Harshi Peiris, Ph.D.

🚨 BREAKING: Scientists just identified what may be the master switch of human aging — and a single antibody that blocks it extends lifespan by 25% in mammals. It just entered human trials. Here is everything you need to know 🧵👇 #Longevity #AntiAging #IL11 #Science #BreakingScience

@BenHe69435073 It targets both ERK and TOR pathways and they are both linked to aging. So very promising. But my personal concern would be the dosing. I think this will differ for different people. And potential biomarker readings for the outcomes are necessary.

@Neuroscope_mp I will definitely take that when it is available on the market, I am looking forward its success.

🚨 BREAKING: Scientists just identified what may be the master switch of human aging — and a single antibody that blocks it extends lifespan by 25% in mammals. It just entered human trials. Here is everything you need to know 🧵👇 #Longevity #AntiAging #IL11 #Science #BreakingScience

@NriaOriol @blepharopsis It definitely is 😊

@Neuroscope_mp @blepharopsis Really wonderful.. Excited future!

One of the most interesting parts of the IL-11 story for me: It seems to activate AMPK (similar to metformin) while also inhibiting mTOR (similar to rapamycin), plus strong anti-fibrotic effects. Hitting multiple aging pathways at once is rare. Curious — do you think multi-pathway drugs like this are the future, or is rapamycin still king? 👇

This one hits close to home. My 10-year-old cat passed away from kidney-related issues, and it was heartbreaking to watch. Chronic kidney disease is one of the top killers of older cats. This Japanese researcher spent years working on reactivating the AIM protein, which cats naturally produce but doesn’t work properly in them. The early trial results look promising, with much better survival rates. It’s beautiful to see science driven by genuine care for animals. Hoping this treatment gets through larger trials and becomes available soon, so other cat parents can have more time with their furry family members.

This is really cool research. I love cats and my 10-year-old died from kidney-related issues. Chronic kidney disease is brutal for older cats and one of the top causes of death. Reactivating the AIM protein so it can actually clear waste properly is a smart way to target the root issue instead of just managing symptoms with fluids and diet. The early survival data looks promising. It’s always inspiring when scientists dedicate years to problems like this out of genuine care. Hoping the larger trials go well and it becomes available soon.

Japanese researcher Dr. Toru Miyazaki has been working on a treatment aimed at one of the biggest health problems in domestic cats: chronic kidney disease, which affects a large proportion of older cats and is a leading cause of death. His work focuses on a naturally occurring protein called AIM, which helps the body clear waste through the kidneys. In cats, this protein exists but does not function properly because it remains bound in an inactive form. Over time, this contributes to a buildup of toxins and gradual kidney failure. To address this, Miyazaki’s team developed an injectable version designed to restore the protein’s activity and support kidney function. In a small trial, cats receiving the treatment showed much higher survival over the following year compared with those who did not receive it, prompting further investigation and regulatory review. The research suggests the therapy may be useful both for cats already affected by kidney disease and potentially as a preventative option in younger animals. While early findings are promising, experts stress that the results are still based on limited trials and longer-term studies are needed. The project, now being advanced through a Japanese research company, has attracted significant public interest and funding support from cat owners after earlier financial challenges threatened to halt development. If it continues to prove successful and receives approval, it could significantly improve treatment options for feline kidney disease and potentially extend healthy lifespans in cats.

100%. This paper shows abstinence from ultra-processed foods isn’t “restrictive” in the harmful way people fear ... it’s restorative. The brain’s reward system resets, cravings drop, and real food starts tasting satisfying again. Nutrient-dense meals (protein + fibre) make it sustainable. Huge implications for metabolic disease and even neurodegeneration. Glad you see it too

indeed an important paper worth paying attention to For many people struggling with food addiction or binge eating, an abstinence-based approach from ultra-processed, hyper-palatable foods can produce meaningful and lasting improvements. By removing the foods that strongly hijack dopamine reward pathways, the brain can gradually reset its sensitivity to normal satiety signals from real food. This challenges the common belief that any form of restriction inevitably leads to worse rebound eating. When done thoughtfully (focusing on nutrient-dense, satiating meals), it often helps restore better control and reduces cravings over time. Ultra-processed foods are engineered to be addictive for a reason. Giving the brain a break from them while prioritising protein, fibre, and whole foods is a legitimate and evidence-supported strategy for many patients dealing with metabolic and eating issues. More of it is needed

