Not sure aging gets cured in my lifetime. I do know where the smart money's betting.

USA
Joined August 2026
Eye rejuvenation gene therapy's first human data: three patients. Phase 1 and open label, with all three patients on the lowest dose and 56 days of follow-up. No paper yet, only a talk at an eye meeting on October 8 and a release from a company that raised $80 million in April. Nothing is approved. ER-100, from Life Biosciences, uses three of the four Yamanaka factors to push old cells toward a younger state without wiping out what kind of cell they are. An antibiotic switches it on and off, and in mouse eyes the approach goes back to Harvard in 2020. Two of the three patients improved on the Humphrey visual field test. In each of those two, at least 28 percent of the tested points gained more than 4 decibels. Point-by-point visual field scores in glaucoma move around from one test to the next, and the scatter grows where the field is already damaged. None of the coverage I read sets those 4 decibels against that scatter, and the release doesn't either. TIME's headline said eye cells may have been rejuvenated for the first time in people. Epigenetic age was not reported for any patient, and there is no control group to compare against. No serious adverse events were reported at the lowest dose, and no dose-limiting toxicity. The safety board recommended moving to a dose three times higher, with no date given for it. Safety is the one thing a Phase 1 is built to show. That April money, per the company's own release, lasts into the second half of 2027. That gives it roughly a year to show the higher dose does more than the lowest one. In 2016 Salk scientists guessed human trials were up to ten years away. They were right on schedule. Ten years of mouse work, and the human number is still three.
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Who gets more years from the same healthy habits? The study is observational, not a trial: 33,541 adults 65 and older in China, followed for 20 years, published this year in Fundamental Research. It can show who gained. It cannot show why. Comparing the healthiest lifestyle with the least healthy at 65, people in the highest socioeconomic group gained 5.65 years of life expectancy. The lowest group gained 3.18. In healthy years the split was 3.90 against 1.40. Lifestyle explained about 20.5 percent of the gap in mortality between low and high status. The rest of that gap falls outside the lifestyle score entirely, and the abstract does not say what fills it. The authors do not draw the next conclusion; it is arithmetic on their numbers. The same habits that help everyone add almost twice as many years at the top, which means a lifestyle campaign on its own could widen the gap in absolute years while improving every group. Michael Marmot made a related point in a 2016 UCL lecture, about a Glasgow man whose life expectancy was 54. Quitting smoking, he said, might get him to 56. That is a problem for the corner of the longevity market that sells lifestyle as the main lever, from clinic packages to coaching apps. They are paid out of pocket, so their customers already come from the group that gains the most here. The study does not test that market, it only shows where the extra years went. It's an older Chinese cohort, with status built from education, finances and occupation. Transfer to US adults is an open question. In this data, healthy habits paid off in every group and paid the most to the people who already had the most.
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Twin-data model says genes explain half of lifespan variation. That is a model fitted to old twin records, not a direct measurement. Ben Shenhar of Uri Alon's lab at the Weizmann Institute published it in Science on January 29, 2026. The headline estimate is about 50%. Earlier twin studies put lifespan heritability at 20 to 25%, and family-tree studies came in near 10%. Shenhar's argument is that early deaths from infection and accidents drown the signal. Strip those out in simulation and the estimate roughly doubles. The preprint used Danish and Swedish twin registries covering births from 1870 to 1935, plus a Swedish cohort with 168 identical pairs raised apart. Its headline came out at 54%, with a standard error of about 0.03, once the cutoff age was set to 15. The final paper's numbers may differ. In the Swedish cohort the corrected estimate runs 33 to 45% at cutoff 50 and 48 to 58% at cutoff 15, so the answer depends on modeling choices. It is also a lifespan figure and does not tell how many of those years are healthy. The paper names no gene, and outside experts quoted by the Science Media Centre say the variants found so far explain only small fractions of lifespan variation. Heritability is a share of variation in one population at one time, and it fixes nothing about any single person. My read on the money: a heritability number tells a lab there is biology to find and tells a pitch deck nothing about a target. Any lifespan gene panel on sale today can read only the small mapped slice of that 50%. ARDD uploaded the talk this clip comes from on January 22, a week before the paper ran, and the slide footer still reads "In revisions." The slide shows the estimate rising to about 50% once extrinsic deaths come off. The next check is cohorts born later, with less extrinsic mortality. The model predicts the number rises, and the Swedish split in the talk shows it climbing to 30 or 40%.
