The Importance of BP Lowering in Intracerebral Hemorrhage Survivors

 You'll need to discuss with your doctor because lower blood pressure means less oxygen for your brain probably allowing more neurons to die. Behind a paywall so can't specifically refute this. 

This is why they are doing this, you'll have to intervene if you'd rather save more neurons and accept this risk.

Intensive blood pressure-lowering cut recurrent stroke risk by around 38% after brain haemorrhage

Has your competent? doctor addressed all the concerns in these! Ask for specific research they have initiated!

hemorrhage cascade of death (15 posts to November 2016)

blood pressure lowering (38 posts to June2013) 

NOT KNOWING OF THIS IS PURE INCOMPETENCE!

The Importance of BP Lowering in Intracerebral Hemorrhage Survivors

Imaging Index Links Blood Flow to Cellular Architecture

 Does your competent? doctor have enough brains to see this need and provide cerebral blood flow protocols?

• cerebral blood flow (51 posts to December 2015)

Imaging Index Links Blood Flow to Cellular Architecture

Summary:

Researchers at USC have created a noninvasive metric called the cerebral blood flow–cell-body staining intensity similarity index (CCSI) to evaluate how blood flow matches cell density across the layers of the living human cerebral cortex.

By combining high-resolution 7-Tesla MRI with cellular, metabolic, and genetic atlases, the team demonstrated that areas with tight vascular-cellular alignment possess higher mitochondrial respiratory capacity and significantly improved models predicting higher-order cognitive brain function.

Key Facts:

• Novel Laminar Metric: The newly developed CCSI uses 7-Tesla arterial spin labeling (ASL) MRI alongside the 3D BigBrain digital atlas to measure how closely laminar blood perfusion mirrors cellular packing depth across 360 cortical regions.
• Metabolic Capacity Over Volume: Higher alignment between blood flow and cell density correlates with greater mitochondrial respiratory capacity (the rate of energy production) rather than simple mitochondrial volume or raw bulk blood flow.
• Predicting Higher-Order Brain Function: Incorporating CCSI into structure-function coupling models significantly enhanced the ability to predict neural activity in association areas responsible for memory, reasoning, and attention.

Source: Keck School of Medicine of USC

The human cerebral cortex is arranged into distinct cellular layers, each populated by varying types and densities of neurons and glial cells. Because neural tissue has virtually no intrinsic capacity to store energy, its survival and function rely on an uninterrupted, precisely regulated delivery of oxygen and glucose from cerebral blood vessels.

Historically, conventional neuroimaging techniques have averaged vascular signals across the entire thickness of the cortex, obscuring how microcirculation meets the metabolic needs of specific cellular layers.

To address this limitation, investigators from the Mark and Mary Stevens Neuroimaging and Informatics Institute (Stevens INI) at the Keck School of Medicine of USC developed a noninvasive framework: the cerebral blood flow–cell-body staining intensity similarity index, or CCSI.

The study, published in Nature Communications, offers a tool to visualize how microvascular perfusion aligns with the brain’s cellular organization.

“The brain has almost no ability to store energy, so its cells depend on a constant and carefully regulated supply from the bloodstream,” explained Fanhua Guo, co-first author of the study and a researcher at Stevens INI. “Our new measure gives us a way to study how well that energy supply is positioned to meet cellular demands in different parts of the cortex.”

Ultra-High-Field Laminar Perfusion

To observe cortical layers in living human participants, the research team used arterial spin labeling (ASL) performed on an ultra-high-field 7 Tesla MRI scanner. ASL magnetically tags water molecules in arterial blood, using them as an endogenous tracer to quantify perfusion at an isotropic spatial resolution of one cubic millimeter.

The team scanned 30 healthy adult volunteers, with 14 participants returning for a second session to confirm test-retest reliability. Researchers divided the cerebral cortex into 360 parcels and tracked blood perfusion from the superficial outer surface to the deeper cortical layers. They matched these laminar blood flow profiles against cell-body staining intensity extracted from BigBrain, an ultra-detailed 3D histological reconstruction mapping cellular packing throughout the human brain.

“Conventional brain imaging often averages information across the full thickness of the cortex, but the cortex is not a uniform sheet,” said Chenyang Zhao, co-first author of the study. “By imaging blood flow at very high resolution, we can begin to see how perfusion changes from the outer surface of the cortex to its deeper layers.”

