u/DadStrengthDaily

Image 1 — My LDL came back at 60 and I finally understand why the new guideline draws the line at 55
Image 2 — My LDL came back at 60 and I finally understand why the new guideline draws the line at 55

My LDL came back at 60 and I finally understand why the new guideline draws the line at 55

Got my lipid panel back a couple weeks ago. LDL 60 mg/dL, calculated with Martin-Hopkins. That sits right on the threshold the new 2026 ACC/AHA dyslipidemia guideline drew for very-high-risk patients: <55 mg/dL. The guideline goes no lower than that.

I had to look into why. The trial evidence keeps going lower. In FOURIER-OLE, the long-term extension of the evolocumab outcomes trial, achieved LDL kept reducing cardiovascular events all the way down past 20 mg/dL. Lower kept being better. So if 30 is biologically better than 55, why didn’t the guideline say so?

The answer, in the editorial accompanying the guideline (Schwartz in JACC), is a cost ladder. From the PROVE-IT data: about 35% of high-risk patients reach LDL <55 on atorvastatin 80mg alone. Add ezetimibe and 55% reach goal. Two generic pills, combined cost of $20-40 a month at most US pharmacies.

To push below 55, about 45% of patients would need a third drug, typically a PCSK9 inhibitor. To push below 30, more than 90% would. Repatha’s cash price via GoodRx is around $2,900 a year right now (list price still around $6,000) — meaningfully cheaper than it was a few years ago but still a real step up from two generics.

The marginal benefit, per FOURIER-OLE, is about 1 percentage point of absolute reduction in cardiovascular death, MI, or stroke over 5 years when you go from LDL 55 down to 40. That’s the math the guideline writers balanced.

For me sitting at 60, this means I’m done. The third drug isn’t worth it for the marginal benefit. For someone with high Lp(a), bad family history, or established CVD with multiple events, the calculus tilts the other way and pushing lower is reasonable.

One thing worth noting: LDL on a routine panel includes the cholesterol carried inside Lp(a) particles. Statins and ezetimibe barely lower Lp(a). So if you’re comparing two people at LDL 80, the one with high Lp(a) has “less modifiable” LDL and a worse forecast. In FOURIER-OLE, patients who achieved LDL <20 had a median Lp(a) of 8 nmol/L; those who landed at 40-55 had a median of 41. Some of the apparent benefit of very-low achieved LDL may actually be the low-Lp(a) phenotype rather than the LDL number itself.

Has anyone here with established CVD or genetically high Lp(a) been pushed below 55 on PCSK9 inhibitor + statin + ezetimibe? Curious what your achieved LDL ended up being and whether the cost felt worth the additional reduction.

u/DadStrengthDaily — 10 hours ago

Lower is better for LDL, but the 2026 cholesterol guideline drew the line at &lt;55 mg/dL. The cost math behind that call is the most useful thing I read this week.

My last lipid panel came back with LDL of 60 mg/dL. That's sitting right on the line the new 2026 ACC/AHA dyslipidemia guideline drew for very-high-risk patients: <55 mg/dL. The guideline does not go lower than that.

My May 2026 lipid panel

That bothered me a little. The trial evidence keeps going lower. In FOURIER-OLE, the long-term extension of the evolocumab outcomes trial, achieved LDL kept reducing cardiovascular events all the way down past 20 mg/dL. Lower kept being better. So if 55 is good and 30 is biologically better, why did the guideline stop at 55?

The editorial that accompanies the new guideline answers this. Gregory Schwartz, JACC. The argument is a cost ladder, and I think it's the most useful piece of cardiology economics I've read this year.

The numbers come from PROVE-IT (the post-ACS lipid trial). On atorvastatin 80 mg alone, 35% of patients reach LDL <55. Add ezetimibe (also generic, $20-30 a month), and 55% get there. Roughly half of high-risk patients can hit the guideline target on two generic pills, combined cost of $20-40 a month.

Beyond that, the math gets ugly fast.

https://preview.redd.it/xgfapm4emh2h1.png?width=1536&format=png&auto=webp&s=1a30d9c76382d5a9f5e4ea478d9f4ac7f4c9a4f1

  To push below 55, 45% would need a third drug. That third drug is almost always a PCSK9 inhibitor. List price is around $6,000 a year, but the realistic cash price through GoodRx for Repatha (the most-prescribed one) runs about $2,900 a year right now. To push below 30, more than 90% would need the third drug.

The benefit you're buying for that money? FOURIER-OLE showed about 1 percentage point of absolute reduction in cardiovascular death, MI, or stroke over 5 years when you go from achieved LDL 55 down to 40. That's the trade: thousands of dollars for a year for a 1-point absolute risk reduction at 5 years.

 Schwartz's conclusion: the 55 mg/dL target is "a judicious distillation of current evidence, balancing clinical efficacy with cost and complexity of care." Translation: the guideline picked 55 because that's where two generic drugs land most people, and going lower as a population-level recommendation still costs meaningfully more than the marginal benefit justifies. For someone with high Lp(a) or strong family history of premature ASCVD, the math at $3K/year tilts more toward "yes" than the list-price math used to.