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Twins born from 1870 to 1935, so the estimate describes that era. Video: "Ben Shenhar at ARDD2025: Heritability of human lifespan is about ~50% when confounding factors...", ARDD on YouTube, Jan 2026
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Younger skin, or just calmer eczema on the clock? That question sits under conference data from an early human trial, with no published paper behind it. Rubedo Life Sciences reported that its topical drug RLS-1496 lowered a skin epigenetic clock by a mean of 2.1 years after four weeks in people with eczema. Its best responder came out 11.7 years younger on day 63. Each patient was measured against their own starting point, eleven paired samples. The trial did have a placebo-cream group of four patients, but it was used for a blood inflammation marker and never for the clock. Those details come from Longevity Technology's report on the talk, and I found no Rubedo release or journal paper with the clock numbers. That missing comparison appears in its write-up and in none of the other coverage I read. The clock Rubedo used is MitraBio's, published in npj Aging and built for tape strips of facial skin. That paper reports an error of about four years for a single reading, and with no control arm, a 2.1-year average can't be separated from what calming the rash does to the sample. Eczema skin is full of immune cells, and when the inflammation settles, the mix of cells in a sample changes. Buck Institute CEO Eric Verdin told Wired he would probably be a little circumspect about what these clocks really measure. RLS-1496 targets senescent cells, the ones Mayo Clinic cleared in mice in the 2016 video attached here, extending life 25 to 35 percent. That's a mouse study. Ten years on, the human version of the headline rests on eleven samples compared with themselves. Rubedo closed a $40 million Series A in April 2024, led by Khosla Ventures and Ahren, and was pursuing a Series B as of February, per a trade interview. It also partners with Beiersdorf, the Nivea maker, so my guess is that the first buyer for a younger-skin claim is the cosmetics shelf. The registry lists this as a Phase 1 trial. Nothing is approved. RLS-1496 may still help eczema, and that alone would be a product worth having. A 2.1-year average shift in eleven people, with no control and a four-year error per reading, is a reason to run a proper trial, not a reason to buy a cream.
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If it helps eczema, that alone is worth the trial.
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Lifespan rose 25%-plus in some tests, none in mammals. Those tests ran on yeast and two kinds of tiny invertebrates, in a paper in Aging Cell at the end of September 2026. The compound, called 991, switches on AMPK, an enzyme the authors compare to a phone's energy saving mode. The paper has no mouse lifespan data at all. In mice the authors report a protein profile they call pro-longevity, and that is where the mammal data stops. One of the senior authors, Filipe Cabreiro, says the field is still a long way from anti-aging trials in humans. There is a specific reason for that caution. In 2017 Merck's pan-AMPK activator MK-8722 improved blood sugar in rodents and monkeys and also enlarged their hearts, as reported in Science. The release on 991 does not mention MK-8722, and none of the coverage I read does either. The authors do note that direct AMPK activators have been used safely in trials for metabolic diseases. A lifespan study runs far longer than a metabolic trial, and MK-8722 is why I would want the hearts examined. The video attached is a 2018 interview with Grahame Hardie, a Dundee biochemist whose lab helped map AMPK. He walks through the worm evidence linking AMPK to aging and calls a role in Alzheimer's disease still quite speculative. His caution from 2018 still fits a 2026 paper that never reaches a mammal's lifespan. Money is already moving around the target. Poxel sold its AMPK activator PXL770 on March 31, 2026, for $8 million upfront and up to $196 million with milestones, for a kidney disease rather than aging. Supplement shelves sell capsules labeled AMPK activator, under the standard note that the FDA has not evaluated the claim. What to check next is a mouse lifespan study with 991, which the team calls the next step, with the hearts examined at the end. Until it runs, the capsules on the shelf are ahead of the science by at least one species.
