Longevity Global

Join us for a live Younger Biological Age Contest 2027 information session via zoom before baseline testing starts! Kits begin shipping Sep 1 and baselines can be completed through Feb 1 2027. The 6 month long contest to become younger can be completed from anywhere in the world. This webinar is your opportunity to meet the scientific teams behind the assessments you'll complete throughout the competition. We'll provide an overview of the testing process, explain what to expect when your kit arrives, and answer your questions before you begin. We'll cover: • ​An overview of the Younger testing experience • ​An introduction to our testing partners: Christin Glorioso, MD PHD (@NeuroAgeTX) Ryan Smith, (@TruDiagnostic) Ray Mak, MD (Harvard's FaceAge) Raghav Sehgal, PhD (Yale) • ​The purpose of each assessment and how they work together • ​What to expect before, during, and after baseline testing • ​Tips for preparing for your baseline assessments • ​Live Q&A with the Younger team Register here: luma.com/6xhp4gzo

Is it harmful to wear polyester and spandex workout clothes? A 2024 TikTok calling polyester "poison" and tying it to infertility and cancer garnered 1.6 million views, and affiliate blogs and wellness press amplified it. Here's what the science says: In short, no one has shown that wearing polyester causes disease in a human being. What exists is a set of real but partial findings about specific chemicals with the answer sitting below the alarmist posts and above "nothing to see here." A few things I found that surprised me: 🧪 The 2024 University of Birmingham study everyone cites as proof did not test clothing at all. It ground down other plastics and applied them to lab-grown skin. It shows a mechanism, that chemicals can move from plastic into sweat and across skin, not that your leggings dose you. 👕 Polyester sheds microplastics as much from being worn as from being washed. About 4,000 fibers per gram in a wash, and hundreds more per gram into the air during 20 minutes of movement, which scales to roughly a billion fibers per person per year going airborne. ⚗️ Antimony, a metal catalyst, sits inside the polyester fiber itself, so it cannot be washed off the way a surface coating can. Most of what leaches into sweat comes off in the first wash, so laundering new synthetics before wearing them actually helps. 🧵 The percentage on your label does not predict the risk. In the antimony work, one entirely-polyester shirt crossed the safety line while others stayed well below it, and the difference was manufacturing, not the blend ratio. 🌱 The properties we want from activewear turn out to be separable. Antimony-free polyester made with a titanium catalyst already exists, and companies like Reprise are chasing zero-spandex stretch. What no brand has done yet is run the cheap, standardized sweat-migration test on a finished garment and publish the number. Where I landed: The environmental case against synthetic shedding is far stronger than the personal-health case, and the two often get blended together. I am swapping my own polyester-spandex pieces (dry fit clothing) for nylon, merino, and cellulose fabrics like modal and rayon. The logic being that when an exposure is easy to reduce and the downside is large, reducing it is reasonable even before the definitive study lands. Link to full post

RT @DrGlorioso: We started filming the #Younger contest instructions and baseline measurements for @NeuroAgeTX 's team and friends. Marah D…

“We need surrogate endpoints. Longevity is a hard thing to prove. If you can give me a test that can predict people’s risk before they get full blown dementia, we’d be very interested in that.” That is roughly what Dr. Mehmet Oz, the Administrator of the CMS, said at The Alliance for Longevity Initiatives H-SPAN conference this week. CMS covers health care for more than 160 million Americans, and dementia is one of the costliest conditions it carries. If we could identify the people at highest risk early and help them act on the modifiable 45%, the savings to the government could reach up to roughly $120 billion a year. The 2024 Lancet Commission put the share of dementia attributable to modifiable risk factors at up to around 45%. A new review in The Lancet Healthy Longevity, published on June 30, 2026, asks whether telling people in mass what to do actually helps. Here is what the review found: 🧠 Messaging reliably raised awareness, in 8 of 11 studies. 📈Whether it changed behavior is still an open question, since almost no study measured behavior objectively. ✅ The one approach with a real behavior signal paired a personal risk profile with a short course, linked to about a 24% drop in risk factors. The barrier people named most often was knowledge, not motivation, and specifically not knowing what to do about their own risk. That is a personalization problem and one we are working on with the Younger Contest NeuroAge Therapeutics. Link to full post: drglorioso.substack.com/p/how-to-get-p…

