-Hz PW. Each session was divided into three phases, namely pre-stimulation, stimulation, and post-stimulation. Changes in cortical excitability were assessed by recording motor evoked potentials (MEPs) before and for up to 30 min after stimulation. Concurrently, behavioral performance and cortical hemodynamic changes induced by tNIRS were evaluated using functional near-infrared spectroscopy (fNIRS) during a finger-opposition task.
Results
Compared to the Sham condition, all active tNIRS protocols induced an increase in MEPs recorded from the right abductor pollicis brevis muscle. At 30 min post-stimulation, the 1064-nm 40-Hz PW condition elicited significantly larger MEP amplitudes than both the 810-nm CW and 1064-nm CW conditions. For behavior, the number of completed cycles during the right-hand finger-opposition task was significantly higher in the 1064-nm 40-Hz PW condition compared to the Sham condition. Regarding cortical hemodynamics, the 1064-nm 40-Hz PW condition showed decreased activation in broad regions of the frontal and motor cortices during the left-hand finger-opposition task compared to baseline. Conversely, the 810-nm 40-Hz PW condition exhibited decreased hemodynamic activation only in the motor cortex during the right-hand finger-opposition task.
Conclusion
The 40 Hz pulsed tNIRS protocol with a wavelength of 1064 nm, irradiance of 120 mW/cm2, duration of 20 min, and stimulation area of 0.24 cm2 induced more pronounced changes in cortical excitability and hemodynamics. This enhanced effect may be attributed to the more significant neurophysiological cumulative response elicited by this specific parameter combination. This specific parameter set represents a promising candidate for future clinical applications of tNIRS.
PrecivityAD2 is the first blood-based biomarker for people as young as 40 with cognitive symptoms
The FDA cleared the PrecivityAD2 blood test to help diagnose Alzheimer's disease as part of a standard clinical workup, C2N Diagnostics announced Thursday.
The test, which measures plasma amyloid beta and tau peptide ratios to assess the likelihood of brain amyloid plaques, is the first Alzheimer's blood-based biomarker for people as young as 40 with cognitive symptoms.
PrecivityAD2 is indicated for adults with signs or symptoms of cognitive impairment being evaluated for Alzheimer's or other forms of cognitive decline. It's intended to be used with a clinical assessment to help healthcare professionals identify patients with amyloid pathology, not as a screening or standalone diagnostic test.
The test uses high-resolution mass spectrometry to quantify Alzheimer's disease biomarkers in blood, producing an outcome called the amyloid probability score 2 (APS2). The APS2 incorporates the ratio of plasma phosphorylated tau 217 (p-tau217) relative to non-p-tau217, combined with a plasma amyloid-beta 42/40 ratio, to rule in or rule out Alzheimer's disease.
In a validation study of 1,142 people with signs or symptoms of cognitive decline, PrecivityAD2 showed a 97.6% positive predictive value (rule-in) and a 93.1% negative predictive value (rule-out) to detect brain amyloid plaques using dual cutoffs measured against amyloid PET or cerebrospinal fluid testing, C2N reported. The test was effective at detecting plaques in a wide range of patients, including people with mild symptoms and those with more advanced cognitive impairment.
PrecivityAD2 showed consistent diagnostic performance as age increased and in people with comorbidities like atrial fibrillation, autoimmune or inflammatory disease, chronic heart failure or kidney disease, coronary heart disease, depression, diabetes, dyslipidemia, history of cancer, history of stroke or transient ischemic attack, hypertension, or obesity, the company added.
A recent study in Sweden showed the test was useful to help primary care physicians rule out Alzheimer's disease. Earlier research showed the APS2 score performed better than primary care doctors or dementia specialists in detecting Alzheimer's disease among people with cognitive symptoms.
In 2025, the FDA cleared two other diagnostic blood tests for Alzheimer's disease: one to help clinicians identify Alzheimer's in people with signs and symptoms, the other to rule out Alzheimer's disease in primary care.
Lab-developed tests not approved by the FDA are also on the market. Last year, the Alzheimer's Association issued guidance outlining sensitivity and specificity parameters for Alzheimer's blood tests to either triage or diagnose people with cognitive impairment.
An estimated 19 to 20 million U.S. adults 65 and older, and hundreds of thousands more between the ages of 45 and 65, have cognitive impairment and may benefit from an early diagnosis, C2N Diagnostics noted.
PrecivityAD2 can be ordered by healthcare professionals experienced in evaluating patients with cognitive impairment, the company stated. It currently is available as a lab-developed test; the FDA-cleared test version is expected to be available later this year.
