The Arising: Health Intelligence

Keto Diet Raised Small Intestine Tumors in Cancer-Prone Mice, MIT Finds

A ketogenic diet sped up tumor growth and shortened survival in mice bred to develop intestinal cancer, according to a new study in Nature, and the cause was not the ketones that the diet is named for.

This is animal research. The authors used mouse models of spontaneous intestinal adenoma formation, meaning the animals were genetically prone to developing these growths. The abstract, the only part of the paper available to us, does not give the number of animals. It also does not say how long the mice were fed the diets. No people were studied.

The question matters because ketogenic diets are popular for weight loss and are sometimes promoted for longevity. They are very high in fat and very low in carbohydrate. The researchers point out that obesogenic high-fat diets are already known to boost the activity of small-intestinal stem cells and tumor formation.

Ketogenic diets contain even more fat, but they also lower circulating insulin and raise ketones. Their effect on intestinal cancer has been poorly understood.

According to the study, the ketogenic diet accelerated tumor burden and shortened survival, regardless of ketone metabolites. The team changed the ketone-making pathway in several ways. They blocked or boosted a key ketogenic enzyme, known as HMGCS2, and they disrupted the breakdown of ketones. None of these changes altered tumor development. That points away from ketones as the driver.

The evidence points instead to how intestinal cells handle dietary fat. When the researchers removed three related fat-sensing proteins (PPARα, PPARδ and PPARγ) from the intestine, the diet's effects on stem cells weakened. Stem cell expansion, proliferation and the ability to form colonies all dropped. Removing an enzyme called CPT1A, which is needed to burn fatty acids, limited adenoma formation specifically on the ketogenic diet. The authors conclude that tumor initiation is linked to burning dietary fat, not to fat simply building up.

The press coverage went further than the abstract in places. According to ScienceDaily, which summarized an MIT release, the small intestine and the colon responded in opposite ways. The ketogenic diet suppressed colon tumors in the mice. The coverage also says the keto-fed mice did not become obese, yet had tumor rates similar to or higher than mice on a high-fat, high-calorie diet. Those details are not in the abstract, so we cannot check them against the study text.

"Ketogenic diets have distinct effects on different tissues even within the gastrointestinal tract," senior author Omer Yilmaz of MIT told ScienceDaily. "What might be beneficial for one tissue may be detrimental for another tissue."

What does this mean for personal choices? The findings come from genetically engineered mice and may not carry over to people with ordinary cancer risk. The study does not show that keto causes cancer in humans. The authors single out people with familial adenomatous polyposis, an inherited condition with a high risk of small-intestinal tumors. They call for careful thought about diet and cancer prevention in genetically susceptible groups. Nobody should start or stop any diet, treatment or supplement without talking to their clinician, and that applies especially to anyone with an inherited intestinal cancer condition.

The study also bears on ketone supplements. According to ScienceDaily, because the effects tracked fat metabolism rather than ketones, ketone drinks would not be expected to reproduce either the harm in the small intestine or the benefit in the colon. That is the coverage's inference, not a test reported in the abstract.

The next step is to learn why the same diet pushes neighboring parts of the gut in opposite directions. Researcher Fangtao Chi told ScienceDaily that this is what the team is working on. Human data on ketogenic diets and intestinal tumors, especially in people with inherited risk, will be the key thing to watch.

Sources: Nature (2026), ScienceDaily (MIT; Nature)

Primary study · Additional reporting

Study Projects 24.7 Million New Dementia Cases in 2050 if Rates Hold

About 24.7 million people worldwide could develop dementia in 2050, according to a new analysis in JAMA Neurology, if today's rates hold. The abstract gives no 2023 baseline, so we cannot say from it how much that figure exceeds today's, and the study finds the risk is not spread evenly across the globe.

The work is an observational study, not a trial. Researchers pooled individual- level data from 22 population-based cohorts in the Cohort Studies of Memory in an International Consortium (COSMIC). The cohorts included 38,418 people in 18 countries or territories on six continents. Participants were followed through the end of 2021. Observational work can show how often dementia occurs. It cannot show why.

Across 287,632 person-years of follow-up, 3,001 participants developed dementia. Aperson-year is one person followed for one year. All diagnoses were clinically based.

After adjusting for age and sex, the overall rate was 9.7 new cases per 1,000 person- years. The 95% confidence interval ran from 7.89 to 11.97. In plain terms, that is roughly 10 new cases for every 1,000 people followed for a year. The researchers standardized the figure to the 2023 global age and sex makeup of the population.