Alzheimer's disease drug development pipeline: 2026 "There are 158 drugs for the treatment of Alzheimer's disease in the 2026 drug development pipeline.... 73% of drugs in the pipeline are disease targeted therapies whose goal is to slow disease progression... A diverse array of AD pathophysiological processes is being addressed by drugs in trials." alz-journals.onlinelibrary.wiley.com/doi/10.1002/tr…

Dental health and dementia prevention (new study) The scientific evidence behind brushing timing, mouthwash, fluoride, and the biological dentistry craze A new study of nearly 1,200 adults found that people with more of a compound their mouth and gut bacteria make had lower cognitive scores and higher Alzheimer's blood markers. It joins gum bacteria showing up inside Alzheimer's brains and large studies tying gum disease to dementia risk. Bottom line. So far this is a pattern in the data, and no study has yet shown that oral care prevents dementia, so the everyday habits carry stronger evidence for the teeth and gums than for the brain. A few things 👇 ⏱️ The routine six-month cleaning is not backed by strong evidence in a healthy mouth. Matching visits to your actual risk works as well as the fixed schedule. 💧 The drop in cavities across the last century tracks fluoride more than the brushing itself. Brushing without fluoride does little against decay. 🩸 Antiseptic mouthwash can wipe out mouth bacteria that help your body make nitric oxide, and some research links regular use to higher blood pressure. 🧴 Bad breath became a condition people worried about after a 1920s ad campaign presented it as a social problem, and Listerine itself began as a surgical antiseptic. 🧠 Plastic toothbrushes shed microplastics, which now show up in human tissue including the brain. A natural-bristle brush removes one source, though the effect on your overall plastic load is unproven. Good oral hygiene carries almost no downside and protects your teeth, gums, and heart whatever way the dementia prevention evidence breaks. Full post: drglorioso.substack.com/p/dental-healt… #BrainHealth #DementiaPrevention #OralHealth

RT @DrGlorioso: NeuroAge Therapeutics is announcing the Younger Contest- 6 months to lower your biological age in partnership with TruDiagn…

The micronutrient essential for brain health that 90 percent of people don't get enough of Almost 90% of us fall short on choline, the nutrient the brain turns into acetylcholine, its memory and attention signal. Don't overdo it though because the risk curve is U-shaped. A few choline facts: 🧠 Acetylcholine is the same messenger that anticholinergic drugs block and that Alzheimer's drugs try to raise. 📈 Dementia risk bottoms out at a moderate intake. Too little is worse, and so is the high end. 🩸 Choline status is hard to test, since the blood level holds steady. Liver enzymes and homocysteine are the closest proxies, and even those are rough. 🥚 One egg gives about a third of a day's target. Skip eggs and most people miss it. 🐟 Fish, poultry, soybeans, and legumes hit the target with little red meat. 💊 The choline supplements, citicoline and alpha-GPC, have some evidence once impairment is present, but none for preventing decline in healthy people. I carry an APOE4 allele, so I track this closely, and I aim for the 425 to 550 mg target from food rather than a pill. At NeuroAge we're studying how choline intake relates to brain aging in carriers. Link to full post: drglorioso.substack.com/p/the-micronut… #BrainHealth #Longevity #Alzheimers

People ask me all the time which medications to avoid if they want to protect their brain. So I sorted the common ones by how much we can trust the evidence, from clear harm to reassuring. The bottom line is that the everyday lever most people can actually act on is cumulative anticholinergic load, and most of those drugs have gentler swaps. 🍷 Heavy alcohol and methamphetamine sit at the severe end. 🧠 Anticholinergics taken for years carry the most consistent everyday signal. The common ones are diphenhydramine (Benadryl, ZzzQuil, the PM in Tylenol PM), oxybutynin for bladder, and amitriptyline. 😴 Benzodiazepines and Ambien show safety signals but these could be driven by the insomnia and anxiety they treat, not the drugs. ♀️ Menopausal hormone therapy looks protective started near menopause. The higher-risk signal came from an older oral formulation begun after 65, and modern bioidentical regimens have not been tested in that group. 💊 Several feared drugs look neutral or protective, including statins and blood pressure medications. Almost none of this comes from randomized trials, so the reasonable approach is to lower the exposures with the most consistent signals while leaving necessary medicines in place. As blood-based markers and brain aging clocks improve, I expect the next few years to finally test these associations directly, which is the work we are building toward at NeuroAge. Link to full post: drglorioso.substack.com/p/what-drugs-a… #BrainHealth #Dementia #Longevity

