I Went Into Research to Study Aging. Then I Needed a Stent at 44.

I went into medicine and research to study aging. In my late 30s I stepped away from fifteen years of running companies in the supplement and wellness industry, because I wanted to understand the biology underneath the products instead of selling them. While working on my PhD project in computational biology, I set out to build what became Calibrated Signal: a consumer-facing tool to help people evaluate their health, wellness and longevity interventions. Many people put together a supplement stack one podcast or Facebook reel at a time. My goal was to give them a tool that analyzes the mechanism and the evidence behind each of those claims.

Then, in January 2025, at 44, I was the one on the table in the cath lab, getting a stent put into a heart artery that was 80 percent blocked.

This post is about what that did to the plan. It also introduces the framework I'll use for everything that comes next: the twelve hallmarks of aging, the biological processes underneath the diseases of getting older, plus a thirteenth I track myself.

The Bottom Line

I was spending thousands of dollars a year on a routine built to keep me healthy longer, and I was confident it was working. The stent doesn't prove that routine was useless. It showed me something more uncomfortable: my confidence had gotten ahead of anything I could actually measure.

If you've built a routine of your own, you've probably asked the same question I couldn't answer: is any of this working? Nobody can fully answer it yet. The study that would prove a supplement or habit makes people live longer would take decades and cost a fortune, and the tests that could tell you whether your routine is slowing your aging mostly don't exist yet either. That doesn't leave you guessing. Some things have real human evidence behind them, and you can learn to tell those apart from the ones that don't.

So I start with the biology. The leading framework breaks aging into twelve processes, the hallmarks of aging, and I add a candidate thirteenth: the aging of the thymus, the gland that trains your immune system. Below, each one gets a short card saying what it is, whether you can test it today, and how far the human evidence has come. My read: the hallmarks are the right place to start, and they're still a working map that the field keeps revising. Everything I grade from here on runs through them.

If you'd rather start with the tour, jump straight to the hallmarks.

Vocabulary that matters

• Healthspan. The years you live in good health. Still walking on your own at 80 counts.
• Hallmark of aging. A process that shows up during normal aging, speeds aging up when it's made worse in experiments, and slows aging down when it's corrected.
• Biomarker. Something measurable in your body, like a blood test or a scan, that tells you something about your biology.
• Proxy. A stand-in measurement, used because the outcome you actually care about takes too long to show up. A proxy can move while the outcome doesn't.
• Epigenetic clock. A test that estimates your biological age from chemical tags on your DNA.

Why I went into aging research

I was hitting my late 30s and starting to feel aging in my own body, and I was reading everything I could about where the science was going. Serious money was moving into it. Google launched Calico, a company built to study aging, in 2013, and in 2016 Jeff Bezos's investment firm backed Unity Biotechnology, a company built to clear out cells that stop dividing but won't die, alongside Mayo Clinic's own venture arm.

Mayo Clinic is the top hospital and one of the top research centers in the world, and it's in my own backyard. It's also a partner in the joint graduate program in bioinformatics and computational biology I enrolled in. In 2017 it launched PhD training in regenerative sciences, including stem cell biology. When a place like that starts training scientists to repair aging tissue, the idea stops looking fringe.

I was also reading futurists, Ray Kurzweil most of all. In 2002 he bet publicly that a computer would pass the Turing test, the classic test of whether a machine can hold a conversation like a person, by 2029, and on artificial intelligence I think he's about to be right again. Next on his list was age reversal, driven by what that intelligence would make possible. In 2024 he put "longevity escape velocity", the point where science adds more than a year of life expectancy for every year that passes, at around 2030. Kurzweil hasn't always been right, but he has been right about a lot. If he's right about artificial intelligence, it might be the key to unlocking some of the mysteries behind the biology of aging. So I'm excited, and I think everyone else should be too.

So I went where I thought the breakthroughs would come from. I chose computational biology, because I believed real progress would take deep molecular biology combined with serious computing power, and I trained in machine learning through that joint program, run with the University of Minnesota, before AI was a household name. Then I went into cancer epigenetics at the Hormel Institute, where my published work looked at chemical marks on the proteins DNA wraps around in melanoma, because cancer and aging run on so much of the same molecular machinery.

The technology behind Calibrated Signal grew out of all of this work, combined with my years in the supplement industry: taking apart, one by one, the interventions people are sold to live longer and stay healthier, to see whether the evidence shows they might actually help. Then my own health took an unexpected detour.