This is a really important paper. An abstinence based approach for food addiction actually improved binge eating symptoms and the benefits lasted at 6 months ... which goes against the common idea that restricting foods makes things worse. Ultra-processed foods hijack the same dopamine pathways as addictive drugs. Giving the brain a break while eating real, satiating food helps restore normal reward signaling for many people. This has big implications for metabolic health and even brain conditions like Parkinson’s, where stable blood sugar and lower inflammation support better cognitive and mood outcomes. More studies like this needed.

Fair point ... many lifelong runners do look weathered. “Runner’s face” is mostly from low body fat (loss of facial padding) + decades of sun exposure, not running itself. What they eat matters hugely ... as we age we need more healthy fats and protein (and I will stress on the need for fat even more than proteins), yet ma ny endurance athletes chronically deplete them. That, plus individual biology (genetics, recovery capacity, inflammation response), creates very different outcomes. No one is one-size-fits-all. The actual data still shows lifelong runners have superior VO₂ max, slower connective-tissue aging, fewer disabilities, and better biological healthspan (Stanford studies + others). Healthspan > mirror age What do you think — appearance or function?

@Neuroscope_mp @Brady_H I challenge anyone who has done 100+ to show a photo of themselves and say their real age. If they are like any of the friends I know who run up the milage regularly, they pretty much always look older than their biological age. Its not sun related either because most protect.

"Multi-marathoners" (people who have completed at least 100 marathons in their lifetime) have a much higher VO₂ max at nearly every age vs. the general population. They also show about a 20-30% lower age-related decline in VO₂ max.

This is a really important paper. The idea that an abstinence-based approach actually improved binge eating symptoms ... and the gains held up at 6 months ... challenges the old belief that cutting certain foods makes disordered eating worse. It makes sense when you look at ultra-processed foods driving dopamine reward pathways similar to addictive substances. Giving the brain a break from that constant stimulation while supporting it with real, satiating food seems to help restore better control for many people. This lines up with what we see in metabolic health and brain conditions too. Stable blood sugar, lower inflammation, and reduced addictive food exposure often improve mood, cravings, and even neuroprotection in areas relevant to Parkinson’s and cognitive health. More studies like this are badly needed.

New paper…an abstinence based treatment for food addiction *improves* binge eating symptoms which is counter to common belief @EllenCalteau @Drdavidwiss @erinlbellamy @lowcarbGP @DoctorTro frontiersin.org/journals/publi…

Exactly. If this antibody can safely slow fibrosis across heart, lung, kidney, and liver at once, it’s not just treating one disease ... it’s attacking one of the biggest common final pathways of aging itself. That’s why I’m so bullish on precision medicine + biomarkers. We’ll measure each person’s fibrosis burden and inflammatory profile, then decide who benefits most. No more one-size-fits-all. This could be game-changing. I think the best approach for this is to find biomarkers for fibrosis and then approach treatment.

@Neuroscope_mp If fibrosis can truly be slowed across multiple organs at once, it could change how we think about aging itself.

Most people don’t die from “old age”. They die when their heart, lungs, kidneys, or liver slowly scar and fail. Fibrosis contributes to ~35% of all deaths. This IL-11 antibody powerfully reduced fibrosis in multiple organs — and added 25% lifespan in mice. Now in human trials. Full thread with the data 👇

This is a really smart advancement in cancer care. MRI-guided cryoablation lets doctors freeze tumors with extreme precision using a thin needle while watching everything in real time. Patients with tumors in tough spots like the spine or pelvis can avoid major surgery, go home the same day, and recover much faster. This fits the bigger shift we're seeing in medicine ... moving toward minimally invasive, root-cause targeted treatments that reduce trauma and complications, especially for older patients or those with other health issues. Hoping this becomes more widely available soon. Less invasive options that actually destroy the tumor are a big win.