June is heating up with our COO, Michael Ringel, JD, PhD, attending @LongevityGL’s AI x Longevity Summit, the Digital Health & AI Innovation Summit, and @Georgetown’s H-Span Summit. Reach out to connect for more on our epigenetic restoration approach: bit.ly/3Z6qT9m

A single dose of psilocybin restored function (for at least a few weeks) in a woman with advanced Alzheimer’s disease 🧠 A case report published in Frontiers in Neuroscience on May 28, 2026 describes a late-stage Alzheimer’s patient recovering function following a “heroic” dose of psilocybin mushrooms. 🇧🇷 ⛪ The work came from the medical department of a São Paulo, Brazil association that public business records list as a religious or philosophical organization founded in 2025, with the senior author as its president- not under IRB so grain of salt is warranted. 👩‍🦳 The woman had chronic urinary incontinence, difficulty swallowing, flat affect, dependent mobility, and very little spontaneous interaction all of which reversed at least for the month or so they reported on. The effects started to fade at 1 month and they re-dosed her with 3 grams. 🐁 🧠 The idea that lost memories can be inaccessible rather than erased has a track record in mice. In 2007, Dr. Li-Huei Tsai's lab at MIT reopened access to old memories in mice with real brain atrophy, using an enriched cage with running wheels. In 2016, Dr. Susumu Tonegawa's group restored memories that looked gone by switching the cells that held them back on. My take. The interesting hypothesis is that part of what looks like permanent loss in late Alzheimer's may be a network access problem, not only tissue that is gone for good and psilocybin may be able to help it. Controlled trials in earlier-stage cognitive impairment are already running and will give us further insight. Full post: drglorioso.substack.com/p/a-single-dos…

The p-tau217 Alzheimer’s clock can now estimate when symptoms are likely to begin (new paper) In a new study in Nature Medicine, a team at Washington University in St. Louis built a model that estimates, from one blood draw, the age at which someone is likely to start showing Alzheimer's symptoms. A marker clinicians already use for diagnosis is starting to look like a timeline. The bottom line is that a single measurement of p-tau217 can now estimate when symptoms might begin within about three to four years. 🩸 p-tau217 is a tau molecule, but what drives its rise is amyloid, so it climbs early, around the time amyloid becomes detectable and well before tau tangles show up on a scan. ⏱️ In the study of 603 older adults, the model estimated the age of symptom onset within about three to four years, a bit like reading tree rings to tell how far along the process is. 📜 In 2025 the FDA cleared the first p-tau217 blood test to aid diagnosis, and in 2026 this work pushed the question from whether the disease is present toward roughly when symptoms may begin. 📉 The number is not fixed. Amyloid-clearing antibodies lower it by 35 to 39 percent, and even oral semaglutide moved tau-related markers, an early hint that the pathway can be reached. 🧬 No single marker carries the whole picture. p-tau217 is strongest read as part of a panel that also captures neurodegeneration and overall brain aging. The timing idea fits how I have long thought about brain aging, placing a person on a trajectory rather than sorting them into positive or negative. One finding I am still a little skeptical of is the claim that becoming positive later in life leaves less time before symptoms, because the age at positivity here was modeled rather than measured directly. I would want longer studies that follow the same people serially with p-tau217 before I take that one as settled. What does hold up is that the marker moves early and reads out from a simple blood draw, which is what prevention has needed. The real gains will come from layering markers rather than relying on one. Combining p-tau217 with neurofilament light and multi-omic signals, including the RNA-based brain aging clock we use at NeuroAge, should sharpen the estimate of where someone sits and where they are heading beyond what any single number can do. That layered, multi-omics direction is where I expect prevention to go. Full post: drglorioso.substack.com/p/the-p-tau217… #BrainHealth #Alzheimers #Longevity

1/4 Speaking at NYC AI x Longevity Summit during NYC Tech Week on Jun 4–5. I’m on the AI in Clinical Practice panel Thu 3:30–4:30p ET w/ @mishalreja, @NeilpDo + Jim Donnelly, hosted by @LongevityGL.