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$12,000 longevity package includes a test FDA hasn't approved. Weill Cornell Medicine's longevity program lists $12,000 for a year and $7,500 for a baseline assessment, both with a multi-cancer blood test, neither covered by insurance. No multi-cancer blood test is FDA-approved, and the only randomized trial of one missed its main goal. That trial is NHS-Galleri, 142,250 people aged 50 to 77. Its main goal was fewer late-stage cancers, stage III and IV together. On that goal, the screened group came out no different from the unscreened one. Stage IV alone fell 14 percent, a secondary measure. GRAIL, the company behind the Galleri test, put that drop in its headline. The miss on the main goal is in the line right under it. An FDA advisory panel voted 6 to 4 on September 23 that the test is effective, and the agency itself has not ruled. Weill Cornell does not name which test it uses, only a blood test that reads fragments of DNA floating in the blood. Its page says every recommendation is grounded in peer-reviewed research, links no studies, and warns that the test does not detect all cancers. The buyers are healthy people paying cash. As reported by STAT on October 6, Northwestern runs a similar program at $5,500 a year, and prices across hospital longevity clinics reach $45,000 a year. None of the coverage I read connects these package prices to the trial result or to the decision FDA has not made yet. What's really being sold is the hospital's reputation. Whoever makes the test gets a prestige channel before any approval. The hospital gets a cash product outside insurance, and the evidence question waits for FDA. A randomized trial says the test finds some cancers earlier. It has not shown that earlier finding moves the outcome it was built to move. Until it does, $12,000 buys a well-run checkup with a hospital's name on it.
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Healthspan Edge retweeted
Did Ozempic slow aging, or did the lost pounds? None of this is peer reviewed yet. Novo Nordisk's semaglutide data is a preprint, and Eli Lilly's tirzepatide data was a conference talk at ARDD in Boston last week. Novo pooled blood from 10,052 people in five placebo-controlled trials and ran it through proteomic clocks, blood-protein scores trained to estimate each organ's risk of dying. Heart age came out about 2 to 4 years younger on the drug. These were high-risk patients from heart and kidney trials, followed for up to three years. Lilly's version is thinner. Per a write-up of Kevin Duffin's talk, the tirzepatide data comes from SURMOUNT-5, and the clocks were checked against the calendar. Over those 1.38 years, all 15 epigenetic clocks ticked forward by less than the calendar did. SURMOUNT-5 ran 72 weeks against Wegovy with no placebo arm, so no untreated group existed to compare against. MIT Technology Review described both results as drug against placebo, and none of the coverage I read notes that Lilly's trial had no placebo to beat. Neither data set measured how long anyone lived. SELECT, the largest of Novo's five trials, cut major heart events by 20%, and that is a real outcome. The clock is a forecast of outcomes, and the preprint's authors write that their result does not establish rejuvenation. Weight loss can move aging clocks too. In 22 bariatric surgery patients, one DNA-based clock showed 4.29 fewer years of excess aging within a year of the operation. Novo's preprint says weight loss does not fully explain its effect, a claim no reviewer has checked. Tirzepatide brought Lilly about $36.5 billion in 2025. Per the same write-up, one of the two labs that replicated Lilly's clock readings was TruDiagnostic, which sells epigenetic age tests to consumers. Vadim Gladyshev, who helped Novo with the measurements, told MIT Technology Review that for healthy people, no one knows whether it is an anti-aging drug. The trial built to answer that, VITAL-H at UT Health San Antonio, will test semaglutide and two other approved drugs against placebo in 726 adults in their 60s. ARPA-H is paying up to $38 million, and enrollment is planned for 2027. What to check next is whether the Novo preprint survives peer review with its weight-loss adjustment intact. Until then, the drug half of those 10,052 patients looks younger than the placebo half on a clock built to predict death, and that is as far as the data goes.