Just bought a 4 level condo, 7 steps to
each level. Absolutely do not believe in removing steps in living
quarters. Don't do steps at home, won't be able to travel to step laden
places like Machu Pichu or restrooms anywhere in Europe!
Maybe you'd rather solve stroke to 100% recovery first when you are the1 in 4 per WHO that has a stroke! Just a thought. Getting 100% recovered would mean a better survival of that second stroke. Cognitive resilience and all.
James E Siegler, MD, FAHA Publish Date August 17, 2026
James Siegler, MD, FAHA, director of the Comprehensive Stroke Center at the University of Chicago, explores the evolving landscape of post-stroke care.
Ischemic stroke remains a leading cause of mortality and long-term disability worldwide, 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. 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 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.
Future State of Stroke Care
Residual Stroke Risk Despite Optimal Care
Even if all barriers to medical care are limited for a given patient, the risk for recurrent stroke remains unacceptably high. This may reflect the chronic and progressive nature of atherosclerotic vascular disease, although the primary drivers of residual stroke risk remain incompletely understood. For example, less than 25% of carotid plaque burden is explained by traditional vascular risk factors.4 Other contributors to vascular disease, inflammation, and stroke risk may include genetic variation, pathologic metabolites originating from the gut microbiome, microplastics, and other patient-level factors.
Although advances in pharmacotherapies for secondary stroke prevention now include individualized antithrombotic regimens, more aggressive lipid targets, and glucagon-like peptide agonists, improvements in stroke prevention remain incremental.
Expanding the Secondary Prevention Toolkit
In addition to the persistent biological drivers of stroke risk, limitations of current therapies highlight the need for continued innovation. Concerns regarding medication toxicity and growing distrust of health care providers have introduced new challenges to sustained treatment.
Nearly a quarter century ago, aspirin became a mainstay of secondary prevention, with a number-needed-to-treat (NNT) of approximately 100 to prevent 1 stroke at 2 weeks.5 However, long-term use is associated with risks for gastrointestinal bleeding or renal dysfunction. A decade later, high-intensity statins expanded the pharmacologic armamentarium, with an NNT of 45 to prevent stroke after 5 years of sustained treatment.6 Yet, more than half of high-risk patients discontinue statins over time due to non-adherence, perceived side effects, or financial barriers.7
Further, glucagon-like peptide agonists have been shown to promote weight loss, reduce tobacco and alcohol use, and lower stroke rates among patients with diabetes and/or obesity, but more than one-third of patients discontinue these therapies at 1 year due to a combination of adverse effects, high out-of-pocket costs, and access barriers.8
There is no single solution or “silver bullet” for secondary stroke prevention. However, emerging therapies may offer new opportunities. Asundexian, a novel factor XIa inhibitor, has been recently shown to reduce recurrent stroke in patients with noncardioembolic stroke.9 With an NNT of 45 to prevent 1 stroke over 19 months and no significant risk for major or minor bleeding, this therapy may represent an important advance in secondary stroke prevention. The Phase III LIBREXIA-Stroke trial (ClinicalTrials.gov Identifier: NCT05702034) evaluating milvexian is ongoing and may provide additional insight into a class effect for factor XIa inhibitors.
Toward Precision Stroke Prevention
As the understanding of stroke biology expands, future approaches will likely move toward more individualized risk prediction and treatment selection. For patients with elevated lipoprotein(a), a low-density lipoprotein molecule largely determined by genetics, Phase III trials are ongoing that are evaluating whether small molecules or small interfering RNA therapies can reduce vascular events. Phase II trials of subcutaneously administered pelacarsen, olpasiran, lepodisiran, muvalaplin, and zerlasirin have demonstrated 30 to 95% reductions in lipoprotein(a) levels, with generally mild injection site pain and flu-like symptoms.10 Whether these reductions translate into meaningful clinical benefit remains uncertain.
The future of secondary stroke prevention will be increasingly personalized. Advances in prolonged cardiac rhythm monitoring, wearable diagnostic technologies, biomarker-based risk stratification, and artificial intelligence-driven predictive modeling may improve identification of patients at highest risk for recurrent cerebrovascular events. Precision medicine approaches are also being explored to guide individualized antithrombotic therapy based on stroke mechanism and patient-specific risk profiles.
In parallel, digital health platforms, remote physiologic monitoring, and telemedicine-based care models may improve longitudinal patient engagement, medication adherence, and access to specialist care, particularly among underserved populations.