The analysis revealed that blood flow and cell density align across most of the cortex, meaning layers with higher cellular density generally receive proportionally greater perfusion. This vascular-cellular alignment was strongest in primary sensorimotor and visual regions, which manage primary sensory processing and motor execution.

Connecting Perfusion to Mitochondrial Power and Glia

To uncover the biological mechanics underpinning CCSI, the team integrated their laminar data with independent multi-scale maps covering mitochondrial respiration, single-cell transcriptomics, and gene expression profiles.

The results demonstrated that regions showing stronger CCSI alignment exhibited higher mitochondrial respiratory capacity, the maximum rate at which cellular power plants generate ATP, rather than merely a larger quantity of mitochondria. Standard total blood flow measurements failed to capture this relationship, indicating that CCSI isolates a dimension of microvascular spatial organization missed by bulk hemodynamic readouts.

At the cellular level, CCSI tracked closely with capillary endothelial cells, which form the blood-brain barrier and regulate local microperfusion, as well as mature oligodendrocytes. Beyond generating insulating myelin sheaths around axons, oligodendrocytes provide metabolic support to nerve fibers, suggesting these glial cells help interface vascular delivery with neuronal metabolic requirements. Transcriptomic profiling further associated high CCSI areas with active gene networks dedicated to angiogenesis, energy metabolism, and mitochondrial integrity.

Decoding Higher-Order Cognitive Circuits

Beyond metabolic mechanics, the researchers tested whether CCSI could help resolve an ongoing challenge in systems neuroscience: structure-function coupling. While structural anatomy closely dictates function in primary sensory and motor cortices, structure and function appear dissociated in higher-order association areas that support complex cognition, such as attention, planning, and abstract reasoning.

By incorporating CCSI into structural-functional coupling algorithms, the researchers observed a marked improvement in their ability to predict actual functional brain activity in these higher-order association networks. The finding highlights that regional vascular and metabolic organization directly shapes neural computations in ways that structural morphology alone cannot account for.

While current CCSI implementations characterize group-level dynamics and rely on postmortem reference atlases for molecular correlations, future work aims to evaluate individual patient trajectories. Disruptions in cerebral hemodynamics, energy production, and oligodendrocyte maintenance are hallmarks of neurodegenerative and neurodevelopmental conditions, including Alzheimer’s disease, multiple sclerosis, and schizophrenia. The researchers hope CCSI can ultimately serve as an early biomarker to monitor neurovascular breakdown and assess metabolic interventions.

About the study

In addition to Guo, Zhao, and Wang, other study authors include Ravi R. Bhatt, Zixuan Liu, Zidong Yang, Kay Jann, Xingfeng Shao, and Neda Jahanshad of the Stevens INI; Mara Mather and Andy Jeesu Kim of the USC Leonard Davis School of Gerontology, USC Department of Psychology, and USC Department of Biomedical Engineering; and Siyi Xu of the University of Washington.

Funding: The research was supported by the National Institutes of Health under grants UF1-NS100614, S10-OD025312, R01-EB032169, RF1-AG084072, R01-MH134004 and R01-NS134712.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this Genetics and Neurology Research:

• Media Contact: Laura LeBlanc
• Source: USC
• Image Credit: Image credited to Stevens INI
• Original Research is Open Access: Nature Communications (September 15, 2026). “Assessing molecular, cellular and transcriptomic bases of laminar perfusion and cytoarchitecture coupling in the human cortex” Authors: Fanhua Guo, Chenyang Zhao, Ravi R. Bhatt, Zixuan Liu, Andy Jeesu Kim, Zidong Yang, Siyi Xu, Kay Jann, Xingfeng Shao, Mara Mather, Neda Jahanshad & Danny JJ Wang.
• DOI: 10.1038/s41467-026-76812-w

Lanark stroke survivor rebuilds strength through pioneering rehab scheme

 Zero understanding what this rehab is. Ask your competent? doctor.

Lanark stroke survivor rebuilds strength through pioneering rehab scheme

A stroke survivor is rebuilding her strength and confidence through a pioneering rehabilitation programme.