For me at LDL 60, this means I'm still done. The math doesn't support adding a PCSK9 inhibitor unless something else changes. For someone with a high Lp(a), bad family history, or established cardiovascular disease with multiple events, the math is different and the case for the third drug is stronger.

I wrote up the full 2026 guideline (PREVENT calculator, CAC scoring upgrade, ApoB targets, all the drugs in plain English) here: Reading Your Cholesterol Panel at 50. The cost ladder above is one piece of a longer story.

reddit.com
u/DadStrengthDaily — 11 hours ago

I keep seeing “cholesterol is debunked” takes pop up. A UW preventive cardiologist just published the cleanest rebuttal I’ve read.

I see at least one of these takes in my feed every couple weeks. The reasoning shifts but the tone doesn’t. Guidelines are wrong, your doctor is hiding something, Big Pharma and the government are pushing statins on everyone, the brave skeptic has cracked the code.
I’ve gone looking for a clean rebuttal more times than I want to admit. James Stein, who ran the UW preventive cardiology program for 21 years.

His core argument is that the U-shaped mortality curve people love to cite, where low cholesterol appears to predict higher death rates, isn’t biology reversing direction. It’s confounding. Low cholesterol can mean low cardiovascular risk. It can also mean cancer, malabsorption, chronic inflammation, or frailty. Mix those people into the data and the left tail goes up. Once you exclude early deaths and adjust for illness markers, the upturn shrinks.

He also picks apart the more sophisticated version. People grab the recent NEJM paper from the Global Cardiovascular Risk Consortium that dichotomized non-HDL cholesterol at 130 mg/dL and showed modest lifetime contrasts. The authors noted the real association is J or U shaped, but the modeling choice flattened it. Read casually, it looks like cholesterol barely matters. Stein’s point: that’s an accounting exercise about one threshold at one age, not a finding about biology.
His closing line, lightly paraphrased: there is no cholesterol debate at the causal level. What keeps coming back isn’t new biology. It’s misreads of risk data.

Worth a read if you’ve ever tried to argue with this stuff: https://jamesstein18.substack.com/p/why-cholesterol-is-debunked-arguments

The “cholesterol is debunked” takes aren’t a scientific position. They’re a content strategy.​​​​​​​​​​​​​​​​

jamesstein18.substack.com
u/DadStrengthDaily — 4 days ago

I have a Wahoo KICKR because my knees won't let me run. A new 479K-person study made my cycling habit more interesting.

I cycle indoors on a smart trainer because my knees and one toe joint won't tolerate running. Until last week I thought of it as a workaround. Then a new dataset landed that made me think about it differently.

Hou et al, JAMA Network Open, June 2025 followed 479,723 UK Biobank adults for a median of 13.1 years and grouped them by how they mostly got around. Compared to nonactive travel, cyclists had a 22% lower risk of Alzheimer's (HR 0.78, 95% CI 0.66 to 0.92), a 40% lower risk of young-onset dementia (HR 0.60, 95% CI 0.38 to 0.95), and measurably larger hippocampi on MRI. Cycling was the only travel mode where the entire confidence interval sat under the reference line. Walking helped less.

The part most coverage skipped: the cycling benefit was much weaker in APOE ε4 carriers. Non-ε4 cyclists got HR 0.74 (CI 0.63 to 0.87, clearly protective). ε4 carriers got HR 0.88 (CI 0.76 to 1.02, crosses 1.0). About 15-25% of people carry at least one copy and most don't know.

The counter-evidence to hold next to this is Zhang/Vidoni, JAMA Neurology, May 2026, the negative RCT I touched on in this sub a few weeks back. 513 older adults at elevated dementia risk, 2x2 design (exercise, intensive BP/LDL reduction, both, usual care), 24 months. None of the active arms beat usual care on cognition.

The two papers don't contradict. Observational cohorts catch decades of habit; RCTs test late-life interventions in people already vulnerable. Anyone selling "exercise prevents dementia" as settled science needs to sit with both. I looked at this a bit and sadly realized that indoor cycling gives up some of the dual-tasking benefit.

I'll be on the KICKR tomorrow morning either way. The math on doing nothing is worse than the math on imperfect evidence.

u/DadStrengthDaily — 4 days ago

Three new Lp(a) papers landed in May 2026. Test everyone once, the aspirin advice doesn't hold up, and three Lp(a)-lowering drugs are in Phase 3.

I had my Lp(a) measured last fall as part of a full lipid panel. Mine came back at 16 nmol/L, well below the actionable threshold. I exhaled and moved on. Then three lipidology papers landed in the past three weeks and made me realize most adults never even get tested.

Wilkinson and Koschinsky in J Clin Lipidol argue that the 2026 ACC/AHA guidelines now formally back universal one-time Lp(a) testing in all adults. About 1 in 5 of us are above the risk threshold (≥50 mg/dL or ≥125 nmol/L) and don't know it.

Shiraki in JAMA Cardiology added a mechanism paper. Common Lp(a) risk variants are associated with specific plaque morphologies and thrombus characteristics in sudden coronary death. In plain language, Lp(a) leaves a different fingerprint on coronary plaque than LDL does.