Then I needed a stent

As I've written before, I thought my routine was optimized. To me it was prevention: using the best information I could find to stay healthy longer and, I hoped, live longer. I was fit, my metabolic health was strong, and my labs looked good to me. My blood pressure ran borderline high and so did my LDL, numbers I now know I under-weighted, which is why I wrote the blood pressure post and the LDL post. I was a keto guy, and I had convinced myself that mildly high LDL was fine on keto.

Then came palpitations and chest pressure, and a CT angiogram found an 80 percent blockage in my right coronary artery. I told that story in my first post. It was a slap in the face. And this August, back in the cath lab, I learned I also have coronary artery spasm, which I wrote about in the diagnosis story.

What does the stent actually prove? Less than you'd think. It doesn't prove my routine did nothing; parts of it may have helped, and the blockage might have been worse without them. It doesn't tell me some longevity supplement would have prevented it, or which of the processes below drove it. What it showed me is that I believed my routine was working and had no real way to know.

So I sped up my PhD. For the last two years my project has been a system, built with computational biology, that checks every supplement, drug and habit in a routine against the biology of aging, the human evidence, and who paid for the studies, and that can grade new ones as they come out of development. It's running in beta, and the first thing I did with it was run my own stack through it. In December I'm opening it to everyone, with early access planned in the coming months. What it can't do is tell you whether your own aging has slowed. Nothing can yet, and the next section explains why. What it can do is show you which claims in your routine have real human evidence behind them, which rest on mechanism alone, and whether the research even studied what you're taking.

Why can't anyone just run the study?

Proving that one supplement or habit makes people live longer would take decades of follow-up and cost a fortune. It would also have to hold up while thousands of people change their diets, jobs, exercise and other supplements for twenty or thirty years, which makes it nearly impossible to pin the result on any one thing. With the way studies are done today, it won't happen. Most of us would be dead before we knew the result.

Even the most famous attempt shows how hard this is. Researchers designed a large trial to see whether metformin, a cheap diabetes drug, delays the diseases of aging in older adults. As of 2024, it still wasn't fully funded. Part of the problem is that regulators approve drugs for diseases, and aging itself isn't treated as one.

What does get run are shorter trials, and some of them answer a question that matters right now: can you stay healthier and more capable, even if nobody can prove you'll live longer? In the LIFE trial, 1,635 inactive adults aged 70 to 89 who already had some physical limitations were assigned to a structured exercise program or to health education classes. Over about two and a half years, 30.1 percent of the exercise group lost the ability to walk 400 meters, about a quarter mile, against 35.5 percent of the education group.¹ That doesn't prove exercise slowed their aging. It does show it kept more of them walking, which is what healthspan is about. Many other short trials only track a stand-in, like a blood marker, for a year or two.

Animal and petri dish studies fill in the mechanism, and mechanism matters, because it tells you what's plausible. But people aren't mice. My years in cancer research taught me that a lot of what works beautifully in a dish or a mouse doesn't transfer to people.

That may not stay true forever. Lab-grown organoids, computer models and approaches nobody has thought of yet may change how fast we can answer these questions. For now, we rely on proxies and stand-ins.

How would we know if something slows aging?

If healthspan gains are coming, how would we even see them? That turns out to be three separate questions, and most of the longevity market only answers the first one or two.

1. Can we measure the process reliably? Does the test give the same answer twice, and does it track the biology we care about?
2. Does an intervention change that measurement in a well-controlled human study?
3. Does that change make people healthier: better function, less disease, longer life?

So where are we on the first question? Mostly noisy consumer tests and a few research tests. Epigenetic clocks are the best known, and the noise is bigger than most people buying them realize. In one analysis, running the same blood sample twice gave readings up to 9 years apart on some of the best-known clocks.² Retrained versions of those clocks brought most repeats within about a year and a half. That's better, and it's still a lot when you're trying to see whether a supplement truly did something to the biology underlying aging.

The rest of the time we use proxies: fitness on a treadmill, a blood marker of inflammation called CRP, how well your artery lining relaxes. All three predict who does well over time. None of them proves that a specific intervention slowed your aging, and a proxy can look fine while the thing you care about isn't. Mine did. My labs read as reassuring to me right up until the CT angiogram.

What are the hallmarks of aging?

So where do you start, if you can't run the trial and can barely measure the result? I start with the biology. The hallmarks of aging break aging into the processes that appear to drive it at the molecular level.