Fiona Wilkie, from Lanark, is taking part in an eight-week scheme at Blantyre LIFE, a facility delivering technology-enriched rehabilitation developed through a partnership between the University of Strathclyde, NHS Lanarkshire, South Lanarkshire Council, and the South Lanarkshire University Health and Social Care Partnership.

Speaking about the programme, Fiona said: "When I first came here, I could only walk tentatively with my stick.

"I can now walk without it, I'm much stronger and my confidence is really good.

"It has given me a safe place to practise with support from the team.

"It has been amazing and I don't think I would have reached this stage without it."

The programme focuses on delivering technology-enriched rehabilitation in a community setting, using technology to aid stroke recovery.

Scott Haldane, non-executive director at NHS Lanarkshire and member of the South Lanarkshire Integration Joint Board, said: "It has been fantastic to see this technology in action and hear directly from the staff and patients involved about the possibilities it presents for people recovering from stroke.

"By bringing together expertise from the NHS, local government and academia, this programme is helping us understand how technology can support recovery and independence after a stroke and what that could mean for community-based rehabilitation in the future."

Professor Soumen Sengupta, chief officer for health and social care for South Lanarkshire, said the programme shows the value of supporting people in familiar surroundings.

He said: "Listening to Fiona and others on the programme has reinforced the difference it can make when people are supported to recover in familiar, local settings.

"This is the kind of care we want to keep developing for the future: leading-edge support brought closer to people, helping them rebuild confidence, regain independence and get back to everyday life in their own communities."

The initiative builds on earlier work by the University of Strathclyde and NHS Lanarkshire.

It aims to strengthen the evidence for technology-enabled rehabilitation in the community.

Dr Andy Kerr, principal investigator for the TERG research at the University of Strathclyde, said: "The learning generated through this partnership will contribute to the evidence base and help inform future rehabilitation services across Scotland.

"We are grateful to our local partners and their teams for their commitment to innovation and dedication to learning."

Low-Dose Digoxin Ameliorates Age-Related Motor Learning Deficits in Mice

 Consult with your doctor if you are using this for atrial fibrillation.

New Concerns About an Old Heart Drug - Digoxin 

The latest here.

Low-Dose Digoxin Ameliorates Age-Related Motor Learning Deficits in Mice

• Junichi Hashimoto,
• Masatake Kai,
• Kazumasa Matsumoto-Miyai &
• Makoto Kondo 

• 67 Accesses

• Explore all metrics

Abstract

Age-related decline in motor learning has been linked to impaired synaptic plasticity in the central nervous system; however, effective pharmacological strategies to restore these processes remain limited. Here, we investigated whether low-dose digoxin improves motor learning performance and dendritic spine structural plasticity in the middle-aged mice. Behavioral analyses revealed that low-dose digoxin (4 and 65 µg/kg) enhanced motor learning performance in the rotarod task, without affecting muscle strength or spontaneous locomotor activity. At the molecular level, digoxin increased sodium-potassium ATPase (Na/K ATPase) activity in the motor cortex. Morphological analyses using Golgi–Cox staining demonstrated a selective increase in filopodia and thin-type dendritic spines, which are associated with structural remodeling. Interestingly, these changes occurred without a detectable increase in the brain-derived neurotrophic factor (BDNF) protein level in the motor cortex as assessed by western blotting. Given the established role of BDNF in synaptic plasticity, these findings suggest that the observed structural changes are not primarily mediated by the BDNF upregulation. Instead, the data are consistent with engagement of activity-dependent structural remodeling pathways, including the neurotrypsin–agrin pathway, which links synaptic activity to dendritic filopodia formation. Furthermore, agrin-derived fragments have been reported to interact with Na/K ATPase, suggesting that this fragment may function as a molecular interface between extracellular signaling and synaptic structural remodeling. Together, these results indicate that modulation of Na/K ATPase activity enhances motor learning and dendritic spine remodeling in the aged motor cortex through mechanisms that do not require increased BDNF protein levels.

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Is It Possible to Prevent Alzheimer’s Disease with Viagra (Sildenafil)?

 I'm not waiting for exact proof, I do Cialis instead.

Check out the research for yourself, when I asked my doctor he pooh-poohed the idea, saying it was to early to tell. I'm ignoring him.