Closing the Evidence-to-Practice Gap
Reducing recurrent ischemic stroke risk and minimizing long-term disability will require more than the continued application of established evidence-based therapies. Persistent implementation barriers, including fragmented care delivery, suboptimal adherence, financial burden, patient mistrust, and uncertainty in individualized therapeutic decisions, continue to limit the effectiveness of current prevention strategies.
Future progress in secondary stroke prevention will depend not only on therapeutic innovation but also on scalable, cost-effective health care delivery models capable of translating scientific advances into durable improvements in cerebrovascular outcomes. Closing the gap between clinical evidence and real-world implementation remains essential to reducing recurrent stroke burden and improving functional outcomes among stroke survivors.
The mitochondria is the “powerhouse of the cell,” but B12 is what keeps the lights on. Here’s the latest science on how it affects your energy levels.
Protein powder, creatine, pre-workouts … There are more supplements than ever promising to elevate your performance in the gym. But if you walked into a supplement shop asking for vitamin B12 for muscle growth, you’d probably raise a few eyebrows.
B12 isn’t typically the go-to nutrient for muscle mass. But recent scientific evidence indicates the “energy vitamin,” may also play a role in powering your muscles. Here’s what we know, and how you can capitalize on it.
What You Should Know About B12 and Your Muscles
When we think of eating to fuel our muscles, you’ve probably heard about eating more protein and consuming enough calories. Physically active folks use their muscles more, so they need larger quantities of these major fuel sources.
But protein alone can’t do it all, and the research shows that other nutrients, like vitamin B12, may matter too. Vitamin B12 is essential for DNA synthesis, healthy nerve function, and red blood cell production — all of which help support normal muscle function.
Particularly, vitamin B12 supports the mitochondria, also known as those famous cellular “power plants” that provide energy.
It’s possible that insufficient vitamin B12 intake can depower your muscles’ capabilities. In fact, researchers believeage-related losses in muscle may have to do with mitochondrial dysfunction.
Are You at Risk of B12 Deficiency?
While the majority of B12 sources in our diet come from animal foods, only about half is effectively absorbed.
What’s more, deficiency is more common in some groups than others. Particularly, adults over 50, vegans and vegetarians, people with digestive conditions, and anyone who’s had stomach surgery may all be at an increased risk for low B12 levels. Plus, some medications may interfere with absorption as well.
There may be a connection between low vitamin B12 status and feeling strong, according to Caroline Thomason Bunn, RD. “Supplementing with vitamin B12 has been shown to improve strength and physical function in elderly adults who were deficient,” she shares.
Vitamin B12 deficiency goes beyond making you feel tired. It’s linked to anemia, nerve symptoms, muscle weakness, and even cognitive impairment in older people. It saps your muscles of an essential mechanistic puzzle piece, according to the latest research.
Going Deeper on the B12–Mitochondria Link
In 2026, scientists from Cornell University and the University of Alabama at Birmingham set out to determine how vitamin B12 deficiency affects skeletal muscle. Rodent subjects were split into two groups:
Young-adult male mice that were either genetically unable to use B12 properly or fed a B12-deficient diet for seven weeks.
Older mice (comparable to senior humans in age) that received weekly B12 injections for eight weeks.
Credit: iStock/Professor25
In the B12-deficient group, the researchers observed that the mitochondria were not functioning at optimal capacity — the mice muscles in this group generated and burned about 25 percent less energy.
But the more useful question is whether that translates to actual strength — and human research suggests it can. In a 2024 pilot study, older adults with mild B12 deficiency who supplemented for three months saw significant gains in muscle strength and quality, reaching about the same level as people whose B12 was already healthy.
Before we get practical, bear in mind the mouse study points to a mechanism rather than proof — and the human evidence, while encouraging, is still one small pilot in people who were already deficient.
The Takeaway
Vitamin B12 supplementation has been recommended by institutions like the Mayo Clinic for years, but when it comes to muscle health and functionality, other supplements tend to steal the spotlight.
Especially if you’re over 50. Incorporate vitamin B12-rich foods into your diet to ensure you meet the recommended daily intake. Some good sources of B12 to include in your diet are:
Clams
Beef liver
Tuna
Salmon
Eggs
Fortified nutritional yeast
Fortified breakfast cereals and other grains
And since B12 supports the mitochondria in your muscles, pairing it with enough protein and regular strength training may help you hold onto muscle function as you age.
Bottom Line
Here’s what we know: Getting adequate micronutrients, such as vitamins like B12, is just as important as hitting the big benchmarks — even if you don’t always feel the effects right away.