A Sydney hospital has introduced a revolutionary new treatment that can destroy tumors and relieve severe pain, without any surgery. Liverpool Hospital is now using Australia’s first MRI-guided cryoablation system. The procedure involves inserting a thin needle (cryoprobe) into the tumor, which then uses extremely cold gas (argon) to freeze and destroy the cancerous tissue, forming a precise “ice ball.” Real-time MRI imaging allows doctors to monitor and control the entire process with exceptional accuracy. This minimally invasive technique is particularly beneficial for patients with painful tumors in difficult-to-reach areas such as the spine and pelvis. Many patients can go home the same day, experience faster recovery, and avoid the risks and trauma associated with traditional open surgery. It’s especially valuable for elderly patients or those with other health conditions who may not be suitable candidates for major operations. A powerful example of how medical innovation is making advanced cancer care gentler, safer, and more accessible.

Cold plunges are no joke for dopamine. That 250% increase and the fact it lasts for hours without the crash is pretty powerful compared to coffee. One of my old Post doc advisors did a jump into San Fran Bay every week day for 30 minutes to an hour and he studies aging and neurodegeneration. What interests me even more is how this ties into brain health overall. For conditions like Parkinson’s where dopamine-producing neurons are vulnerable, anything that supports natural dopamine pathways, reduces inflammation, and builds resilience is worth paying attention to. Cold exposure also boosts norepinephrine and BDNF, which help with focus, mood, and neuroprotection. I recommend this because the body adapts if you overdo it. Short and intense seems to work best. Definitely one of the highest return practices once you get past the initial shock.

Your morning coffee gives you a 30% dopamine boost. You know what else does? A cold plunge. Studies show that cold water immersion increases dopamine levels by 250% — and unlike caffeine, the effect lasts up to two hours and doesn't crash. The most alert, focused, unstoppable version of you is a few uncomfortable minutes away. Nobody said it would be warm.

28% body weight loss is absolutely wild. Retatrutide is pushing the boundaries with that triple receptor action. The “too much weight loss” issue is interesting, though. It shows we’re getting so powerful at driving fat loss that the challenge is now shifting from “how do we make people lose weight” to “how do we personalize it so they lose the right amount and protect muscle.” This is where precision medicine really matters. People respond very differently based on their starting metabolism, muscle mass, age, and genetics. For brain health, especially, we want to avoid rapid sarcopenia or nutrient deficiencies that could affect long-term outcomes in Parkinson’s, Alzheimer’s, and cognitive function. Excited to see the full data on muscle preservation and long-term metabolic effects.

Retatrutide, a triple receptor drug for GLP-1, GIP, and glucagon, is the most powerful weight loss drug yet. A significant issue is too much weight loss among the trial participants. New randomized trial results announced today with 28% body weight loss. gift link nytimes.com/2026/05/21/sci…

Wow ... turning 75 and still this excited about the future? That’s inspiring as hell. Wishing you an amazing next 75 🙌 You’re right ... it’s all of the above. And this is exactly why I keep hammering precision medicine + biomarkers. No universal treatment exists because every disease (and every person) manifests differently. What works beautifully for one 75-year-old may do nothing for another. That’s where biomarkers come in: we measure your biology, then decide if/when a therapy like anti-IL-11 actually makes sense for you. Science really is beautiful. Excited you’re here for it.

when i was born 75 years ago i figured they would figure it out before i died. science is beautiful. . ...all of the above. these are exciting times and the introduction of AI will speed things up. i have been taking DHEA fo 35 years and when i compare my aging to my two younger siblings i am convinced it has powerful anti-aging effects

This is one of the most important ways to think about aging. Cells still hold the original youthful program — they just lose access as epigenetic marks get scrambled over time. What’s exciting is this opens the door to restoration instead of replacement. We’re already seeing partial reprogramming restore function in tissues. The same idea could apply to brain cells in Parkinson’s and Alzheimer’s, where the youthful gene patterns are still there if we can safely restore access. I’ve been looking at IL-11 lately as another piece of the puzzle. As this cytokine rises with age it drives chronic inflammation and tissue scarring. Lowering it extended lifespan in mice by around 25%. I put together a short thread on it today if you’re interested: x.com/Neuroscope_mp/… Blocking these inflammatory signals might help keep youthful gene access open longer when combined with reprogramming approaches. The future is definitely going to be layered strategies.

Cells do not forget how to be young, they lose access

@blepharopsis Haha love the decisive “yes.” What tipped it for you> the 25 % lifespan extension in middle-aged mice, the fibrosis reversal, or the fact that it’s already in human trials? Curious what sealed the deal for you.

