Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,080 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.
Showing posts with label 5 lost years of brain cognition. Show all posts
Showing posts with label 5 lost years of brain cognition. Show all posts
New research shows theobromine, a compound found in dark chocolate, may support longevity.
Reaching for a piece of dark chocolate can offer an afternoon pick-me-up, but chocolate lovers may also get longevity support from their favorite treat. A recent study published in the journal Aging found there may be a connection between a naturally occurring compound in chocolate and the speed of your biological aging — how your body ages on the cellular level.
Research associates dark chocolate (and coffee) consumption with heart-healthy benefits, and that’s often thanks to theobromine, a compound found in both of these — let’s face it — daily essentials. Theobromine benefits include reduced blood pressure and healthier cholesterol levels. But does the chocolate itself slow aging, or are dark-chocolate lovers just more likely to practice other habits that support longevity?
What You Should Know About Theobromine
You’ve probably heard about the heart-healthy benefits of dark chocolate. The antioxidants, such as flavanols, found in cocoa can help reduce inflammation, protect the health of your cells, and even support your cardiovascular system and healthy blood flow.
As it turns out, it may even help slow your body’s biological aging process, essentially the age your body is considered when factoring in health markers such as heart rate and blood pressure, which may be different than your chronological age, or the number of candles on your birthday cake each year.
This may be due to the presence of theobromine, another natural compound found in cocoa, coffee, and tea, with the highest concentrations in dark chocolate; it’s what gives it that bitter taste. Think of this lesser-known compound as a cousin of caffeine, since it’s a much milder stimulant and acts differently in the body. Theobromine is found primarily in cocoa, and moderate to high intake of the compound has been linked with heart health benefits.
More good news for chocolate lovers: The study referenced links higher theobromine levels, which may come from your favorite dark chocolate bar, to slower biological aging.
Going Deeper on Theobromine and Aging
Researchers at King’s College London analyzed data from roughly 1,700 adults across the U.K. and Germany to see if theobromine plays a part in healthy aging and longevity. The discovery group was made up of women, with the findings then replicated in a larger mixed-sex cohort.
Comparing both biological-age measures against theobromine levels in the blood, researchers found that people with more theobromine looked younger than their chronological age on DNA-methylation aging clocks, which help predict disease and mortality risk more accurately than birthdays alone. Higher theobromine also showed a more modest link to longer telomeres, the protective caps on chromosomes that shorten with age or chronic stress.
While the association appeared specific to theobromine, it’s important to note the study is observational, so it doesn’t necessarily prove the compound, or eating dark chocolate, actually slows aging or show exactly how it may support your biological age. And, it raises more questions, like if it’s a marker for other known markers of antioxidants in cacao, like flavanols, that weren’t measured in this study.
The Takeaway
While higher theobromine correlates with slower biological aging in this study, more research is needed to establish why exactly this is the case. Until it’s established exactly why the two are linked, it’s (unfortunately) not a prescription to eat more chocolate. To get health-boosting benefits we already know about, nutritionists suggest looking for dark chocolate that contains at least 70 percent cacao and less than 8 grams of sugar. A daily serving is about one to three squares, or 10 to 30 grams, of your favorite dark chocolate bar.
Bottom Line
Since this study was observational, the results can’t definitively establish that a higher intake of dark chocolate (and theobromine) is the reason study participants saw a younger biological age than their chronological age. Essentially, it’s not yet known if the compound truly is the secret ingredient to better aging or if it’s perhaps due to overall flavanols you consume when eating dark chocolate. While dark chocolate may not be the answer to keeping your body younger — yet — you can still consume it in moderation as part of an overall healthy diet. There’s just no need to load up on the sugary stuff in an effort to pause aging.
Experts Who contributed
Lauren Keary, NASM-CNC, reviewed this article for accuracy.
Jordan Smith, an ISSA certified running coach, wrote this article.
Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!
Summary: Researchers unmasked a profound breakdown in the body’s internal garbage clearance system. As we age, tissue-resident macrophages lose their ability to engulf and dispose of expiring white blood cells, specifically short-lived neutrophils. Left un-cleared, these old cells transform into highly toxic, zombie-like “organ aging(2) neutrophils” that damage healthy tissues.
By blocking a single pro-inflammatory receptor known as EP2 exclusively on these long-lived macrophages, the team successfully revived their youthful cellular cleanup capabilities. This targeted intervention halted chronic inflammation and preserved the functional youthfulness of multiple vital organs throughout the body.