In 2013, a team led by the Spanish biochemist Carlos López-Otín proposed nine of them. In 2023 the same team updated the list to twelve, adding disabled macroautophagy (the cell's recycling slowing down), chronic inflammation and dysbiosis (a disrupted community of gut microbes), and stressed that the hallmarks are interconnected.³ If you've seen a list of nine, that's the 2013 version. Cancer research has its own list, the hallmarks of cancer, and that's part of why this framework clicked for me: cancer and aging run on much of the same machinery.

To count as a hallmark, a process has to pass three tests. It shows up during normal aging. Making it worse in experiments speeds aging up. And correcting it slows aging down. That third test is the hard one, and in people it mostly hasn't been passed. It's also the one some supplement marketing is built around, with claims that a product can move the biology underlying a particular hallmark.

The twelve fall into three groups. The first five are forms of damage. The next three are the body's responses to damage, which help at low levels and cause harm when they run too hard or too long. The last four are what happens when tissues and organs stop coordinating.

For now, each hallmark gets a short card with two lines at the bottom that answer the same questions every time. Measured today says whether you can get a test for it, and which one. Evidence today says, in plain words, the furthest the human evidence has gotten for anything aimed at that process: only animal or lab studies, tried in people without a benefit, a treatment that changed a measurement in people, or a real health benefit in a specific group of people. It reflects the best evidence for the process, not a verdict on every product that claims to touch it. If you'd rather skip the cards, jump to where we head next.

The damage

Hallmark 1 · The damage

Genomic instability

DNA damage builds up

Your DNA takes damage every day, from sunlight, tobacco smoke, normal metabolism and copying mistakes when cells divide. Your cells repair almost all of it, but over decades some damage slips through and mutations pile up. One result hit close to home for me: CHIP, where a single blood stem cell picks up a mutation and its descendants take over a growing share of your blood. People who carry it have a higher risk of heart disease, which I covered in the CHIP post.

Measured today

No direct test. CHIP sequencing of blood shows one piece of it.

Evidence today

Animal and lab studies only so far

Hallmark 2 · The damage

Telomere attrition

The protective ends of your chromosomes wear down

Telomeres are the protective caps on the ends of your chromosomes, like the plastic tips on shoelaces, and they wear down a little each time a cell divides. Cancer hijacks this system: most cancer cells switch telomerase, the enzyme that rebuilds telomeres, back on, which lets them keep dividing almost indefinitely. So this is interesting biology with a lot of nuance. Short telomeres go with aging, so longer sounds better, but genetic studies suggest people born with longer telomeres have a higher risk of several cancers, along with a lower risk of some other diseases, including heart disease.⁴ A drug has lengthened telomeres in people with a rare inherited telomere disease, but nobody has shown that longer telomeres make an ordinary person healthier. Keep that in mind before you pay for a telomere test, or for anything that promises to lengthen them.

Measured today

Consumer telomere tests (noisy); a clinical test exists only for rare telomere diseases

Evidence today

A drug lengthened telomeres in people with a rare disease; no health benefit shown in normal aging

Hallmark 3 · The damage

Epigenetic alterations

The switches that control your genes drift

Every cell in your body carries the same DNA. What makes a heart cell a heart cell is a layer of chemical tags on the DNA, and on the proteins it wraps around, that switch genes on and off. With age, that pattern drifts, and epigenetic clocks read the drift. A few trials have nudged a clock a little; none has shown that moving it makes people healthier. In mice with a premature-aging disease, partly resetting these tags extended life, and the first human safety trials of that idea are just getting started. This is the hallmark I spent years on in the lab, and my bet for one of the most upstream drivers of aging. The evidence hasn't settled that yet, but I'm hopeful.