Will you be in NYC during @Techweek_? Don't miss the @LongevityGL AI x Longevity Summit on June 4-5, bringing together researchers, founders, investors, and more. Agenda and registration: ow.ly/eBQT50Z5JIw

Nootropics and neurorestoratives graded by the evidence The question I get most about brain supplements and drugs is about what works and what people should take. The simplest way to classify a compound is to ask what happens after you stop taking it. If the benefit disappears within days, it was tuning the function of circuits that were already intact, which makes it a nootropic. If the benefit holds, the intervention changed something durable about the tissue, its connectivity, its vasculature, or its cellular state, which makes it neurorestorative. Nootropics with best evidence in order: 1. Caffeine: blocks adenosine receptors to reduce the sense of fatigue and raise arousal, and it has more controlled trials behind it than any other cognitive enhancer, which makes it the reliable choice for alertness and sustained attention. 2. Caffeine with L-theanine: A 2025 meta-analysis of randomized trials found small-to-moderate improvements in attention and task switching. 3. Prescription stimulants- In people without ADHD a meta-analysis of 48 placebo-controlled trials found only small effects on inhibitory control and memory, and its authors noted that much of what healthy users feel may be improved energy and motivation rather than faster thinking. 4. Modafinil: A 2015 systematic review found measurable gains in attention and executive function in people who are not sleep deprived 5. Guanfacine: its effect is clearest in ADHD and minimal in healthy people 6. Creatine: A 2024 randomized trial found that a single high dose reduced the decline in processing speed and memory during overnight sleep deprivation, with a smaller effect in rested people. 7. Bacopa monnieri: A meta-analysis of nine trials found improvements in memory and attention 8. Nicotine: an agonist at nicotinic acetylcholine receptors, produces a measurable improvement in attention. 9. L-tyrosine, citicoline, alpha-GPC, and the racetams have thinner support, though not none. Neurorestoratives: 1. Aerobic exercise: in a one-year randomized trial in older adults, a walking program increased anterior hippocampal volume by about 2 percent, while the same region shrank by about 1.4 percent in the control group. 2. Speed-of-processing training: In the randomized ACTIVE trial in older adults it lowered the risk of dementia by roughly 29% over 10 years 3. Mindfulness meditation and 3D video game training: controlled studies found gray matter increases on MRI 4. Anti-amyloid antibodies: In phase 3 trials, lecanemab and donanemab slowed clinical decline in early Alzheimer’s 5. B vitamins: In the VITACOG trial, high-dose B vitamins in older adults with mild cognitive impairment and elevated homocysteine reduced atrophy in the gray matter regions most vulnerable to Alzheimer’s disease 6. Omega-3: a 2025 analysis from the DO-HEALTH trial showed slowing of several DNA methylation agin clocks Full post: drglorioso.substack.com/p/nootropics-a…

Just back from the Aging Code Summit during @Techweek_ If you've been watching longevity from the sidelines, this is where the actual conversation is. Omniscope is busy decoding the immune system, the definitive marker of health and aging. omniscope.ai/lifetime @LongevityGL

Longevity medicine has a major bottleneck. And it's not even the science. It's care delivery. Because most health decisions don’t happen in a doctor’s office. Spent the last two days at the Aging Code Summit in Cambridge with scientists, founders, investors, and clinicians working across biomarkers, therapeutics, AI, neurodegeneration, inflammation, regenerative medicine, and clinical trials. The discovery engine is real. But as a practicing longevity clinician, I kept thinking about the layer after discovery: How does any of this actually reach people? Not just the patient with time, money, and medical literacy. Not just the person who can find the right concierge doctor. And not just once a year, during a visit. People make health decisions every day: in grocery stores, gyms, group chats, supplement aisles, lab portals, algorithm feeds, and anxious 11pm searches. Most of those moments do not involve a physician. So if the future of longevity is “clone more doctors,” we’re going to fail. There will never be enough of us. And that’s not how people live. The real opportunity is to build better surfaces for healthcare: - tools that translate evidence into action - systems that support follow-through - guardrails against overtesting, overtreatment, and false certainty - care models that meet patients where they already are That’s the part I care most about building. Longevity needs great science. It also needs delivery models that make the science usable. @gocarecore Thanks so much to @LongevityGL for another amazing meeting, and fellow speakers, organizers, and attendees: @Mindvyne @3cubedAi @DrGlorioso @justinqtaylor @NeuroAgeTX @agingdoc1 @usnehal @CoreViva @agelessrx_ @kpfortney @bioagelabs @lifebiosciences @JamieHeywood @microbeminded2 @polybioRF @mahdi_moqri @agingbiomarkers @manoliskellis @MIT_Picower @DrDorisDay @VincereBio @InSilicoMeds @hevolution_f @CellinoBio @MariZazzer