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Did Ozempic slow aging, or did the lost pounds? None of this is peer reviewed yet. Novo Nordisk's semaglutide data is a preprint, and Eli Lilly's tirzepatide data was a conference talk at ARDD in Boston last week. Novo pooled blood from 10,052 people in five placebo-controlled trials and ran it through proteomic clocks, blood-protein scores trained to estimate each organ's risk of dying. Heart age came out about 2 to 4 years younger on the drug. These were high-risk patients from heart and kidney trials, followed for up to three years. Lilly's version is thinner. Per a write-up of Kevin Duffin's talk, the tirzepatide data comes from SURMOUNT-5, and the clocks were checked against the calendar. Over those 1.38 years, all 15 epigenetic clocks ticked forward by less than the calendar did. SURMOUNT-5 ran 72 weeks against Wegovy with no placebo arm, so no untreated group existed to compare against. MIT Technology Review described both results as drug against placebo, and none of the coverage I read notes that Lilly's trial had no placebo to beat. Neither data set measured how long anyone lived. SELECT, the largest of Novo's five trials, cut major heart events by 20%, and that is a real outcome. The clock is a forecast of outcomes, and the preprint's authors write that their result does not establish rejuvenation. Weight loss can move aging clocks too. In 22 bariatric surgery patients, one DNA-based clock showed 4.29 fewer years of excess aging within a year of the operation. Novo's preprint says weight loss does not fully explain its effect, a claim no reviewer has checked. Tirzepatide brought Lilly about $36.5 billion in 2025. Per the same write-up, one of the two labs that replicated Lilly's clock readings was TruDiagnostic, which sells epigenetic age tests to consumers. Vadim Gladyshev, who helped Novo with the measurements, told MIT Technology Review that for healthy people, no one knows whether it is an anti-aging drug. The trial built to answer that, VITAL-H at UT Health San Antonio, will test semaglutide and two other approved drugs against placebo in 726 adults in their 60s. ARPA-H is paying up to $38 million, and enrollment is planned for 2027. What to check next is whether the Novo preprint survives peer review with its weight-loss adjustment intact. Until then, the drug half of those 10,052 patients looks younger than the placebo half on a clock built to predict death, and that is as far as the data goes.
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Healthspan Edge retweeted
Observational data: wealth falls six years before dementia. The study is an NBER working paper, not yet peer-reviewed, so treat it as early evidence. It tracked 2,312 Americans classified as developing dementia and 8,431 who didn't, using survey data from 2000 to 2016, and the two groups' wealth starts to split about six years before onset. At onset the gap is about $124,000, and about 63 percent of it is financial wealth, mostly money held in investment and bank accounts. Eight years out the groups differed by about $30,000, a gap too small to be statistically meaningful, and it barely moved until year six. Earnings barely move: at onset the gap is $947. Before onset, out-of-pocket medical bills run about $1,000 to $1,600 a year higher, too little to explain it. Retirement accounts like IRAs, which are hard to touch, show no relative change, and none of the press coverage I read mentions that result. Onset here comes from a statistical model built on memory test scores. No doctor made that call, and the NBER's own summary still puts "before dementia diagnosis" in its title. It fits earlier work. A JAMA Internal Medicine study of 81,364 Medicare beneficiaries found missed bill payments up to six years before diagnosis, though the absolute gap at that point was 7.7 percent against 7.3 percent. Brokerages already have rules for this. Since 2018 FINRA lets them put an initial hold of up to 15 business days on a payout from the account of a customer 65 or older if they suspect someone is exploiting that customer. Account-watching subscriptions for older people start around $7.49 a month. Healthspan is usually told as a medical story. Mayo Clinic researchers put the US gap between lifespan and healthy lifespan at 12.4 years, the widest of 183 countries, and this paper suggests part of the cost lands in household money years before onset. The six-year timing looks solid; the cause is inferred by ruling out alternatives, as the authors write themselves. The money that held up was the money that was hardest to get at.
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Observational data: wealth falls six years before dementia. The study is an NBER working paper, not yet peer-reviewed, so treat it as early evidence. It tracked 2,312 Americans classified as developing dementia and 8,431 who didn't, using survey data from 2000 to 2016, and the two groups' wealth starts to split about six years before onset. At onset the gap is about $124,000, and about 63 percent of it is financial wealth, mostly money held in investment and bank accounts. Eight years out the groups differed by about $30,000, a gap too small to be statistically meaningful, and it barely moved until year six. Earnings barely move: at onset the gap is $947. Before onset, out-of-pocket medical bills run about $1,000 to $1,600 a year higher, too little to explain it. Retirement accounts like IRAs, which are hard to touch, show no relative change, and none of the press coverage I read mentions that result. Onset here comes from a statistical model built on memory test scores. No doctor made that call, and the NBER's own summary still puts "before dementia diagnosis" in its title. It fits earlier work. A JAMA Internal Medicine study of 81,364 Medicare beneficiaries found missed bill payments up to six years before diagnosis, though the absolute gap at that point was 7.7 percent against 7.3 percent. Brokerages already have rules for this. Since 2018 FINRA lets them put an initial hold of up to 15 business days on a payout from the account of a customer 65 or older if they suspect someone is exploiting that customer. Account-watching subscriptions for older people start around $7.49 a month. Healthspan is usually told as a medical story. Mayo Clinic researchers put the US gap between lifespan and healthy lifespan at 12.4 years, the widest of 183 countries, and this paper suggests part of the cost lands in household money years before onset. The six-year timing looks solid; the cause is inferred by ruling out alternatives, as the authors write themselves. The money that held up was the money that was hardest to get at.