• Erectile Dysfunction Drugs (5 posts to February 2024) 

The latest here:

Is It Possible to Prevent Alzheimer’s Disease with Viagra (Sildenafil)?

The descent into dementia is horrific. It can creep up gradually, robbing people of their personalities as well as their memories. Friends, family and co-workers have a hard time dealing with the forgetfulness and cognitive dysfunction. Family members often struggle to help their loved one stay safely at home, but frequently that becomes an overwhelming task. For those who have had to deal with dementia, the question we get most often is, “How can I prevent Alzheimer’s disease myself?” A study in the Journal of Alzheimer’s Disease (March 19, 2024) was titled “Sildenafil as a Candidate Drug for Alzheimer’s Disease.”

In case you don’t recognize the drug sildenafil, it is the generic name for Viagra! That’s right, the medication that the FDA approved for erectile dysfunction in 1998.

The Pharmaceutical Industry Dropped the Ball:

With nearly 7 million people suffering from Alzheimer disease it should come as no surprise to learn that drug companies have been trying hard to come up with effective treatments. It would be a billion-dollar bonanza for any drug company if it had a medication that actually improved memory and/or helped keep people out of nursing homes. Families would be ecstatic if there were ever such a breakthrough.

A nursing home can cost any where from $80,000 to $120,000 a year. Many people would be willing to spend their life savings to stay out of such a facility. If there were a medicine that could accomplish that, a pharmaceutical manufacturer could charge $100,000 a year or more. Do the math. That would equal $500,000,000,000. If you lost count of the zeroes, that is $500 billion, which is a mind-boggling amount of money.

Drug companies are thrilled if a medication earns a billion dollars in a single year. A $5 billion drug is a blockbuster. A $500 billion dollar drug would bankrupt insurance companies and families. If it worked, though, people would likely pay, just as they now are paying over $100,000 a year for some cancer drugs.

The Anti-Amyloid Drug Disappointment

We have written a lot about the disappointing results from anti-amyloid drugs. The FDA approved three medications in recent years. One, Aduhelm, was discontinued. You can read about this hot mess at this link. The others include donanemab (Kisunla) and lecanemab (Leqembi). Estimating price is tricky, but we have seen numbers like $32,000 for Kisunla and $26,500. That is not the full story, though. CBS News did an in-depth report (Aug. 1, 2023) titled: “The real costs of the new Alzheimer’s drug, Leqembi — and why taxpayers will foot much of the bill:”

“In addition to the company’s $26,500 annual price tag for the drug, treatment could cost U.S. taxpayers $82,500 per patient per year, on average, for genetic tests and frequent brain scans, safety monitoring, and other care, according to estimates from the Institute for Clinical and Economic Review, or ICER.”

“To qualify for Leqembi, patients must undergo a PET scan that looks for amyloid plaques, the protein clumps that clog the brains of many Alzheimer’s patients. About 1 in 5 patients who took Leqembi in the major clinical test of the drug developed brain hemorrhaging or swelling, a risk that requires those taking the drug to undergo frequent medical checkups and brain scans called MRIs.”

More about anti-amyloid drugs shortly.

What About Generic Sildenafil (Viagra) To Prevent Alzheimer’s Disease?

The pharmaceutical industry and a lot of neuroscientists don’t seem terribly excited about the paper in the Journal of Alzheimer’s Disease (JAD) (March 19, 2024) involving Viagra. Maybe that’s because sildenafil is relatively inexpensive (anywhere from $15 to $30 for 30 pills with a coupon). It does not fit the classic anti-amyloid model of AD that has prevailed for so long.

The JAD study was ambitious. It suggests that the ED drug Viagra might reduce the risk of developing Alzheimer disease. Researchers at the Cleveland Clinic identified genes involved in the development of amyloid plaques and tau tangles in the brain. These are distinctive markers of dementia. Analysis showed that sildenafil (the generic name for Viagra) had the potential to interact with these genes in a positive way.

Then the investigators evaluated two large patient databases of insurance claims. People taking sildenafil were substantially less likely to be diagnosed with Alzheimer disease than those taking the blood pressure pill spironolactone. Test tube research had previously shown that the drug could improve neuron growth and reduce the accumulation of toxic tau.