Key Facts
The Neutrophil Garbage Crisis: The body produces roughly 100 billion neutrophils daily as frontline immune responders. Because their active lifespans rarely exceed 12 to 24 hours, long-lived tissue-resident macrophages are tasked with continuously clearing these defunct cells. With advanced age, an unrelenting surge of the pro-inflammatory hormone prostaglandin E2 (PGE2) binds to heavily concentrated EP2 receptors on macrophages, shutting down their cellular engulfing (phagocytosis) mechanism.
The Rise of Zombie Neutrophils: Starved of proper macrophage clearance, expiring neutrophils undergo a swift transition into an intensely toxic, senescent state. These zombie cells accumulate within the liver, spleen, bone marrow, and other major organs, where they damage surrounding tissues by leaking destructive chemicals and propagating systemic inflammation.
Widespread Multi-Organ Rejuvenation: Disabling or pharmacologically blocking the EP2 receptor exclusively on tissue-resident macrophages triggered sweeping systemic preservation in aged mice. Rejuvenation and a stark reduction in inflammation metrics were confirmed across a vast network of organs:
Neurological Preservation: Deeply reduced hippocampal inflammation, preventing age-related memory loss and maintaining baseline spatial navigation and cognitive processing speeds.
Metabolic Recovery: Drastically lowered visceral fat accumulation, preserved youthful skeletal muscle mass, and normalized 59 out of 71 age-altered blood proteins, primarily driven by restored liver homeostasis.
Somatic Vitality: Aged mice treated with an experimental EP2 inhibitor looked leaner and exhibited physical speed, balance, and forelimb grip strength matching their youthful counter-cohorts.
Human Translation Confirmed: Transitioning from mice to humans, the Stanford team analyzed comprehensive human hepatic databases. The dataset confirmed that older and diseased human livers exhibit the identical pathological cascade seen in the animal models: a dramatic neutrophil buildup, widespread cellular senescence, and heightened macrophage EP2 receptor activity.
The Precision Medicine Alternative: Dr. Katrin Andreasson emphasizes that while current everyday painkillers (like aspirin or NSAIDs) reduce inflammation by blocking PGE2 production upstream, they are too clumsy, shutting down multiple beneficial prostaglandins and companion receptors. Developing a safe, highly selective drug that targets the EP2 receptor directly, without interfering with broader hormone systems, represents an outstandingly high-priority therapeutic path to extend human health spans.
Source: Stanford
We may age at different rates, but none of us escapes aging. A study in mice and in human cells by Stanford Medicine researchers pins much of the blame on a particular type of immune cell’s increased inability, with advancing age, to gobble up another immune cell type.
So-called tissue-resident macrophages appear to be central coordinators of age-related organ decline. Blocking a single receptor on these cells preserved the youthfulness of multiple organs in mice including the brain, heart, skeletal and heart muscle, liver, spleen, bone marrow, kidney, and colon. The receptor binds specifically to a hormone known to cause inflammation and pain in humans as well as mice.
Targeting the pro-inflammatory EP2 receptor on tissue-resident macrophages restores the clearing of senescent neutrophils, successfully reducing systemic inflammaging to preserve youthfulness across the brain, liver, heart, and skeletal muscles. Credit: Neuroscience NewsIn mice, selectively disabling this receptor exclusively on tissue-resident macrophages prevented chronic-inflammation-driven disorders of age including frailty, excessive fat accumulation and heart trouble; it also substantially slowed cognitive decline, said Katrin Andreasson, MD, the Edward F. and Irene Thiel Pimley Professor in Neurology and Neurological Sciences.
“We’ve been trying to figure out why we age,” Andreasson said. “Now we know at least one big reason for it.”
The study’s findings are described in a paper to be published online July 16 in Science. Andreasson is the senior author, and the lead author is Jessy Tan, PhD, an instructor in neurology.
This discovery clarifies systemic inflammation’s outsized contribution to aging and the debilities that accompany it. And it suggests a pharmaceutical approach that could restrain our organs’ ineluctable march to senescence, extending our overall health spans.
A tale of two cell types
The most abundant white blood cells in our immune system are neutrophils, our bodies’ main first responders. Born in the bone marrow, new neutrophils hop into the bloodstream, where they circulate and, if they come across a bacterial, viral or fungal pathogen, go all medieval on it: They squirt out poison and perform a hara-kiri horror act, spilling their guts out and unloading long, stringy macromolecules that form weblike nets and trap the pathogen.
Perhaps unsurprisingly, neutrophils are extremely short-lived: They’re lucky to survive 24 hours (12 hours is more typical). Some 90% of circulating neutrophils end up in the liver, spleen and bone marrow, awaiting execution and riddance by another batch of immune cells.