Measured today

Consumer epigenetic clock tests (noisy)

Evidence today

Some treatments nudged a clock in people; no health benefit shown

Hallmark 4 · The damage

Loss of proteostasis

Proteins lose their shape and clump

Proteins are the cell's working machines, and each one only works if it's folded into the right shape. With age, the systems that fold, repair and clear proteins slip, and misfolded proteins clump together. Those clumps are a feature of Alzheimer's and Parkinson's disease. Nothing measures your protein quality control as a whole. The clearest human win so far is narrow: in one form of heart failure caused by a single misfolding protein, a drug that holds that protein in shape lowered deaths.⁵

Measured today

No overall test; only disease-specific tests, like an Alzheimer's blood test

Evidence today

A drug lowered deaths in one protein-misfolding heart disease; nothing shown for aging itself

Hallmark 5 · The damage

Disabled macroautophagy

Cell recycling slows

Your cells have a recycling system, called autophagy, that wraps up worn-out parts and hauls them to the lysosome, the cell's recycling center, to be broken down. With age it slows, and damaged parts linger. In mice, turning autophagy up extended both lifespan and healthy years. Fasting and a long list of supplements get credit for "boosting autophagy" all the time. Nobody can measure whether they did it in you, and a year-long randomized trial of spermidine, one of the most popular autophagy supplements, found no benefit on memory in older adults, its main goal.

Measured today

No test in people

Evidence today

Tried in people; no benefit shown yet

The responses that overshoot

Hallmark 6 · Responses that overshoot

Deregulated nutrient sensing

Growth signals lose their balance

Your cells constantly read fuel gauges, signaling pathways with names like insulin, mTOR and AMPK, to decide whether to grow or to hold back and repair. With age, and with food always available, those gauges fall out of balance. Fasting glucose and HbA1c, a three-month average of your blood sugar, read the insulin side indirectly; nothing you can order reads mTOR. In people at high risk of diabetes, a lifestyle program and metformin both cut how many went on to develop it. Metformin and rapamycin, two of the most talked-about longevity drugs, both act on this hallmark, and neither has been shown to slow aging in people. You met the metabolic side in the metabolically healthy post.

Measured today

Indirect only: fasting glucose and HbA1c

Evidence today

Lifestyle change and metformin cut new diabetes cases in high-risk people; not shown to slow aging

Hallmark 7 · Responses that overshoot

Mitochondrial dysfunction

The cell's engines make less energy

Mitochondria are the small engines inside your cells that turn food and oxygen into usable energy, and with age they make less of it. In older muscle, that decline tracks with weaker legs and slower walking. A direct test takes a muscle biopsy or a specialized MRI scan in a research lab. VO2 max, the fitness number your watch estimates, reflects your mitochondria only in part. Hard interval training has raised mitochondrial capacity in older adults' muscle, which makes exercise the clearest lever we have here. You met this in the training post.

Measured today

Research only (muscle biopsy or a special MRI); VO2 max is a partial stand-in

Evidence today

Exercise raised mitochondrial capacity in older adults; not proven that's why exercise helps

Hallmark 8 · Responses that overshoot

Cellular senescence

Damaged cells that won't die pile up

Some damaged cells stop dividing but don't die, which is why people call them zombie cells. They sit in your tissues sending out inflammatory signals that irritate the cells around them. Early in life, stopping a damaged cell from dividing helps block cancer; with age, these cells pile up. Clearing them extended healthy lifespan in naturally aged mice, and that result launched a wave of senolytic drugs and supplements, built to clear them. Clearing them may not be the simple answer, though. In one mouse study, wiping out a type of senescent cell that lines blood vessels in the liver broke down the vessel barriers, scarred the tissue, and made the mice sicker.⁶ Two other approaches are being studied: quieting the inflammatory signals these cells send, and resetting them to a younger state, which so far has worked only in cells in a dish. In people, one small study in patients with diabetic kidney disease found fewer senescent cells in fat tissue after treatment, while a randomized trial in older women missed its main goal. You met these cells in the zombie cells research note.

Measured today

No accepted test

Evidence today

A small human study lowered senescent cells; no health benefit shown yet

The system stops coordinating

Hallmark 9 · The system stops coordinating

Stem cell exhaustion

The body's repair reserves run low

Your body keeps reserves of stem cells that rebuild worn-out blood, muscle and gut lining, and with age those reserves restock and repair less well. In blood, the number of stem cells doesn't seem to fall much. What drops is diversity: in old age, a handful of stem cell lines can come to make most of your blood, and CHIP, from the first card, is one version of that. No test grades your stem cell reserve; blood counts are the closest stand-in. In old mice, sharing a blood supply with young mice revived aged repair cells. In people, there's no good evidence yet that anything restores the reserve.