Women had a higher rate than men: 10.6 versus 8.6 per 1,000 person-years. Low- and middle-income countries had a higher rate than high-income countries: 13.6 versus 8.3. The confidence intervals in both comparisons overlap, so the exact size of these

gaps is uncertain. The abstract does not say whether the differences passed a formal test.

The 24.7 million figure comes from applying today's age- and sex-specific rates to the projected 2050 population. It assumes incidence stays constant over time. So it is a projection of what the same rates would mean in a larger and older world, not a forecast that individual risk will climb. Whether rates rise or fall is unknown.

Because the abstract does not give the 2023 baseline, any claim that cases will "double" rests on a comparison we could not verify here.

The authors say many earlier estimates underrepresented low- and middle-income countries and used mixed methods. They describe these harmonized figures as a comparable benchmark. They say it can inform planning for prevention, diagnosis and memory-care services, especially in those underrepresented settings.

What does this mean for individuals? The study did not test any way of lowering dementia risk. It cannot say which habits or treatments help. What it does show is that dementia is common, and that the number of new cases will grow with ageing populations unless rates fall. Prevention planning is the use the authors point to.

Advice on individual risk reduction is outside what this analysis tested, and this is the weakest point of any personal takeaway. The full text was not available to us, so details beyond the abstract are unverified.

Watch next for studies that track whether dementia incidence is falling or rising within countries over time. That would test the constant-rate assumption behind the 2050 projection.

Sources: JAMA Neurology (2026), Medical Xpress (reporting on JAMA Neurology, UNSW Sydney)

Primary study · Additional reporting

Study of 300 Million Lab Tests Finds Abrupt Body Changes at Menopause

Menopause may change the body more suddenly than doctors have long thought. A new analysis of routine blood tests reports a sharp, step-like shift in several body systems at a woman's final menstrual period, and that finding is already being challenged.

The work was published in Nature Medicine in 2026. It is an observational, cross-sectional analysis of existing laboratory data from two independent cohorts, totalling 300 million laboratory tests. It is not a clinical trial. Nobody was assigned to a treatment, so the results show patterns, not cause and effect. We had access only to the study's abstract, so details beyond it are not covered here.

The problem the authors set out to solve is a practical one. Most of what we know about menopause comes from small studies that follow women over time. These have tended to describe menopause as a gradual transition. Large medical databases hold far more data, but they rarely record the age at which a woman had her final menstrual period. Without that, the data cannot be lined up around the event.

The researchers built a computational method, which they say was inspired by astronomy, to get around this. Women reach their final period at different ages.

Averaging across them blurs any sharp change into a smooth slope. The method reconstructs trajectories anchored to the final period, removing that blurring.

Using it, the authors report a step-like physiological "cliff" at the final menstrual period. It appeared in the endocrine (hormone), skeletal, hepatic (liver), renal (kidney) and lipid (blood fat) systems. In plain terms, that covers sex hormones, bone, liver and kidney measures and cholesterol-type fats.

Three other findings stand out. The same jumps were absent in men. They were concordant across the two populations studied. And they appeared markedly attenuated in women using menopausal hormone therapy. The authors also report that dysregulation began more than a decade before the final period, with sex hormone changes starting more than 10 years before menopause.

For You

For personal health, the point is timing. If changes begin a decade or more early, the years before the final period may matter for bone and metabolic health, not only the years after. The abstract does not say what screening or treatment schedule should follow. That question is where the debate lies. Readers should not start or stop any medication or hormone therapy without speaking to their clinician.

ABC News (Australia), which reported on the study, quoted its lead, Uri Alon of the Weizmann Institute in Israel. According to ABC, he said bone density is usually checked around age 60, and that the findings would support checking around 40 or 45 and then considering hormone therapy as prevention, on a physician's advice.

That recommendation comes from the coverage, not the abstract. The abstract reports that hormone therapy users showed smaller changes. It does not test whether starting therapy earlier protects bones.

Australian experts quoted by ABC were unconvinced by the framing. Martha Hickey of The Women's Hospital in Victoria said "physiological cliff is not a scientific or medical term" and called the claim "unnecessarily alarming". Elina Safro of the Australasian Menopause Society said the cliff idea is "not plausible". ABC noted that the study used existing data and self-reported information about the last period, unlike the long-running SWAN study, which was designed to follow women through the transition. Hickey described retrospective studies as "poor-quality" and not designed to answer this question, and Safro agreed. ABC also reported Hickey's caution that healthier women may be more likely to use hormone therapy, which could affect comparisons.