This neutrophil clearance is critical. In aged animals, the vast bulk of neutrophils that never see combat undergo a fast transition to senescence, a zombie-like state in which they injure, age and inflame neighboring cells by vomiting toxic chemicals and otherwise behaving like an addled rock star punching holes in a hotel room wall.
The older we get, the more our neutrophil counts rise, with senescent neutrophils constituting an ever higher percentage.
“Senescent neutrophils are killing our tissues,” Andreasson said. “Clearance of these cells is essential for preventing chronic inflammation.”
That’s a job for another type of immune cell called a macrophage. These cells are by turns soldiers, builders, medics and garbage collectors. They comb the tissues for pathogens, chew them up, spurt signaling substances that summon other cells to lend a hand, and pump out growth factors that help repair damaged tissue.
First and foremost, Andreasson said, “They’re the body’s garbage collection crew. A lot of that garbage is defunct cells.” And a lot of those cells are neutrophils — to the tune of 100 billion a day.
Macrophages come in several subtypes. Tissue-resident macrophages are long-lived and ubiquitous. They take up residence in each of the body’s organs during fetal development and remain for their lifetimes in whatever organ they’ve inhabited, adapting their roles to fit that organ.
One of tissue-resident macrophages’ prime responsibilities is to swallow senescent cells. Especially important targets for this operation, the study showed, are some 100 billion neutrophils, produced daily, which start showing signs of senescence within 8 to 12 hours after entering the bloodstream. (Neutrophils that haven’t arrived at senescence yet but have lived long enough and seen enough to put out “kill me now” flags of surrender on their cell surfaces are fair game.)
But tissue-resident macrophages also grow old and tired and dyspeptic. As Andreasson and associates showed in a 2021 Nature paper, over the advancing years these long-lived cells become ever more prone to succumb to aging-associated inflammation and to propagate it.
A distress signal
Immune cells produce hormones called prostaglandins. One of the five varieties of prostaglandin, called PGE2, can exert diverse effects on a cell, depending on which type of surface receptor is expressed on that cell’s surface.
Of the various subtypes of receptors for PGE2, one designated EP2 is highly pro-inflammatory. Tissue-resident macrophages are loaded with EP2.
Infection, injury and toxic chemicals including the ones produced by our aging bodies increase PGE2 output. As the 2021 Nature paper showed, that output grows substantially as we grow older. So does the concentration of EP2 on tissue-resident macrophages.
It’s a one-two punch: PGE2’s pro-inflammatory influence increases with age. The resulting unrelenting inflammatory PGE2 stimulation on tissue-resident macrophages, the new study showed, downshifts these voracious cells’ ability to wolf down neutrophils. Senescent neutrophils then accumulate in tissues and blood.
Andreasson and her colleagues have previously shown that with aging, tissue-resident macrophages undergo a slow decay in their energy metabolism. “Once that starts, there’s a steady decline in a macrophage’s performance,” she said.
In the new study, she continued, “We’ve shown that when tissue-resident macrophages don’t have EP2 on their surfaces anymore or when that receptor is plugged up by a drug, this decline doesn’t happen.”
Block one receptor, rejuvenate many organs
Andreasson’s lab has bioengineered a mouse in which, at a time of the scientists’ choosing, the gene that’s a recipe for EP2 gets deleted — but only in tissue-resident macrophages. The subsequent disappearance of EP2 from these cells, the new study proves, reinvigorated the neutrophil-devouring process that PGE2 undermines.
For their experiments, the Stanford Medicine researchers studied younger normal mice (age 6 to 8 months) corresponding to late adolescence or early adulthood in humans; older normal mice (23 to 25 months), whose human counterparts would be in their 60s or 70s; and otherwise virtually identical older mice whose EP2-encoding gene had been deleted at 4 to 6 months of age (their “teenage” years).
The scientists identified 71 proteins, found in blood, whose levels were significantly altered in older normal mice. Of those proteins, 59 stayed at youthful levels in older mice whose tissue-resident macrophages lacked EP2. Many of these proteins originated in the liver.
“The liver is one of the body’s most tissue-resident-macrophage-enriched organs and a major contributor to aging-related changes in blood chemistry,” Andreasson said. “It’s the central organ determining the body’s metabolic rate.”
Smoldering senescent neutrophils, the study showed, accumulated in normal old mice’s livers, spleens and bone marrow — and, to a lesser extent, in all the many other bodily organs the researchers looked at.
But the organs of older mice lacking EP2 on their tissue-resident macrophages retained the lower neutrophil numbers of youth. These mice looked younger, leaner and more physically fit compared with control littermates. They evidenced less visceral fat and greater muscle mass. Their performance on tests of multiple organs’ function equaled that of young mice.