The authors describe their research in somewhat technical, but understandable language:

“Sildenafil is a selective PDE5 inhibitor and PDEs are broadly expressed in human brain. Recent studies have shown that sildenafil has beneficial effects in various preclinical models of AD by modulating neuronal plasticity, reducing tau phosphorylation, improving cognitive impairment, decreasing amyloid betaplaque accumulation, and enhancing the level of BDNF [brain-derived neurotrophic factor]. Our previous study found that sildenafil increased neurite growth and decreased phospho-tau (pTau181) in AD patient iPSC-derived neurons, mechanistically supporting its potential beneficial effect in AD.

“Furthermore, two pilot trials demonstrated beneficial effects of sildenafil in treatment of AD, where a single dosage of 50 mg sildenafil reduced spontaneous neural activity in the right hippocampus in 10 patients; and increased the cerebral metabolic rate of oxygen and cerebral blood flow in 12 patients; and decreased cerebral vascular reactivity in 8 patients.

“Recent observations involving data from over 30 million insured members validates the association between sildenafil use and reduced risk of AD. This study showed that sildenafil could reduce the risk of AD by 60% which in consonant with our findings.”

We grant you that this is pretty technical. The authors sum up their research by suggesting that:

“…sildenafil can be a potential repurposable drug for the treatment of AD and warrants further testing in more functional models and randomized controlled clinical trials.”

Sadly, we do not expect any drug company to take them up on this suggestion. Sidenafil is incredibly cheap compared to anti-amyloid drugs. And drug companies cannot make money on medications that have lost their patents. It remains to be seen whether other funding groups will sponsor randomized controlled trials to demonstrate whether sildenafil or other ED drugs that inhibit PDE5 could be truly effective against Alzheimer’s disease.

A Recent Visitor to This Website Wanted a 2026 Update:

We received this question from a visitor to www.PeoplesPharmacy.com:

Q. A few years ago you wrote about a Viagra study. It looked really promising, because it showed a 30 to 54 percent reduction in Alzheimer’s disease from a drug that isn’t even taken daily! I really hope that researchers will follow up with a clinical trial.

Meanwhile, men could try taking Viagra. But what about women?

A. Back in 2024 researchers reported preliminary results suggesting that sildenafil (Viagra) might help protect against Alzheimer’s disease (AD). One report noted that sildenafil reduced phosphorylation of tau, one of the important risk factors neurologists note for this dementia (Journal of Alzheimer’s Disease, 2024). In addition, the investigators analyzed medical records in two large databases and found, as you wrote, a significant reduction in AD.

Another study also relied on medical records and found that men taking sildenafil or a similar drug were also less likely to develop AD over five years (Neurology, Feb. 7, 2024).

 The researchers concluded:

“…a randomized controlled trial including both sexes and exploring various PDE5I [sildenafil-like drugs] doses would be beneficial to confirm the association between PDE5I and AD.”

So far as we can tell, only one such study has been published (Journal of Prevention of Alzheimer’s Disease, Nov. 2025). The study of mirodenafil was small and did not show benefit in people who had already been diagnosed with AD. We are still waiting for a large, well-controlled, long-term trial.

The Anti-Amyloid Bet: A Big Disappointment

The results of anti-amyloid drugs have been disappointing at best. One experimental treatment that struck out was solanezumab. This monoclonal antibody (“mab”) was designed to harness the brain’s immune system to attack and remove amyloid.

Researchers know that beta-amyloid protein clumps together to form plaques in the brains of people with Alzheimer disease. They made the assumption that getting rid of these plaques would protect the brain against dementia. Unfortunately, although solanezumab was quite good at reducing brain levels of amyloid, it was no better than placebo at slowing cognitive decline.

A Familiar Failure:

This is not the first time an anti-amyloid drug has produced disappointing results. Since 2000, the pharmaceutical industry has tested more than 200 compounds.

Some investigators are beginning to question the amyloid theory of Alzheimer disease. There is even a suggestion that amyloid might play a protective role when the brain is under attack by pathogens. That is because it seems to have antimicrobial activity (Molecular Pharmaceutics, April 2012; Biological Chemistry, July 2012).

The Prevagen Promise:

Prevagen has been widely advertised on television as a “breakthrough” that is “clinically shown to improve short term memory.” The active ingredient, apoaequorin, was originally derived from a protein in jellyfish.