Where the critics and the study agree is on the value of earlier attention. ABC reported that Safro saw the early start of change as a reason to stay alert to health in midlife. Ada Cheung of the University of Melbourne said menopause is a good time to review bone health, cholesterol, blood pressure and blood sugar. Those points reflect the experts' views, not new findings.

What To Watch Next

Alon told ABC his team is planning a clinical trial of hormone therapy started before the final period, which would be a far stronger test of whether earlier treatment protects bone and other systems.

Sources: Nature Medicine (2026), ABC News (Australia), reporting on a Nature Medicine study

Primary study · Additional reporting

Gut Bacteria Fatty Acid C15:0 Halved Artery Plaque in Mice

A fatty acid made by a common gut bacterium cut artery plaque by around 50% in mice, according to a study in Nature. It is an early result, and it is not a reason for anyone to stop a prescribed statin, start a C15:0 supplement, or make any other change to their treatment without talking to their clinician.

This is animal research. The authors used a mouse model of atherosclerosis, the build-up of fatty plaque in artery walls. The abstract available to us does not give the number of animals, so we cannot report group sizes. The work also included human comparisons, but these were observational: they looked at differences between patients and healthy people, not at a treatment given to people.

The starting point was a known pattern. Bacteroides, a dominant genus in the human gut, is depleted in patients with atherosclerosis. Until now it was unclear whether that loss was a cause of the disease or just a sign of it. In mice, the researchers report, giving one species, Bacteroides uniformis, eased atherosclerosis.

They link this to higher levels of the LDL receptor in the liver. That receptor pulls LDL cholesterol, the harmful kind, out of the blood.

The team then screened for the bacterium's active ingredient. They identified pentadecanoic acid, also called PA or C15:0. It is a saturated fatty acid with an odd number of carbon atoms. According to the study, PA supplementation reduced

plaque burden by around 50% and significantly improved plasma lipid profiles in the mice.

The proposed mechanism is familiar. The authors report that PA directly inhibits HMG-CoA reductase, the liver enzyme that statin drugs target. That slows the liver's own cholesterol production and helps clear LDL cholesterol from the blood. The authors describe this as gut–liver crosstalk, meaning chemical signals from gut microbes that change how the liver handles cholesterol.

Two further findings add context. Across 100 gut bacterial strains, PA production occurred in multiple genera within the Bacteroidota group, not just one species. And PA was markedly depleted in patients with dyslipidaemia, meaning unhealthy blood fat levels. That last finding is an association. It does not show that low PA causes high cholesterol, or that raising PA would fix it.

The study's own wording is cautious about benefit. It says the work underscores PA's "therapeutic potential" and that changing the microbial–metabolic axis has "atheroprotective potential". It does not claim a treatment.

The coverage went further in places. Lifespan.io, which reported on the paper, called the molecule a "natural statin". It also said atorvastatin, a widely used statin, worked noticeably better than C15:0 at the same dose in the mice. It added that C15:0 appears to be a weaker inhibitor of the enzyme. These comparisons come from Lifespan.io's account, not from the abstract we reviewed. Lifespan.io also noted, about the 12- week B. uniformis experiment, that results were compared with vehicle-fed controls at the end rather than with baseline. That shows slowed plaque growth, not necessarily reversal. We do not know whether the same applies to the C15:0 experiment.

That is why this matters for personal choices. C15:0 can be bought as a supplement, but nothing here shows that taking it helps people's arteries. Mouse doses, gut absorption and long-term safety in humans are all untested in this work. Lifespan.io put it plainly: "it is not clear that C15:0...is superior to statins in any way." Statins have large human trials behind them. Anyone prescribed one should talk to their doctor before changing it, and anyone considering a C15:0 supplement should talk to their clinician before starting it.

The more useful takeaway is the direction of the science. Gut bacteria may help set cholesterol levels through the molecules they make. If that holds up, it could eventually lead to new ways to support heart health. Lifespan.io quotes study co-

author Wenjing Zhao of Sun Yat-sen University as saying the findings underline new ways the microbiome might be harnessed to protect the heart. Lifespan.io itself adds that more studies, especially in humans, are needed.

What To Watch Next

Human trials that test whether raising C15:0, or the bacteria that make it, lowers LDL cholesterol safely, and how that compares with statins.