EP2 deletion reduced inflammation in the blood, liver, colon, heart, kidney and hippocampus (a brain region tightly tied to memory and navigation ability) in the older mice. Their speed, balance and forelimb grip strength resembled that of young animals.
Reducing EP2 action in older mice also preserved their memory capabilities. They could thread their way through a maze or recall previously encountered objects almost as well as younger mice — and far better than similarly old mice in whose tissue-resident macrophages EP2 remained functional.
Seeking drugs to target EP2
There are, today, no approved drugs that selectively shut down EP2 activity, although there are several that target PGE2. Non-steroidal anti-inflammatory painkillers work by blocking PGE2 production, Andreasson said. (That’s how aspirin and similar drugs reduce pain, fever, swelling and redness, the “four horsemen” of inflammation.) But to greater or lesser degrees they all block other vital prostaglandins. Even PGE2 has beneficial properties when it binds to receptors other than EP2, rather than the detrimental inflammatory one examined in this study.
The investigators treated otherwise normal 22-month-old mice for two months with an EP2-inhibiting experimental drug.
This drug reduced total and senescent neutrophil counts in old mice toward youthful levels. In culture dishes, old age diminished — but the EP2-blocking drug likewise significantly restored — the mice’s tissue-resident macrophages’ ability to engulf and digest burnt-out neutrophils.
Finally, the team turned to a large database characterizing goings-on in all cell types in young, old and diseased human livers. This database revealed the same age-related neutrophil buildup, increased neutrophil senescence, tissue-resident-macrophage decline and heightened EP2 activity in older — and even more so, diseased — livers that the Stanford Medicine researchers had seen in mice. It was a first-time observation in human cells, according to Andreasson.
Targeting neutrophil clearance may yield big therapeutic benefits, she said: “We need to develop a safe drug” that incapacitates EP2 without disrupting upstream events such as PGE2 production.
A researcher from the University of Munster in Germany contributed to the work.
Funding: The study was funded by the National Institutes of Health (grants 1RF1AG080742, 1RF1AG070839 and P30AG066515), the American Heart Association, the Phil and Penny Knight Initiative for Brain Resilience (at the Wu Tsai Neurosciences Institute), Stanford University, the Arc Institute, and the Chan-Zuckerberg Biohub. The research was conducted in part at the Neurosciences Preclinical Imaging Community Laboratory at the Wu Tsai Neurosciences Institute.
Key Questions Answered:
Q: Why are neutrophils so helpful in youth but so incredibly destructive to our tissues as we get older?
A: Think of neutrophils as the kamikaze first-responders of the immune system. When you are young and get an infection, they swarm the site, unleash toxic chemicals to melt away pathogens, and deliberately burst open to form weblike nets that trap invaders. Because they are so intensely destructive, they are designed to die within 12 to 24 hours, at which point the body’s macrophage cleanup crews instantly sweep them away. However, as we age, the cleanup crew goes on strike. Left floating in our organs past their expiration date, these un-cleared neutrophils transform into hyper-toxic “zombie cells.” They wander through healthy tissues, punching holes in cell walls, vomiting inflammatory chemicals, and accelerating the physical aging of everything around them.
Q: If we already have anti-inflammatory drugs like aspirin that block this hormone pathway, why can’t we just use those to stop aging?
A: While everyday painkillers like aspirin or ibuprofen do reduce inflammation by shutting down the production of the prostaglandin PGE2, they act like biological sledgehammers rather than precision tools. PGE2 is a complex hormone that does many different jobs depending on which receptor it latches onto. When it hits the EP2 receptor on macrophages, it causes damage and shuts down clearance; however, when it binds to other receptors, it can actually support healing, protect the stomach lining, and assist blood vessel health. Blanket NSAIDs shut down the entire system, causing long-term side effects like ulcers or kidney stress. The Stanford team’s ultimate goal is to develop a hyper-targeted drug that leaves the helpful pathways completely alone, acting like a shield that plugs up only the problematic EP2 receptor.
Q: What makes this discovery a true paradigm shift for the future of longevity and preventative medicine?
A: For decades, the medical community viewed the aging of different organs—like cognitive decline in the brain, fatty buildup in the liver, and frailty in our muscles, as separate, distinct illnesses that required completely different treatments. This study completely upends that reductionist model. By demonstrating that deleting a single receptor on one type of immune cell simultaneously preserved the youthful function of the brain, heart, liver, muscles, colon, and kidneys, Stanford has exposed a universal master key to aging. It proves that we do not necessarily have to treat every organ disease individually; by simply fixing the body’s natural cellular garbage disposal system, we can halt systemic inflammation at its root, unlocking a future where overall human health spans can be extended in unison.