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Who backed the $173 billion longevity drug forecast? That figure comes from a forecast model by a trade publisher, reviewed by experts the publisher chose, outside any journal. Longevity Technology's Longevity Biotech Report came out last month. It projects $173 billion a year in extra revenue for drugs aimed at aging itself, once regulators create a way to approve them, which it models from around 2035. The publisher says the report was supported by MuseCell Innovations. MuseCell sells stem cell products given by IV only through authorized clinics, and its own site says the products "have not been evaluated or approved" by the FDA. None of the coverage I read connects that disclaimer to a forecast that only pays out through the FDA. That approval route does not exist yet for people. Neither the FDA nor Europe's regulator has a category for aging, and the report says so itself. At the ARDD conference in Boston last week, FDA officials said aging will feature in the agency's next update of research priorities, due in the coming months, and sketched trial designs but no formal approval pathway. The only lifespan drug to clear an FDA effectiveness step so far is for large dogs, Loyal's, in 2023. The $173 billion is also easy to confuse with a much bigger number. The longevity economy, the economic activity of people over 50, came to $45 trillion in 2020 by AARP and Economist Impact's estimate, about 34 percent of global GDP. That money exists today, while the $173 billion waits on a rule. Investment is real and much smaller: $18.4 billion into longevity biotech in 2025 and $12.1 billion so far in 2026, by the same publisher's count. The publisher also sells the dataset behind those numbers. Sponsorship does not make the model wrong, and the publisher says it kept editorial control. The condition is the weak part. The headline number depends on a decision no regulator has made, and it travels without that condition attached. Without a pathway, $173 billion describes a policy outcome, not a market. That FDA update, due in the coming months, is the next thing to read for any way to measure aging in a trial, and the $173 billion forecast rests on what it says.
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$173 billion is conditional on pathways modeled from around 2035.
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Mouse anti-aging molecule shows up in human diabetes data. The anti-aging result is a mouse study, published in Nature Aging in late August. Researchers in Beijing gave naturally aged mice either a gut bacterium (Bifidobacterium pseudocatenulatum) or a molecule it makes, 5-AVAB, and reported that inflammation fell in six organs. The human part was observational only: in Chinese cohorts, older people simply had less of the bacterium and the molecule. The institutional release said the bacterium was found to "delay aging." The abstract itself calls the bacterium a candidate and says the molecule alone only partially reproduced its effects. 5-AVAB turns up in other journals under a second name, delta-valerobetaine. In a 2023 Nutrition and Diabetes study, 143 people with overweight or obesity were followed for 18 months after a weight-loss program. Those with higher levels were more likely to develop diabetes, an odds ratio of 3.26. In the top third, 35.4 percent saw their glucose status worsen; in the bottom third, 17 percent. That is an association study, not a trial. A 2021 Nature Metabolism paper went further in mice. On a Western diet, the molecule increased visceral fat and worsened fatty liver. In people, levels were higher with obesity and tracked visceral fat. I want to be precise about my objection. Nobody hid anything here; these are separate literatures, in different populations and models. But a molecule presented as a youth signal in one journal and flagged as a metabolic risk in two others is not ready for a capsule. The capsule market does not wait for that. Novonesis, one of the biggest probiotic suppliers, grew its human health sales 10 percent organically in 2025, to roughly $584 million, led by North America. The business that should exist here is unglamorous: independent screening of a strain's own metabolites against the published risk literature before a longevity claim goes on the bottle. Six organs looked calmer in old mice. The number I would want explained first is 3.26.