Sources: Nature (2026), Lifespan.io (reporting on a study in Nature)

Primary study · Additional reporting

AI Reading Heart Signals During Sleep Studies Predicts 10-Year Cardiovascular Risk

A night in a sleep lab already records the heart. Researchers now report that a computer model reading those rarely examined heart traces can help estimate a person's risk of atrial fibrillation, heart failure and early death over the next 10 years.

The work was published in the journal SLEEP in 2026. It is a retrospective study of patient records from three U.S. hospitals, not a trial. The model was fine-tuned on 15,809 patients at Massachusetts General Hospital. It was then tested on two separate groups: 9,810 patients at Emory University Hospital and 12,576 at Beth Israel Deaconess Medical Center. Outcomes came from electronic health records, using diagnosis codes.

The recordings come from polysomnography, the overnight test used to diagnose sleep disorders such as sleep apnea. During the test, a single-lead electrocardiogram (ECG) tracks the heart's electrical activity. According to the authors, these ECGs are recorded but rarely analyzed. Sleep disorders are recognized as risk factors for heart disease, so the team asked whether the data could do more.

The researchers used a deep learning model, a type of artificial intelligence, that had first been trained to detect arrhythmias, or abnormal heart rhythms. They combined its ECG analysis with information on sleep stages. The goal was to predict 10-year risk of atrial fibrillation, stroke, heart attack, heart failure and death from any cause.

The model's output was strongly associated with long-term risk (p < .0001). This held after the team adjusted for age, sex, body mass index, smoking, hypertension and diabetes. It also held after adjusting for sleep measures, including the apnea- hypopnea index, which counts breathing pauses, as well as arousals, limb movements, time in each sleep stage and sleep efficiency.

The sizes of the associations are reported as hazard ratios. A hazard ratio above 1 means a higher rate of the outcome. For each one-standard-deviation increase in the model's output, the hazard ratio for atrial fibrillation was 2.03 at Emory and 2.72 at Beth Israel Deaconess. For heart failure, it was 1.69 and 2.33. For death from any cause, it was 1.82 and 1.65.

Results for stroke and heart attack were weaker. The stroke hazard ratios were 1.19 and 1.40. For heart attack, they were 1.38 at Emory and 1.10 at Beth Israel Deaconess, and the second figure had a confidence interval (0.86 to 1.40) that includes no effect.

The abstract does not describe the model as ready to predict these two outcomes.

What does this mean for someone referred for a sleep study? Nothing changes today.

The abstract describes a research tool, and it does not say the score is available in clinics. The authors conclude that building such predictions into polysomnography could improve detection and support personalized clinical decision-making. That is the authors' proposal, not something this study has tested in patients.

There are limits. Only the abstract was available to us, so details such as how well the model separates high-risk from low-risk people are not known here. The outcomes came from health records and diagnosis codes, which can miss or misclassify cases.

The study shows association, not that the score causes or changes anyone's outcomes.

The next test is whether acting on such a score leads to better outcomes for patients, and whether the model performs as well for stroke and heart attack.

Source: SLEEP (2026)

Primary study

England and Wales Mortality Hits Record Nine-Month Low, Pressuring Annuity Pricing

People in England and Wales are dying at the lowest rate on record for the first three quarters of a year, and that is bad news for the firms that have promised to pay them pensions for life.

According to the latest update from the Continuous Mortality Investigation (CMI), cumulative standardised mortality to September 25 was 6.4% below the ten-year average for 2016 to 2025. The record holds for both males and females across nearly all age groups tracked by the monitor. The figure comes from the CMI's Q3 2026 mortality monitor, reported by Insurance Business.

The trend has run most of the year. Q1 2026 had lower mortality than any previous first quarter. The H1 update showed mortality 5.4% below the ten-year average through June. The Q3 data, which covers week 39, shows the gain held despite summer heatwaves that pushed deaths higher in parts of the period.

Respiratory causes stand out in the data. There were 944 deaths involving COVID-19 in the first 39 weeks of 2026. The same period saw 3,215 in 2025 and 7,591 in 2024.

Deaths from influenza and pneumonia were around 54,900, against a range of roughly 62,900 to 67,500 over 2023 to 2025. The CMI does not attribute causes to changes in mortality rates, so the data shows where the improvement sits but does not explain it.

Steve Bale, chair of the CMI Mortality Projections Committee, said mortality across the third quarter was at a similarly low level to 2025. "Mortality for the first three quarters of the year is at record low levels in 2026 for most age groups considered in the mortality monitor," he said. Young males are the exception. Their mortality remains around 1% above the record low set in 2012, having been rising before the pandemic.