@Neuroscope_mp yes

Reversing the biological age of 50-year-old skin cells by about 30 years while keeping them functional as skin cells is a big step. The key here is the short 13-day exposure to Yamanaka factors so they don’t lose their identity and turn into stem cells. What’s especially exciting is they saw improvements in collagen production, wound healing, and even reversal of some gene markers linked to Alzheimer’s. This kind of partial reprogramming could have huge potential for aging tissues and diseases like Parkinson’s and Alzheimer’s in the future. We’re slowly moving from just treating symptoms to actually addressing the root causes of aging at the cellular level. Still early days, but very promising.

Scientists made 50-year-old skin cells behave like they’re 20 again. Researchers at the Babraham Institute in Cambridge have developed a groundbreaking method to reverse the biological aging of human skin cells by approximately 30 years, all while keeping them as fully functional adult skin cells. The team used a carefully controlled, short-term version of the Nobel Prize-winning Yamanaka reprogramming technique. By exposing adult skin fibroblasts to a specific set of reprogramming factors (the Yamanaka factors) for just 13 days—and then stopping the process early—they successfully “reset” many molecular markers of aging without pushing the cells all the way back to a stem cell state. After this brief treatment, the rejuvenated cells displayed a dramatically younger profile: their epigenetic clock (a measure of chemical tags on DNA that tracks biological age) and their gene expression patterns (the transcriptome) closely resembled those of cells from much younger individuals. Even more impressively, the cells behaved younger too. The treated fibroblasts produced significantly higher levels of collagen—the protein essential for skin firmness, elasticity, and wound healing—and they migrated faster to close an artificial “wound” in laboratory dishes compared to untreated older cells. The researchers also observed reversal of age-related changes in genes associated with diseases such as Alzheimer’s and cataracts, suggesting the technique could have broader therapeutic implications. While this work is still in its early stages and the precise mechanisms remain under investigation, the findings open exciting possibilities: one day, scientists may be able to selectively rejuvenate aging cells in the body to enhance tissue repair, improve healing, and potentially slow or mitigate some effects of age-related diseases—without the risks associated with fully reprogramming cells into stem cells. [Gill, D., Parry, A., Santos, F., Okkenhaug, H., Seale, M., Dobbs, L. J., Reik, W., & Ocampo, A. (2022). Multi-omic rejuvenation of human cells by maturation phase transient reprogramming. eLife, 11, e71624. DOI: 10.7554/eLife.71624]

This is fascinating. The idea that dropping protein to ~9% of calories can ramp up energy expenditure by hundreds of calories per day without major muscle loss is wild. It really challenges the standard “calories in, calories out” thinking. I’m especially interested in the potential mechanisms like FGF21, mitochondrial efficiency, and how this interacts with overall metabolic health. It also makes me think about protein needs in different contexts — athletes vs people optimizing for longevity or specific diseases. Curious to see how this plays out long term and whether we can get some of the benefit without going extremely low protein. Great self-experiment as always.

How I Ate 6,000 Extra Calories and Lost Weight 1/5) Last year, I read a paper last year and immediately thought, “this can’t be right.” It was a human controlled study that found people who ate less protein burned dramatically more calories—without any meaningful muscle loss. I was curious. So, I decided to test it on myself. I was wrong.

This is really fascinating. I have been reading MS trials recently and we need more interventions ... but there's a lot of hope. Irisin, the exercise-induced hormone from muscle, showing strong neuroprotective effects and preventing brain cell loss in an MS model, makes a lot of sense. It helps explain why regular exercise is one of the most powerful tools we have for brain health. We see similar benefits in Parkinson’s and Alzheimer’s research ... exercise boosts BDNF, reduces inflammation, improves mitochondrial function, and now apparently irisin as well. It’s another reminder that physical activity hits multiple root causes at once. The more we understand these molecular pathways, the better we can design exercise protocols and potentially irisin-based therapies for neurodegenerative diseases. Great share.

An exercise hormone derived from muscle—irisin— is neuroprotective, preventing brain cell loss, as seen in the experimental model of multiple sclerosis @NatMetabolism nature.com/articles/s4225… nature.com/articles/s4225…