Editorial Notes:
This article was edited by a Neuroscience News editor.
Journal paper reviewed in full.
Additional context added by our staff.
About this aging research news
Author: Bruce Goldman Source: Stanford Contact: Bruce Goldman – Stanford Image: The image is credited to Neuroscience News
I do lots more than this anemic 3-4 cups daily, mainly to prevent Parkinsons and dementia and since nobody knows the amounts for that, I'm not taking chances.
Your morning coffee ritual might be doing more than waking you up—researchers found the optimal daily amount associated with cellular markers of living 5 years longer.
Summary: In an era dominated by generative AI, smartphones, and short-form digital media, the way humanity consumes text has transformed more over the past decade than in the entire century preceding it. While modern wellness trends heavily emphasize meditation, biohacking, and neurostimulation to achieve peak mental clarity, a new book points to an overlooked cognitive tool. Reading is not simply a neutral pathway for receiving information; it is a profound neurological catalyst that fundamentally rewires memory, attention, executive reasoning, and visual perception.
Bringing together decades of cross-disciplinary research spanning psychology, linguistics, education, and cognitive neuroscience, researchers detail how literacy reshapes the physical architecture of the human brain. The work challenges traditional neural “invasion” theories, which assumed reading intrusively steals space from older visual systems, by demonstrating that learning to read actually sharpens overall visual processing, including our ability to recognize human faces.
Key Facts
The Cognitive Enhancer: Huettig frames literacy as one of the most potent, evidence-backed tools for cognitive enhancement available to humans, driving broad structural upgrades across multiple neural networks.
The Visual Recycling Myth: Cognitive neuroscience long held that because reading is an evolutionary newcomer, it must destructively “co-opt” or crowd out older visual real estate, such as the brain networks dedicated to face recognition.
Enhanced Face Recognition: Huettig’s field research comparing literate and illiterate adults in India proved the opposite: learning to read triggers a functional fine-tuning that structurally adapts and improves face and object recognition performance.
The Continuous Literacy Spectrum: True reading proficiency is an unfolding continuum, not a binary on/off switch. Avid readers constantly automate and refine sub-cortical processes, shifting how they physically perceive and interpret the world.
The Screen Effort Disconnect: Meta-analyses show inferior comprehension when reading on digital screens compared to print. The root cause is psychological self-regulation: readers instinctively view paper print as “serious,” causing them to exert greater cognitive effort.
Audiobook Limitations: While listening to audiobooks successfully exposes the brain to rare vocabulary and complex narrative structures missing from everyday speech, Huettig emphasizes that the full spectrum of neurological benefits is only unlocked by actively processing written text.
The Danger of Over-Simplification: The author warns that relying heavily on AI readability scores, autocorrect, and simplifying text to match shrinking vocabularies dilutes the richness of written expression, ultimately stalling neural development in young people.
Source: Max Planck Institute
Smartphones, online learning, generative AI: the way we read has changed more in the last decade than in the previous century. So what do we actually know about what reading does for the mind?
In his new book, Falk Huettig, Senior Investigator at the Max Planck Institute for Psycholinguistics, brings together research spanning psychology, linguistics, neuroscience, and education to answer that question.
The result is a systematic account of how literacy reshapes memory, attention, language processing, and reasoning – and even abilities readers might not expect, like face recognition.
Cognitive enhancement is having a moment, with people turning to better sleep, exercise, nutrition, stress management, and tools like caffeine or neurostimulation in search of a sharper mind.
According to Huettig, one of the most powerful enhancers of all has largely flown under the radar: “One of the most powerful cognitive enhancers, with broad and increasingly well-documented effects, is rarely emphasized in these discussions: the ability to read.”
An unexpected finding: reading and face recognition
One of the more surprising threads in the book concerns face recognition. A long-standing idea in cognitive neuroscience holds that because reading is a relatively recent cultural invention, the brain has no dedicated reading network of its own, so literacy training has to borrow space from older visual systems, including the one used for recognising faces.
“Neuroscientists have proposed that the development of reading expertise may therefore partially displace or encroach upon the face recognition network in the brain,” Huettig explains.
“This postulated cortical ‘invasion’ could result in a measurable decline in face or object recognition performance, as neural resources are reallocated to support the newly acquired reading skill.”
Huettig’s own research points the other way. “Our alternative perspective challenges the idea of destructive competition by proposing that learning to read may actually enhance sensitivity to faces and other visual object categories, rather than intrusively co-opting existing face recognition territory,” he says.
In studies conducted in India comparing literate and illiterate adults, his team found that “such co-opting leads to functional fine-tuning, where older networks are not diminished but rather adapted and even enhanced. We confirmed this explanation in behavioral studies: literate people were better at face recognition than illiterate people.”