The market consequence runs through longevity models. According to the source, the CMI_2025 projections model, published earlier this year, already reflected 2025 data. It raised life expectancy at age 65 by around eight weeks for males and six weeks for females compared with the prior version. WTW estimated that scheme liabilities would rise by around 0.5% for schemes adopting it.

If 2026 mortality stays at its current level, the source says the CMI_2026 model is likely to face the same upward pressure on life expectancy projections. That would carry consequences for reserving and pricing. That is a projection, not a published result.

The effect differs by business line. Lower mortality reduces near-term claim volumes for protection writers. Annuity providers and longevity reinsurers face higher present values on guaranteed income streams they have already committed to pay.

The pressure arrives in a busy market. WTW's 2026 De-risking report forecast pension risk transfer volumes of about £70 billion for the year. That includes an estimated £50 billion in bulk annuities and up to £20 billion in longevity swaps. Both types of deal reference CMI projections, adjusted for each scheme's own experience.

A further year of lower-than-expected mortality tightens the assumptions behind them.

What the source does not say is how any single insurer or scheme will respond, or how far pricing will move. Those answers depend on each party's own experience data and model choices.

The next marker to watch is the publication of the CMI_2026 model, and whether it lifts life expectancy again as the 2026 data suggests it might.

Source: Insurance Business (citing the Continuous Mortality Investigation)

Additional reporting

Parkinson's Stem Cell Developer Aspen Neuroscience Files for Nasdaq IPO

Aspen Neuroscience, a San Diego company that makes a Parkinson's cell therapy from a patient's own skin cells, has filed publicly for a Nasdaq IPO, according to Renaissance Capital. The therapy, sasineprocel, is investigational and not approved or available outside clinical trials.

The company filed on October 9, 2026, after a confidential submission on March 30, 2026. It plans to trade under the ticker ASPE. Renaissance Capital estimates the deal at up to $100 million. Leerink Partners, Piper Sandler and Stifel are the bookrunners.

Aspen's lead product is sasineprocel. According to the source, it is a single-dose therapy designed to replace the dopamine-producing neurons lost in Parkinson's disease. It is made from the patient's own cells.

The product holds two FDA designations, RMAT and Fast Track, according to the source. As of August 18, 2026, 15 patients had been dosed in an open-label Phase 1/2a trial. Open-label means patients and doctors know what is being given.

The company says that, after FDA feedback, it expects to dose its first Phase 3 patients in the second half of 2027. Renaissance Capital lists Aspen as founded in 2018, with about 120 employees.

For investors, the offering is a direct test of appetite for a regenerative approach in an age-related neurodegenerative disease. The company is selling shares with only 15 patients dosed and a pivotal trial still ahead. The size of the raise, the pricing and the demand will show how much weight the market gives to early data and regulatory designations at this stage. Those outcomes are not yet known. Readers with Parkinson's should not start or stop any medication or treatment without consulting their clinician.

What To Watch Next

Whether Aspen sets a price range and completes the listing, and what FDA feedback means for its Phase 3 timing.

Source: Renaissance Capital

IMF Says AI Productivity Gains Could Outweigh Asia's Aging-Driven Workforce Decline

Asia's aging populations may not drag down its growth if artificial intelligence delivers, according to the International Monetary Fund. This account rests on a secondhand summary of Investing.com's report, because the underlying page could not be fetched.

On October 12, 2026, IMF Managing Director Kristalina Georgieva launched an IMF book on Asia's economic outlook, as reported by Investing.com. The book names three forces reshaping the region: demography, economic integration and technology.

According to the IMF, AI could add 0.5 to 1 percentage point to growth in Asia's advanced economies. The IMF says that if countries capture those productivity gains, "these benefits will more than compensate for demographic pressures." Those pressures include aging populations and shrinking workforces.

The IMF attaches a condition. The gains depend on AI adoption spreading evenly across Asia, rather than widening the gaps that already exist between nations.

For markets and strategy, the point is that the IMF frames the outcome as one of adoption, not just technology. It is our inference, not the IMF's stated view, that countries falling behind would struggle to offset their labor losses. The report as

summarized does not specify which economies are best placed, or what policies the IMF recommends.

What To Watch Next

Whether the IMF's full analysis shows how adoption is spread across Asian economies, and whether the gap between leaders and laggards narrows or widens.