The Federal Trade Commission and the New York Attorney General charged the maker of this dietary supplement with “making false and unsubstantiated claims that the product improves memory, provides cognitive benefits, and is ‘clinically shown’ to work.”

The company, Quincy Bioscience, “vehemently disagrees with these allegations…” and maintains that “Prevagen improves memory and supports healthy brain function.”

ConsumerLab.com wrote an article titled: “Does Prevagen really improve memory?”

“According to the Prevagen website, ‘Prevagen is an over-the-counter supplement for healthy brain function and memory improvement.” A disclaimer indicates that these statements are “Based on a clinical study of subgroups of individuals who were cognitively normal or mildly impaired.’ Its package also claims that Prevagen supports ‘healthy brain function, sharper mind, and clearer thinking.’

“However, as discussed below, there is little evidence that Prevagen (from Quincy Bioscience) provides any meaningful benefit in terms of memory improvement, and the extent of potential improvement appears to be minimal. Due to actions by the FTC, the marketing claims for Prevagen have been scaled back from earlier claims that it treats conditions such as head injuries and Alzheimer’s disease.”

ConsumerLab.com goes on to discuss litigation:

“In March 2024, a jury verdict for another case brought against Prevagen by the state of New York (Federal Trade Commission et al v. Quincy Bioscience Holding Company, Inc. et al, Case #1:17-cv-00124) found that all eight statements challenged in the suit, including “Prevagen improves memory” and “Prevagen improves memory within 90 days,” lacked support by “competent and reliable scientific evidence.” Furthermore, the jury found two of the statements to be deceptive or materially misleading: These were that “Prevagen reduces memory problems associated with aging” and “Prevagen is clinically shown to reduce memory problems associated with aging.”

You can read the full ConsumerLab.com report at this link.

These days, Prevagen commercials are very careful about the language that is used. What you will see and hear are the words:

“Prevagen For Your Brain“

Another 2026 commercial asks: “What do you do to take care of your brain?” 

It recommends:

“Daily Brain Care” with Prevagen because “It’s made for your brain.”

The asterisk on the screen states: “not evaluated by the FDA. Not intended to treat/prevent disease.”

Can You Prevent Alzheimer’s Disease?

A Finnish study recruited older people with average or below-average cognitive scores. It demonstrated through a randomized trial of improvements in diet, exercise, cognitive training, blood pressure and cholesterol control that these could lead to significant improvement in cognitive scores (Lancet, June 6, 2015).

A Researcher Who Claims to Have Reversed Dementia:

Readers who would like to learn more about how a variety of preventive strategies may wish to listen to our interview with Dale Bredesen, MD. It can be found at PeoplesPharmacy.com. In it, he describes his multifactorial interventions to reverse dementia.

You may also find a more recent interview with Dr. Bredesen of interest as well:

Show 1412: Beyond Amyloid: The Science That Could Change the Course of Alzheimer Disease
A personalized approach considering multiple factors may be helpful for changing the course of Alzheimer disease.

You can listen to the podcast on Apple Podcasts at this link or on Spotify.

We would be grateful if you would share this article with someone you think might find it helpful.

Citations

• Greeley, D., et al, "A phase 2 randomized, placebo-controlled study on the efficacy and safety of AR1001, a phosphodiesterase-5 inhibitor, in patients with mild-to-moderate Alzheimer's disease," Journal of Prevention of Alzheimer's Disease, Nov. 2025, doi: 10.1016/j.tjpad.2025.100337
• Gohel, D., et al, " Sildenafil as a Candidate Drug for Alzheimer’s Disease: Real-World Patient Data Observation and Mechanistic Observations from Patient-Induced Pluripotent Stem Cell-Derived Neurons," Journal of Alzheimer's Disease, March 19, 2024, doi: 10.3233/JAD-231391

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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One body measurement could help reveal your diabetes risk—it's not weight

 Your could try figuring it out yourselves, but ask your competent? doctor instead.