A continuum, not a switch
The book argues that literacy keeps developing long after someone learns to decode text. “Reading proficiency does not end once a reader can fluently decode a writing system,” says Huettig. “Avid readers continue to automatize and refine these subprocesses and their coordination, training both lower- and, with increasing practice, higher-level cognitive functions.
As a result, literate people come to ‘see’ the world through a fundamentally different lens than those who are illiterate or less literate.” Few people, he notes, ever reach the very top: “only a small proportion of individuals reach the highest levels of critical reading in international assessments such as the PISA tests.”
Content matters too: “It matters a great deal what people read,” Huettig says. “Reaching these advanced levels of literacy requires regular engagement with sophisticated texts, along with the development of strong critical thinking and reasoning skills.”
Print, screens, and audiobooks
On format, the picture is more nuanced than “print good, screens bad. Meta-analyses have found inferior reading comprehension when text is read on digital screens,” Huettig notes, but he points to self-regulation as the likely driver: “Readers tend to regard analogue print as a more appropriate medium for ‘serious’ reading than screens, and monitor their behavior accordingly. As a result, they exert more cognitive effort for the task at hand.”
Still, he’s cautious about overstating the case: “The existing body of research does not support the simplified inference that print always results in better reading outcomes than digital reading.”(I hate digital reading, hard to scan backwards to pick up missed context.)
Audiobooks, meanwhile, can deliver some of reading’s benefits at a distance. “Listening to audiobooks can expose listeners to rare and sophisticated words, infrequent grammatical constructions, and complex narrative structures: elements that are not commonly found in everyday speech,” he says. But the full picture requires the real thing: “The full spectrum of the benefits of reading is only obtained from reading text.”
A message for parents and educators
Huettig’s advice runs counter to a popular instinct: don’t over-simplify. “Simplifying texts to align with shrinking vocabulary and declining grammatical proficiency among young people may be counterproductive,” he warns.
“Relying too heavily on human- or AI-generated readability scores, or defaulting to autocorrect for ‘better words’ and ‘better grammar,’ can dilute the richness of written expression. Instead, prioritizing quality writing, memorable prose, and the use of complex, uncommon, and sophisticated language may be a more effective strategy for maintaining and enhancing literacy.”
More broadly, he wants readers to come away with a sense of just how much is at stake: “Reading and writing are not merely neutral tools that humans use: they take hold of the mind and profoundly reshape it.”
What comes next for reading?
The book closes by asking what happens to these benefits as reading habits keep shifting. Huettig is cautious about firm predictions but draws a parallel with vinyl records: “What once was the standard medium for music has become a niche interest, sustained by a small group of enthusiasts… In a similar way, the written medium may persist in pockets of culture, or even become a nostalgic fad for future generations, before largely fading from everyday use.”
If literacy continues to decline globally, he suggests, the kinds of skills current intelligence tests measure may decline with it, and he’s doubtful new technologies will simply compensate: “Mastering new, future technologies may compensate for the loss in cognitive abilities, but personally, I wouldn’t bet on that happening.”
Early praise
Early endorsements describe the book as an original and accessible contribution to the science of reading, with reviewers from Oxford, the University of Illinois at Urbana-Champaign, and CNRS/Aix-Marseille University praising its scope and clarity.
Key Questions Answered:
Q: How does learning to read actually improve a person’s ability to recognize faces?
A: For a long time, neuroscientists believed in the “cortical invasion” theory. Because reading was invented relatively recently in human history, the brain hasn’t had time to evolve a built-in reading network. Scientists assumed text recognition had to aggressively crowd out older visual systems, like the face recognition network. Dr. Huettig’s research in India proved the opposite. By comparing literate and illiterate adults from identical backgrounds, his team found that learning to read acts like an intensive gym workout for your entire visual system. It refines the brain’s visual sensitivity, functionally fine-tuning older networks so that literate individuals actually become measurably better at identifying faces and distinct objects.
Q: Why does reading on a physical piece of paper yield better comprehension than reading on a digital screen?
A: It isn’t necessarily a limitation of the screen technology itself, but rather a reflection of human psychology and self-regulation. Meta-analyses consistently show that people retain less information when reading digitally. Huettig explains that our brains treat mediums differently based on habit. We instinctively view analog print as the proper medium for “serious” reading, which subconsciously prompts us to invest more cognitive effort and monitor our focus closely. When reading on screens, where we are used to skimming fast social media feeds or clicking away, we drop our cognitive guard, read more superficially, and fail to deeply process the material.
Q: What is the danger of using simplified language and AI readability tools for children?