Source: Investing.com (reporting on IMF)

UCSF Details How FDA's Bone Density Endpoint Will Shrink Osteoporosis Trials

A late-stage osteoporosis trial that once needed up to 15,000 patients may now need about 750. According to UCSF News, that is the effect of an FDA decision that lets drug developers use changes in hip bone density, rather than fractures, as the main measure of success.

This article is based on UCSF News' report of the research. The underlying paper was not reviewed. Readers should not start or stop any osteoporosis treatment without talking to their clinician.

The scale of the change is large. According to UCSF News, a typical Phase 3 trial has enrolled 6,000 to 15,000 patients for three to five years, so that enough fractures occur to judge whether a drug works. Under the new approach, trials can enroll about 750 patients and follow them for a year and a half to two years.

For now, the change covers trials in postmenopausal women with osteoporosis, UCSF News reports. The FDA made the decision late last year.

The market logic is plain, though it is interpretation rather than reporting. Smaller and shorter pivotal trials should cost less. A lower cost of entry could draw in new bone-drug developers, including smaller firms that could not fund a multiyear

fracture trial. It could also create openings for licensing deals and acquisitions. UCSF News does not make these forecasts itself.

What UCSF News does report is that development had stalled. Dennis Black, PhD, a UCSF professor of epidemiology and biostatistics and co-lead of the SABRE Project, said the most recent osteoporosis drug approval was romosozumab in 2019. He said no new drugs have entered the pipeline since then because of the expense and time required. "Everything just stopped," he said.

The demand side is sizable. According to UCSF News, osteoporosis affects about 10 million Americans over age 50, including 1 in 5 women. The report says the share of Americans 65 and older is expected to rise from 18.9% to 23.4% by 2060.

The evidence behind the decision came from SABRE, the Study to Advance Bone Mineral Density as a Regulatory Endpoint. UCSF News describes it as a public- private collaboration of academia, the National Institutes of Health, the FDA, industry and nonprofits. Black said the team assembled data from more than 50 randomized trials involving about 170,000 patients, much of it held by private companies.

Black said the analysis found a strong link between larger bone density gains and larger fracture reductions. According to UCSF News, when a drug raised bone density above a certain threshold, there was more than a 95% chance it reduced fractures. He said this held across drugs that work in different ways, some slowing bone breakdown and others building bone.

Incumbents may face more competition. Black said new drugs could differ in dosing, duration and side effects, and that more competition could mean lower prices and better access. He framed this as a hope, not a certainty. Existing drugs work, he said, but some patients have rare side effects or find dosing inconvenient.

The precedent may matter beyond bones. UCSF News describes bone density as the first surrogate endpoint the FDA has formally qualified in any therapeutic area since its formal biomarker qualification process began. Black said the acceptance could set a precedent for faster development in areas such as cancer or Alzheimer's disease. That is his view. The report does not say whether the FDA will treat other endpoints the same way.

UCSF News describes the change as more than a decade in the making. Black named two hurdles: gathering the data and moving through an FDA process with no close precedent and several levels of review. Other disease areas would likely face similar work.

Watch for the first pivotal osteoporosis trials designed around the bone density endpoint. The UCSF report does not say whether any are under way, so the first announcements and financing deals will show how quickly the market responds.

Source: UCSF News

Tiny Health Raises $33 Million Series B as Adult Microbiome Testing Overtakes Pediatric

A company that began by testing babies' guts now sells more tests to adults. Tiny Health, based in Austin, has raised a $33 million Series B, according to Longevity.Technology.

B Capital Group led the round. Total funding now stands at $46 million. Other investors include Spero Ventures, The Venture City, Overwater Ventures and new backers, according to the source.

The shift in customer mix is the strategic point. Adult testing volumes now exceed pediatric volumes, according to the report. Longevity.Technology reports that nearly 200,000 customers and more than 6,000 healthcare practitioners use the platform.

The company has added longevity-focused products, including Gut Microbiome Age and Gut Resilience scores, according to Longevity.Technology. The source does not say how these scores are calculated or validated, and the notes do not address regulatory treatment.

Its business-to-business arm, called Powered by Tiny, grew fourfold last year, according to the source. That suggests practitioners and partners are a growing sales channel alongside direct consumers. The notes give no revenue figures, so the scale

of that growth is unclear.

CEO Cheryl Sew Hoy said, according to the source: "no one else was building for the whole lifespan." That is the company's own account of its positioning. The notes do not assess competitors.

What To Watch Next

Whether Tiny Health discloses revenue or evidence supporting its new longevity scores as it deploys the new capital.

Source: Longevity.Technology