Feeling strong and energetic can make a massive difference in your overall quality of life, but requires you to pay attention to more than just calories or protein. If you’re feeling fatigued and are part of a cohort that tends to suffer from B12 deficiency, upping your intake might make a noticeable difference.
That said, the clearest human evidence so far is a small pilot where three months of B12 brought deficient older adults’ strength up to match non-deficient peers — promising, but larger trials are the next step, especially on whether B12 supplementation helps people who aren’t prone to deficiencies. In the meantime, there’s no harm in keeping your bases covered.
Experts Who Contributed
Jake Dickson (BS-EXS, NASM-CPT), wrote this article.
Lauren Keary, NASM-CNC, reviewed this article for accuracy.
Caroline Thomason Bunn, RD, CDCES, founder of Caroline Thomason Nutrition, reviewed this article for accuracy.
supports the mitochondria, also known as those famous cellular “power plants” that provide energy.
It’s possible that insufficient vitamin B12 intake can depower your muscles’ capabilities. In fact, researchers believeage-related losses in muscle may have to do with mitochondrial dysfunction.
Are You at Risk of B12 Deficiency?
While the majority of B12 sources in our diet come from animal foods, only about half is effectively absorbed.
What’s more, deficiency is more common in some groups than others. Particularly, adults over 50, vegans and vegetarians, people with digestive conditions, and anyone who’s had stomach surgery may all be at an increased risk for low B12 levels. Plus, some medications may interfere with absorption as well.
There may be a connection between low vitamin B12 status and feeling strong, according to Caroline Thomason Bunn, RD. “Supplementing with vitamin B12 has been shown to improve strength and physical function in elderly adults who were deficient,” she shares.
Vitamin B12 deficiency goes beyond making you feel tired. It’s linked to anemia, nerve symptoms, muscle weakness, and even cognitive impairment in older people. It saps your muscles of an essential mechanistic puzzle piece, according to the latest research.
Going Deeper on the B12–Mitochondria Link
In 2026, scientists from Cornell University and the University of Alabama at Birmingham set out to determine how vitamin B12 deficiency affects skeletal muscle. Rodent subjects were split into two groups:
Young-adult male mice that were either genetically unable to use B12 properly or fed a B12-deficient diet for seven weeks.
Older mice (comparable to senior humans in age) that received weekly B12 injections for eight weeks.
Credit: iStock/Professor25
In the B12-deficient group, the researchers observed that the mitochondria were not functioning at optimal capacity — the mice muscles in this group generated and burned about 25 percent less energy.
But the more useful question is whether that translates to actual strength — and human research suggests it can. In a 2024 pilot study, older adults with mild B12 deficiency who supplemented for three months saw significant gains in muscle strength and quality, reaching about the same level as people whose B12 was already healthy.
Before we get practical, bear in mind the mouse study points to a mechanism rather than proof — and the human evidence, while encouraging, is still one small pilot in people who were already deficient.
The Takeaway
Vitamin B12 supplementation has been recommended by institutions like the Mayo Clinic for years, but when it comes to muscle health and functionality, other supplements tend to steal the spotlight.
Especially if you’re over 50. Incorporate vitamin B12-rich foods into your diet to ensure you meet the recommended daily intake. Some good sources of B12 to include in your diet are:
Clams
Beef liver
Tuna
Salmon
Eggs
Fortified nutritional yeast
Fortified breakfast cereals and other grains
And since B12 supports the mitochondria in your muscles, pairing it with enough protein and regular strength training may help you hold onto muscle function as you age.
Bottom Line
Here’s what we know: Getting adequate micronutrients, such as vitamins like B12, is just as important as hitting the big benchmarks — even if you don’t always feel the effects right away.
Feeling strong and energetic can make a massive difference in your overall quality of life, but requires you to pay attention to more than just calories or protein. If you’re feeling fatigued and are part of a cohort that tends to suffer from B12 deficiency, upping your intake might make a noticeable difference.
That said, the clearest human evidence so far is a small pilot where three months of B12 brought deficient older adults’ strength up to match non-deficient peers — promising, but larger trials are the next step, especially on whether B12 supplementation helps people who aren’t prone to deficiencies. In the meantime, there’s no harm in keeping your bases covered.
Experts Who Contributed
Jake Dickson (BS-EXS, NASM-CPT), wrote this article.
Lauren Keary, NASM-CNC, reviewed this article for accuracy.
Caroline Thomason Bunn, RD, CDCES, founder of Caroline Thomason Nutrition, reviewed this article for accuracy.