A: There is a popular instinct among modern educators and content creators to simplify text, strip away rare words, and use AI tools to smooth out complex grammar to accommodate declining attention spans. Huettig warns that this approach is completely counterproductive. Written text is unique because it exposes the mind to intricate sentence structures and rare vocabulary that almost never occur in casual spoken conversation. If we constantly sanitize text and rely on autocorrect to fix expressions, we dilute the cognitive challenge. To keep human intelligence sharp, we must prioritize memorable prose and sophisticated language, as these are the exact ingredients that force the mind to grow.
Editorial Notes:
This article was edited by a Neuroscience News editor.
Journal paper reviewed in full.
Additional context added by our staff.
About this reading and cognition research news
Author: Anniek Corporaal Source: Max Planck Institute Contact: Anniek Corporaal – Max Planck Institute Image: The image is credited to Neuroscience News
Original Research: The Perks of Being a Bookworm: The Science of the Benefits of Reading by Falk Huettig is available to purchase online
Do you really think your doctor is competent enough to get you recovered enough to do this and at least recover some of your 5 lost years of brain cognition due to your stroke? I can almost guarantee that your incompetent? doctor HAS NOTHING FOR 100% RECOVERY! Ask him/her and not politely!
Following a simple, guideline-based aerobic workout programme for a year could make the brain “measurably younger”, scientists claim in a new study.
Researchers found that regularly following the exercise regimen for a year led to participants’ brains appearing nearly a year younger on MRI scans.
Studies have previously shown that regular exercise plays a meaningful role in slowing ageing and keeping the mind sharp as one grows older.
In particular, a consistent aerobic workout routine has been proven to prevent the brain from ageing faster. Aerobic exercises have been linked to sharper thinking, stronger memory, and better overall well-being.
But structured long-term studies looking into measurable brain effects of such workouts have been limited, say researchers.
In a new study, scientists subjected 130 healthy adults(So your doctor needs to get further research going on stroke subjects! I bet your doctor will fail at that!) aged 26 to 58 to a 12-month intervention involving moderate-to-vigorous intensity aerobic exercise and measured changes to their brains via Magnetic Resonance Imaging (MRI) scans.
Participants in the exercise group attended two supervised 60-min sessions per week in a laboratory setting, along with at-home workouts to achieve 150 minutes of exercise per week.
They were guided to walk, jog, or run on a treadmill, as well as to record their use of aerobic exercise equipment such as bikes, elliptical machines, stair climbers, and rowers.
For the first six weeks, each participant was prescribed an exercise intensity that took them to 50 to 60 per cent of the maximum heart rate reserve (HRR), which is the difference between one’s maximum heart rate and resting heart rate.
The maximum heart rate is typically calculated using the formula of “220 – one’s age”, scientists explained.
“For the remainder of the intervention, participants increased their intensity to 60 to 75 per cent of HRR,” researchers wrote in the study published in the Journal of Sport and Health Science.
Participants’ fitness was estimated at the beginning and end of the 12-month study by measuring their peak oxygen uptake.
Brain ages of the participants were determined by estimating how old their brains appeared on MRI scans compared to their actual age.
Scientists found that the exercise group showed a measurable decrease in brain age after one year, while the control group experienced a slight increase.
“We found that a simple, guideline-based exercise programme can make the brain look measurably younger over just 12 months,” said Lu Wan, an author of the study from the AdventHealth Research Institute in the US.
“Studies like this offer hopeful guidance grounded in everyday habits,” Dr Wan said, adding that “even a one-year shift in brain age could matter over the course of decades”.
“From a lifespan perspective, nudging the brain in a younger direction in midlife could be very important,” said Kirk I. Erickson, another author of the study.
Researchers suspect exercise could be acting through additional mechanisms that haven’t been captured yet in studies.
Some subtle changes in brain structure, inflammation, vascular health, or other molecular factors due to routine exercise could be behind the slower ageing effects, they theorise.
They hope that larger studies conducted in the future with longer follow-up can determine whether exercise can reduce the risk of stroke, dementia, or other age-related brain diseases.
“If we can slow brain ageing before major problems appear, we may be able to delay or reduce the risk of later-life cognitive decline and dementia,” Dr Erickson said.
“Our findings support the idea that following current exercise guidelines – 150 minutes per week of moderate-to-vigorous aerobic activity – may help keep the brain biologically younger, even in midlife,” he added.
Did your competent? doctor give you a protocol on sleep, diet and exercise? NO? So, your doctor IS FUCKING INCOMPETENT? No question about it! You lost 5 lost years of brain cognition due to your stroke , at a minimum your doctor can provide these protocols!