Measured today

No direct test; blood counts are the closest stand-in

Evidence today

Animal studies only so far

Hallmark 10 · The system stops coordinating

Altered intercellular communication

Cell-to-cell signals get garbled

Cells and organs coordinate through messages: hormones, nerve signals and factors carried in the blood. With age, those messages weaken, shift or get garbled. The example closest to my own story is the lining of your arteries, which tells the vessel wall to relax using nitric oxide, a signal that fades with age even in healthy people. The "young blood" idea lives here too. Factors in young blood revived old tissue in mice, while the first small human trials of filtering plasma point in opposite directions. You met this in the blood pressure post.

Measured today

Single signals only, like hormone levels or an artery-relaxation ultrasound

Evidence today

Small human trials of plasma filtering gave mixed results; no health benefit shown

Hallmark 11 · The system stops coordinating

Chronic inflammation

The alarm that doesn't shut off

With age, many people develop a low-grade inflammation with no infection behind it, a state researchers call inflammaging. Think of the immune system's alarm never fully switching off. It's tied most clearly to heart disease, and a routine blood test, CRP, tracks it, though bluntly. In heart patients, some anti-inflammatory drugs have lowered repeat heart attacks and strokes, and others have failed. That's real evidence in heart disease, and it still isn't proof that calming inflammation slows aging. You met this in the CHIP post and the microvascular post.

Measured today

Routine blood test (CRP), a blunt measure

Evidence today

Some anti-inflammatory drugs lowered repeat heart attacks and strokes; not shown to slow aging

Hallmark 12 · The system stops coordinating

Dysbiosis

Your gut's microbe community shifts

Trillions of microbes live in your gut and mouth, helping with digestion, immune defense and even blood vessel chemistry, and the community shifts as you age. The clearest proof that a disturbed community causes disease comes from a stubborn gut infection, C. difficile, where a stool transplant from a healthy donor beat antibiotics. Consumer gut tests are noisy: when researchers sent the same standardized sample to seven services, the results differed about as much as different people's guts do.⁷ If you've paid for one, that's worth knowing before you rebuild your diet around it. Your mouth counts too, which is why I wrote the mouthwash post.

Measured today

Consumer stool tests (they disagree with each other)

Evidence today

Stool transplant treats a stubborn gut infection; not shown to slow aging

Our candidate thirteenth

The 2023 framework stops at twelve. In the system I've been building, I track a thirteenth: thymic involution, the aging of the thymus. It isn't on the official list, and you could argue it belongs under immune aging in general. I think the research points to a process of its own. The thymus ages early and on its own timeline, it has a measurable output, and losing it as an adult appears to have real consequences. Treat it as a candidate, not a settled hallmark.

Hallmark 13 · Our candidate

Thymic involution

The gland that trains your immune cells shrinks

The thymus is a small gland behind your breastbone where T-cells, the immune cells that learn to recognize specific threats, are trained and checked so they don't attack your own body. It starts shrinking early in life, and fat gradually replaces its working tissue, so fewer fresh T-cells come out. Does an adult thymus still matter? In a 2023 study, adults whose thymus was removed during heart or chest surgery were nearly three times as likely to die within five years as similar patients who kept theirs, 8.1 percent versus 2.8 percent, and they had more cancer.⁸ That's observational, so it can't prove the missing thymus caused it, but it's hard to ignore. The test that estimates thymic output screens newborns for severe immune deficiency; in adults it's a research tool. Turning one gene back on regrew an old thymus in mice. In people, the best-known attempt reported thymus regrowth on MRI in nine men, with no comparison group.

Measured today

Research test only (the same test used to screen newborns)

Evidence today

One tiny study reported thymus regrowth in people; no comparison group, no health benefit shown

What to do with this

You don't need to memorize thirteen processes. You need three questions for anything in your routine, and the next few posts teach each one properly:

• Which hallmark is it supposed to touch, and how? If the answer is "supports cellular health," that isn't an answer.
• How far up the ladder has the human evidence climbed? A dish, a mouse, a moved biomarker, or a health benefit in people?
• Who paid for the studies? In this space, the company selling the product often funded the research behind it.

The Final Signal

• What the framework gets right: it organizes aging into twelve interconnected processes you can look up, sometimes measure, and grade interventions against. I add a thirteenth candidate, the aging thymus.
• What it doesn't do: it doesn't measure your aging, and it isn't a finished theory. The test of whether correcting a hallmark slows aging is the hardest one, and in people it mostly hasn't been passed.
• What I changed: I sped up my PhD and ran my own routine through it first.
• What would change my mind: an aging biomarker shown to predict outcomes and respond to treatment, or a human trial showing that correcting one hallmark extends healthy life.
• What's next: how to judge a longevity claim, one question at a time.