MEDWACS (Machineborne Early Diabetic Warning And Control System) is a free, non-invasive machine learning tool published in the Journal of Clinical Epidemiology in April 2026. Developed by researchers at the Technical University of Denmark (DTU) and the University of Parma, it predicts prediabetes or undiagnosed type 2 diabetes risk using seven at-home measurements without any blood tests. [1, 2]

The 7 Required Parameters

Age
Gender
Body Mass Index (BMI)
Waist circumference
Systolic blood pressure
Upper arm circumference
Upper leg (thigh) length [1]

One body measurement could help reveal your diabetes risk—it's not weight

The length of a person’s thigh could help reveal whether they are at risk of type 2 diabetes, according to a new study from researchers in Denmark who have built an at-home test based on the finding.

The tool, called MEDWACS, was developed to help identify people with prediabetes or undiagnosed type 2 diabetes without requiring a blood test or a doctor’s visit, ultimately enabling earlier access to vital health information and steps to improve their health. Users have to answer a short set of questions, several of which can be measured at home with nothing more than a tape measure, a bathroom scale and a standard blood pressure monitor.

The push to develop MEDWACS stems from a gap in diagnosis.

According to the Danish Diabetes Association, roughly 100,000 Danes have type 2 diabetes without knowing it, and about half a million more are estimated to have prediabetes, a precursor condition. Type 2 diabetes accounts for 80 percent of all diabetes cases in Denmark, making early detection a public health priority.

In the U.S., around 31.3 million people aged 65 years or older have prediabetes.

How MEDWACS Works

The test was built using artificial intelligence trained on 30 years of U.S. health data from the National Health and Nutrition Examination Survey, covering adults aged 18 and older of both sexes. From nearly 3,700 possible health indicators, researchers narrowed the test down to seven parameters, including age, gender and body mass index.

The tool was then externally validated using separate data sets from the U.S. and South Korea, where actual diabetes rates were already known.

According to the findings, published in the Journal of Clinical Epidemiology, MEDWACS performed on par with, or better than, other established screening methods at identifying people with prediabetes or undiagnosed type 2 diabetes.

The Thigh Connection

Among the seven parameters, the one researchers describe as most unexpected is thigh length.

Umberto Maggiore, an Italian physician and kidney disease specialist who worked on the tool, explained the link in a statement. He said the length of the femur reflects nutrition in early childhood, and that poor nutrition in the first years of life slightly restricts bone growth, a pattern that is closely tied to a higher risk of diabetes decades later.

Maggiore also pointed to muscle mass. The body’s largest muscle group sits in the thighs, and those muscles play a key role in clearing sugar from the blood. Shorter legs, he said, generally mean less muscle available to absorb that sugar, raising diabetes risk.

statement. “Poor nutrition in the first years of life slightly inhibits bone growth and is closely linked to an increased risk of diabetes decades later.

“Furthermore, the body’s largest muscle group is also located in the thighs, and these muscles are responsible for removing sugar from the blood. Overall, shorter legs mean that a person has less muscle mass to absorb that sugar, which increases the risk of diabetes.”

Daniel Yoo, data scientist at the Technical University of Denmark, spoke with Newsweek about his team’s findings.

“We wanted to create an early warning system that requires zero blood tests or doctor visits,” Yoo said. “By removing those barriers, we can empower people to check their risk right from their living room and prompt them to seek clinical testing before serious complications develop.

“While traditional clinical screening guidelines often target middle-aged or older adults, MEDWACS is validated for anyone aged 18 and up. This is a crucial advantage because type 2 diabetes is increasingly affecting younger populations who might otherwise slip under the radar.”

The researchers built MEDWACS on U.S. and South Korean data, so they say the thigh measurement’s relevance to the Danish population is still an assumption rather than a confirmed fact. To be fully certain the tool works as effectively in Denmark, it would need to be validated against Danish health data specifically.

Even so, the team behind the test says it has good reason to believe the tool will prove accurate for Danes as well, given how consistently it performed across the two very different populations already tested.

Reference

Yoo, D., Maggiore, U., Jolliet, O. (2026). Enhancing prediabetes and diabetes detection through a machine learning-enabled self-assessment approach. Journal of Clinical Epidemiology. https://doi.org/10.1016/j.jclinepi.2026.112266.

Contact Newsweek editors on this story: Kara Dolman and Gray R. Thomas

Update, 08/03/2026 09:55 a.m. ET: This article was updated with comment from Daniel Yoo.

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