Sleeping, eating, and exercise are crucial to health — and improvements in any of those categories can have big impacts. Now we’re learning that minimal changes to all three can improve health better than focusing on just one area alone.
That’s the takeaway from new work from Australian researchers that suggests strong synergistic effects. The research is among the first to calculate the effects of lifestyle changes in combination. Findings suggest that adding just 5 minutes of sleep, 2 minutes of moderate activity, and half a serving of vegetables a day can add a full year to your life.
Emmanuel Stamatakis, PhD
“The central clinical message is that modest combined changes across three behaviors may matter more than trying to overhaul one behavior in isolation,” said Emmanuel Stamatakis, PhD, a professor of physical activity and population health at the University of Sydney and Monash University in Australia.
In 2025, Stamatakis gained notice with a Nature Communications paper that showed each dose of 60 seconds of daily vigorous exercise could add years to lifespan and reduce the risk for cardiometabolic disease and cancer.
Now, drawing from UK Biobank data, his team’s latest findings show a synergistic effect that “argues against an all-or-nothing approach,” Stamatakis said. “If a patient is struggling to make a large change in one area, it may still be worthwhile to pursue smaller gains across several domains at once.”
The Bare Minimum for Longer Life
The researchers started from a low baseline, creating a composite score for diet, physical activity, and sleep for study participants in the fifth percentile. These people slept about 5.5 hours a night, logged 7.3 minutes of daily moderate activity, and received a diet quality score of 36 out of 100. From there, the researchers set out to find the bare minimum improvements needed to improve lifespan and healthspan.
Here are some conclusions, from the paper published in eClinicalMedicine:
The minimum: People who added 5 minutes of sleep, 2 minutes of at least moderate activity, and a small diet change such as a half serving of vegetables daily lived 1 year longer than those with the lowest baseline.
The optimum: Getting 7.2-8 hours of sleep, 43 minutes of moderate activity, and a high-quality diet (score, 57.5-72.5 out of 100) was linked to more than 9 years of additional healthspan and lifespan.
The synergy: The math shows that these changes multiply each other’s powers. For example, if you rely on sleep alone to add a year to your life, you need an extra 25 minutes a night. But if you combine it with 2 minutes of activity and half a serving of veggies, you need only 5 minutes of additional sleep to get that same extra year.
“What stood out most was how small the estimated combined changes were for a meaningful signal,” Stamatakis said. “We are used to lifestyle advice sounding large, difficult, and sometimes discouraging. Seeing that a few extra minutes of sleep, a couple of minutes of moderate-to-vigorous activity, and a modest diet improvement were associated with an extra year of lifespan was striking.”
“Equally striking was that the combination mattered so much,” he said. “Scientifically, that reinforces the idea that everyday behaviors interact in the real world, and practically it suggests a more hopeful, less overwhelming message for patients and clinicians.”
The researchers published a separate analysis in the European Journal of Preventive Cardiology that showed similarly small synergistic changes in sleep, activity, and diet lowered the risk for major cardiovascular events.
Call It ‘Progress Over Perfection’
That mindset, plus the flexibility of making several small changes, can be important, said Meagan L. Grega, MD, a lifestyle and family medicine physician in Easton, Pennsylvania, and chief medical officer of the Kellyn Foundation, a healthy neighborhood nonprofit initiative that she co-founded. She serves on the governing board of the American Board of Lifestyle Medicine and wasn’t involved in the study.
Meagan L. Grega, MD
Increased moderate-to-vigorous physical activity, is the strongest driver of improvement in lifespan and healthspan, she said, noting dramatic lifespan gains for each 5 minutes daily. Adding improvements in sleep and nutrition could achieve similar benefits with lower amounts of moderate-to-vigorous physical activity — “a more flexible and attainable path for many patients.”
To coach your patients toward small changes, start by asking, “What matters most to you?” Grega suggests. It could be strength and vitality to stay active with the family, or protecting cognitive health. Choosing the behavior gives the patient autonomy and helps them access their internal motivation.
From there, examine barriers and strategies, Grega said. Improving sleep might mean “creating a consistent wind-down routine or setting a reminder to transition toward bedtime,” she said. “Reviewing a typical day together can uncover opportunities for brief ‘exercise snacks,’ or short bursts of movement woven into existing routines.”
For diet, take a cue from the recent study and suggest adding half a serving of vegetables a day. That’s about one medium carrot, half a bell pepper, or 4 ounces of vegetable juice.
Stamatakis made the following relevant disclosure: He is a paid consultant and holds equity in Complement 1, a US-based startup whose products and services relate to physical activity promotion and other lifestyle changes. Grega had no relevant disclosures.