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Healthspan Edge retweeted
Growth signaling cut, female mice lived 8 percent longer. Mouse study, out this September in Aging Cell from John Kopchick's lab at Ohio University. The receptor for growth hormone was switched off at 12 months, roughly middle age, in 30 to 35 animals per sex per group. In females, median lifespan rose 8 percent, from 929 to 1,003 days. The p value was 0.049, just under the usual 0.05 cutoff for calling a result significant. Males gained 7 percent, which did not reach significance on that measure. The paper's title says it extends healthy lifespan. In females, the healthy part did not show up: no gains in grip strength, balance, frailty or bone. Males improved on insulin sensitivity, grip and balance, and both sexes carried more body fat. Anti-aging clinics have sold growth hormone injections for years, pushing that signal up. These mice lived longer with it turned down. In the US, distributing growth hormone for anti-aging is a federal felony. The classic version, mice born without the receptor, has been one of the most replicated lifespan results in mammals since the late 1990s. Switching the receptor off in midlife, the only timing a human drug could realistically copy, gives a much smaller effect. Humans with the same receptor defect exist. In Ecuador, about 100 people born with it (Laron syndrome) were followed for 22 years, and none developed diabetes, against 5 percent of their relatives. Cancer appeared once, and it was not fatal, against cancer in 17 percent of relatives. They did not live longer, mostly because of accidents, alcohol and other causes unrelated to age. This is observational data, not a trial. So the pathway with nearly three decades of mouse data, switched off in midlife, produces a modest, borderline result. Meanwhile the field's hottest idea, cell reprogramming, got New Limit $435 million in June at a $3.1 billion valuation, with no human data yet and a first trial planned for 2027. A drug that turns growth hormone signaling down in midlife without the extra fat would be a real business. That is a concept. Nobody has one built for aging yet. A modest effect in one cohort of mice, with a cost attached. An 8 percent gain in one sex at p equal to 0.049 is a reason to repeat the experiment, and not a reason to buy anything a clinic is selling.
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Growth signaling cut, female mice lived 8 percent longer. Mouse study, out this September in Aging Cell from John Kopchick's lab at Ohio University. The receptor for growth hormone was switched off at 12 months, roughly middle age, in 30 to 35 animals per sex per group. In females, median lifespan rose 8 percent, from 929 to 1,003 days. The p value was 0.049, just under the usual 0.05 cutoff for calling a result significant. Males gained 7 percent, which did not reach significance on that measure. The paper's title says it extends healthy lifespan. In females, the healthy part did not show up: no gains in grip strength, balance, frailty or bone. Males improved on insulin sensitivity, grip and balance, and both sexes carried more body fat. Anti-aging clinics have sold growth hormone injections for years, pushing that signal up. These mice lived longer with it turned down. In the US, distributing growth hormone for anti-aging is a federal felony. The classic version, mice born without the receptor, has been one of the most replicated lifespan results in mammals since the late 1990s. Switching the receptor off in midlife, the only timing a human drug could realistically copy, gives a much smaller effect. Humans with the same receptor defect exist. In Ecuador, about 100 people born with it (Laron syndrome) were followed for 22 years, and none developed diabetes, against 5 percent of their relatives. Cancer appeared once, and it was not fatal, against cancer in 17 percent of relatives. They did not live longer, mostly because of accidents, alcohol and other causes unrelated to age. This is observational data, not a trial. So the pathway with nearly three decades of mouse data, switched off in midlife, produces a modest, borderline result. Meanwhile the field's hottest idea, cell reprogramming, got New Limit $435 million in June at a $3.1 billion valuation, with no human data yet and a first trial planned for 2027. A drug that turns growth hormone signaling down in midlife without the extra fat would be a real business. That is a concept. Nobody has one built for aging yet. A modest effect in one cohort of mice, with a cost attached. An 8 percent gain in one sex at p equal to 0.049 is a reason to repeat the experiment, and not a reason to buy anything a clinic is selling.