Where we head next

Over the next couple of months, before the December launch, I'll be mixing two kinds of posts. One kind teaches how to judge a longevity claim: what a mechanism can and can't tell you, how to grade evidence when nobody funds the big trial, how conflicts of interest run through this space, and what you actually bought when you picked a form and a dose. The other kind covers the things to stop doing before you buy anything new, each tied to the hallmarks. We started with mouthwash; alcohol, smoking, poor sleep and chronic stress are coming. People know smoking is bad, and most of them think of lung cancer. We'll look at what it does to the hallmarks.

After the launch, each hallmark gets its own deep dive, and then we start grading the things that claim to help.

The science that pulled me into this field is still moving. If Kurzweil is right that AI will speed up biology, the number of health claims you'll be asked to believe is about to grow fast, and being able to judge them honestly will matter more than it ever has. That's what this series is for.

More on the biology of aging: the Aging Biology series, and the Evidence Critique posts on how claims hold up.

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References

1. Pahor M, Guralnik JM, Ambrosius WT, et al. Effect of structured physical activity on prevention of major mobility disability in older adults: the LIFE study randomized clinical trial. JAMA. 2014;311(23):2387-96. PMID: 24866862 [Finding: The LIFE randomized trial in 1,635 sedentary adults aged 70 to 89 with physical limitations. Major mobility disability occurred in 30.1 percent with structured activity versus 35.5 percent with health education, over about 2.6 years.]
2. Higgins-Chen AT, Thrush KL, Wang Y, et al. A computational solution for bolstering reliability of epigenetic clocks: Implications for clinical trials and longitudinal tracking. Nat Aging. 2022;2(7):644-661. PMID: 36277076 [Finding: In human blood datasets, technical noise produced differences of up to 9 years between replicate samples for six prominent epigenetic clocks; retrained principal-component versions kept most replicates within 1.5 years.]
3. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. Hallmarks of aging: An expanding universe. Cell. 2023;186(2):243-278. PMID: 36599349 [Finding: The 2023 update of the framework, by the original team: twelve hallmarks of aging, defined by three premises, and described as interconnected. A framework review, not an experiment.]
4. Haycock PC, Burgess S, Nounu A, et al. Association Between Telomere Length and Risk of Cancer and Non-Neoplastic Diseases: A Mendelian Randomization Study. JAMA Oncol. 2017;3(5):636-651. PMID: 28241208 [Finding: A genetic (Mendelian randomization) study: longer telomeres likely increase risk for several cancers while reducing risk for some non-cancer diseases, including cardiovascular disease.]
5. Maurer MS, Schwartz JH, Gundapaneni B, et al. Tafamidis Treatment for Patients with Transthyretin Amyloid Cardiomyopathy. N Engl J Med. 2018;379(11):1007-1016. PMID: 30145929 [Finding: In 441 patients with transthyretin amyloid cardiomyopathy, a heart disease caused by an unstable, misfolding protein, tafamidis lowered all-cause mortality compared with placebo.]
6. Grosse L, Wagner N, Emelyanov A, et al. Defined p16(High) Senescent Cell Types Are Indispensable for Mouse Healthspan. Cell Metab. 2020;32(1):87-99.e6. PMID: 32485135 [Finding: In mice, continuous or acute elimination of p16-high senescent cells, mostly blood-vessel cells lining the liver, disrupted blood-tissue barriers, caused liver and perivascular fibrosis, and worsened health. Animal evidence: some senescent cells do structural work.]
7. Servetas SL, Gierz KS, Hoffmann D, Ravel J, Jackson SA. Evaluating the analytical performance of direct-to-consumer gut microbiome testing services. Commun Biol. 2026;9(1). PMID: 41748906 [Finding: Seven direct-to-consumer gut microbiome services, sent the same standardized fecal material, produced major discrepancies; variation between providers was on the scale of variation between different donors.]
8. Kooshesh KA, Foy BH, Sykes DB, Gustafsson K, Scadden DT. Health Consequences of Thymus Removal in Adults. N Engl J Med. 2023;389(5):406-417. PMID: 37530823 [Finding: Adults whose thymus was removed during cardiothoracic surgery, compared with matched patients who had similar surgery without thymectomy: five-year all-cause mortality 8.1 versus 2.8 percent and cancer 7.4 versus 3.7 percent, with less new T-cell production in a subgroup. Observational.]