@DrDorisDay Much fun to reunite with fellow longevity physicians and brilliant speakers @agingdoc1, Dr. Jay Luthar, @MariZazzer @LongevityGL - can't wait till our next panel together 💪

NeuroAge Therapeutics featured in Stat News article on Vitalist Bay. Body scans, blood tests, and bodyoids Most people in the longevity community are focused on preserving their health as long as they can — either to make it to the current outer limits of longevity, about 120 robust years or so, or to last long enough that science achieves what’s known as longevity escape velocity, where advancements keep piling up so that there’s no limit on how long life might last... I stopped to talk with NeuroAge founder and CEO Christin Glorioso, a neuroscientist who was inspired to start the company because her grandmother developed Alzheimer’s. (Peterson’s mother had Alzheimer’s too; it was a common thread among attendees.) Using brain MRIs and blood biomarkers, the NeuroAge tests aim to help give people the tools to prevent dementia with both data and recommended interventions. Glorioso said she’d been able to grow her own hippocampus 1.5%, which she credited to some combination of hormone replacement therapy, better sleep, statins, VO2 max training, Norwegian 4X4 high-intensity interval training, and GLP-1 drugs. Beside her was Stephen Hubbard, a buff director of business development at NeuroAge and leader of the Biotech Barbell Club, who was also leading weightlifting sessions elsewhere on the Lighthaven premises. I asked about the political breakdown of the longevity crowd, having just wandered away from a speech by the grandson of economist Milton Friedman about seasteading and charter cities. There were a fair amount of libertarians and some fans of the Make America Healthy Again movement, Hubbard said, though he did not count himself among their ranks. “Can’t we have sanity around vaccines and pullups?” he said. Whatever one’s goal, it was clear from the companies with booths set up at Vitalist Bay that there are ample opportunities in the business of longevity. Most of these were focused on personalized medicine. Along with Rythm ($79 a month), I spotted biological age testing company TruDiagnostic ($499 for a one-time test), brain age testing company NeuroAge ($1,398 for the most popular plan), and sleep testing company Empower Sleep ($1,200 for the basic plan)... What motivated many people at Vitalist Bay was not so much the chance to live forever, it seemed, but more freedom to enjoy all the different things that make them feel happy and fulfilled in abundance. For that, the typical human lifespan simply isn’t long enough. One ebullient woman at a weight-lifting session predicted she’d live about 5,000 years. I asked what she’d do with all those bonus millennia. “I don’t know,” she said. “But I’d like to find out.” Full article: statnews.com/2026/05/27/lon…

Exercise Timing and Your Chronotype I have historically been a night owl, and early-morning exercise left me yawning by 10am and depleted for the rest of the day. Also my Oura ring data flags my evening workouts as detrimental to recovery, showing suppressed overnight heart rate variability and elevated nocturnal resting heart rate, which leads me to feel pressured to shift my workout earlier on the assumption that exercising at night is harmful. What the science shows: 📱 📉 For Oura, WHOOP, or similar device users, suppressed HRV after evening exercise represents information about acute autonomic recovery rather than a verdict on long-term harm 🕐 Midday-afternoon exercise had lower all-cause mortality than morning-dominant timing in the general population 🌙 Evening exercise had the strongest mortality benefit in adults with obesity (61% lower) ⏰ The biggest risk signal was chronotype-exercise mismatch (early workouts in night owls, late workouts in larks) ⏱️ Learn your chronotype through MCTQ and/or genetic testing and match your workout to it Full post: drglorioso.substack.com/p/exercise-tim…