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Plasma swaps cut 2.61 years of biological age, briefly. That's a 42-person pilot in adults over 50, published in Aging Cell and measured on aging clocks in the blood rather than on disease or lifespan. And the company selling the procedure advertises the result at exactly the point where it disappeared. The procedure is therapeutic plasma exchange: blood is drawn and its plasma swapped out for a 5% albumin solution before the blood goes back in. Circulate Health funded the study, and three of the authors are Circulate members. Circulate's site advertises "an average 2.6-year reduction in biological age after just six TPE sessions." Six sessions is where it breaks. The 2.61 comes from the measurement after session four, in the group that also got IVIG, pooled donor antibodies given by infusion. After session six, the preprint of the same trial reports no significant difference from a sham procedure in any group. The published paper leads with the earlier timepoint, and the authors suggest the body compensates. In August Viome bought Circulate, and the acquisition release repeats the 2.6. Sessions have run about $8,000 to $10,000 each by GeekWire's reporting, so a six-session course comes to roughly $48,000 to $60,000. Next Health sells its own six-session bundle for $45,000. My objection is narrow. Plasma exchange is an established procedure for specific diseases, and this single-blind trial logged one mild allergic reaction across 240 procedures. The Mayo Clinic clip in the first comment shows that established use, with neurologist Brian Weinshenker on multiple sclerosis and neuromyelitis optica: 1:13 the clinical background 3:04 the plasma exchange itself The objection is to the number: a lab clock instead of health outcomes, about ten people in each of four groups, a headline figure that needed IVIG, and an effect that did not survive to the session count the sales page advertises. What would settle it is a larger sham-controlled trial, run by people who do not sell the sessions, that still shows the drop after session six. Until somebody runs it, 2.61 is a four-session number.
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2.61 is from session four. The sales page says six.
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Healthspan Edge retweeted
Dead bacteria made old mice look younger on paper. Nature Aging published the study on September 24, 2026. It comes from Jing-Dong Han's lab at Peking University, and the organism is Neisseria flavescens, a bacterium that already lives in your mouth. No human picked this bacterium. The team built an AI aging clock they call AURORA, had it model what would happen if you added or removed each microbe, and this one came out on top as the predicted winner. Screening by model is normal practice and fine on its own. What matters is what the screen got followed with. In people, nothing. The human data is associative, with no intervention at all. The closest thing to a longitudinal check tracked 132 participants over a year, and it is still a correlation. And in the study's own supplementary figures, when they ranked people directly by how old they looked biologically, N. flavescens did not come out as a top correlate. The headline exists because the model put it there. In worms, live bacteria did extend lifespan and healthspan. Movement was scored on 30 worms per group. In mice it gets thin. Heat-killed bacteria, ten weeks, 20-month-old animals, six per group and five in some panels. Blood chemistry and liver gene activity shifted toward the patterns of younger mice, and the gut bacteria shifted too. Survival was never measured, and there is no mouse lifespan curve anywhere in the study. Food intake was recorded per cage with no statistics run on it. The supplementary notes say the P values weren't corrected for testing many things at once, which is how findings that aren't there get published. The authors' own figure title calls the reversal partial. Worms got live bacteria and mice got dead ones, and the sections I can read don't say why the switch was made. That's the first thing I'd want answered. No company is attached to this, and no investor. The funding is Chinese public money. The one commercial fact in the study is a pending patent, number 202611084872X, filed by the senior author and a colleague and not yet publicly viewable. It was filed before a single human had been given anything. The selling started years ago regardless. Viome runs a $399 test that reads your oral microbiome and hands back a biological age score, plus lozenges at $79 a month on subscription. Pendulum sells Akkermansia muciniphila for $54, and Akkermansia turns up inside this very study as a loose correlation rather than a result. Bristle sells a $169 oral microbiome test and makes no aging claim at all, which deserves credit. Keep the two markets apart. The longevity economy means everything sold to older people, and it is enormous. Biotech that actually treats aging is a much smaller thing that mostly hasn't worked yet. The products above sit in the first market while borrowing the language of the second. There's a history here too. In 2018 this same bacterium was pulled from gastritis patients and written up in Current Microbiology as a possible pathogen, with the authors asking someone to study whether it causes disease. Nobody appears to have run that study, and nobody has established what a live strain does in a person. This is worth watching and not worth buying. An AI model nominated the bacterium, worms lived longer on it, and six old mice per group had younger-looking blood work after ten weeks of dead cells. That's a hypothesis with a patent attached, and the readout that matters is whether anyone runs it in living humans. Zero survival curves in the study. One $399 test already on the shelf.
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