The surprise: Lopes in EJPC published a meta-analysis showing aspirin doesn't significantly reduce events in primary-prevention adults with high Lp(a). The intuition (clot-prone blood → aspirin helps) is real, but the data doesn't back it up. Despite being the cocktail-party advice for this population, the bleeding risk and the lack of clear benefit make it a real conversation to have with your cardiologist, not a foregone conclusion.

The reason the testing push is happening now and not five years ago is that the drug pipeline finally has something to offer the high-Lp(a) population. Olpasiran (Amgen, siRNA), pelacarsen (Ionis/Novartis, antisense oligonucleotide), and lepodisiran (Eli Lilly, siRNA) all knock Lp(a) down by roughly 95% in Phase 2. Their Phase 3 cardiovascular outcomes trials read out in the next two to three years. For the first time, knowing your number could mean having something to do about it.

Full breakdown with the threshold math and what to do if yours is high: What is LP(a)

u/DadStrengthDaily — 5 days ago

I like Rhonda Patrick. This “receipts are castrating men” video is still absurd.

I like Rhonda Patrick, and I think microplastics are a real public-health concern. We should probably touch fewer thermal receipts, stop putting hot food and coffee in plastic, and take plastic exposure more seriously.

But this Jack Neel video is a mess. Neel’s creator/agency page describes him as the “largest horror/true crime genre influencer on TikTok,” which explains the whole vibe. This is health content packaged like a murder documentary.

The video opens with sperm counts down, testosterone down, microplastics in semen and testicles, and “chemicals quietly castrating American men.” Then it asks whether we’re raising the “least masculine generation” of men. A few minutes later, the endocrine-disruptor segment cuts into a sponsor read for “clean” men’s shampoo with “no hormone disruptors.” That is almost too perfect.

Some of the concern is real. Sperm counts do appear to have declined. Microplastics have been detected in human reproductive tissue. Thermal receipts and hot plastic packaging are reasonable things to avoid when it’s easy.

But the testosterone-collapse story is much shakier. Barbell Medicine’s recent series makes the boring point that the scary headline version is overstated, and that low testosterone in adult men is often better explained by visceral fat, poor sleep, sleep apnea, illness, medications, low energy availability, or overtraining than by one scary modern toxin.

That distinction matters. “Sperm counts are down” and “young men are being chemically castrated by receipts” are not the same claim.

So yes: digital receipts, don’t microwave plastic, avoid hot food in plastic, use glass or stainless when practical, consider a real water filter, sleep more, lift weights, eat fiber, and keep your waist under control.

That’s useful. The horror-podcast packaging is not.

youtu.be
u/DadStrengthDaily — 5 days ago
▲ 26 r/ProactiveHealth+1 crossposts

I hit my goal on Zepbound 18 months in. ATTAIN-MAINTAIN is the first trial that speaks to what comes next.

I posted about ACHIEVE-3 back in February. That one was the head-to-head of Lilly's oral orforglipron against oral semaglutide in type 2 diabetes. Interesting result, not my question.

My question, after 18 months on Zepbound and now at the weight and body fat I actually want to hold, is the boring and slightly terrifying one. What does maintenance look like, and is it really lifelong.

ATTAIN-MAINTAIN, published May 13 in Nature Medicine, is the first trial that goes after that directly. Patients who finished SURMOUNT-5 on injectable tirzepatide or semaglutide came off the shot and were randomized to daily oral orforglipron or placebo for a year.

The headline says the pill worked. The numbers are more honest. People switching from tirzepatide kept 74.7 percent of their body weight reduction. People switching from semaglutide kept 79.3 percent. The pill mostly holds the line, but you give back roughly 20 to 25 percent of what you lost. The tirzepatide arm gained about 11 pounds back over the year. The semaglutide arm about 2.

For me, stopping is not on the table. The real choice is keep injecting at the current dose, drop to a lower maintenance dose, or move to the pill and accept some giveback. ATTAIN-MAINTAIN does not test a lower-dose injectable arm, which is the comparison I actually want to see. It also does not break out how much of the regain is fat versus muscle and bone.

A Lilly-funded trial at Lilly's preferred academic centers. Definitely interesting, but not the last word.

news.weill.cornell.edu
u/DadStrengthDaily — 5 days ago

I built this sub because nobody here is selling you a supplement. A new Pew study shows how unusual that is.

I started this sub because I wanted a place to talk about preventive health where the people on the other side of the screen both knew what they were talking about (or at least did sincere research) and wasn’t selling me anything. Pew Research dropped a study last week that confirms how rare that combination is online.

Pew analyzed nearly 13,000 health and wellness accounts with at least 100,000 followers on Instagram, TikTok, and YouTube. Forty percent of U.S. adults, and half of those under 50, now get health information from influencers and podcasts. Fewer than one in five are conventional medical professionals. Sixteen percent list no credentials at all. The rest of Pew’s “healthcare professional” bucket is padded with chiropractors, naturopaths, massage therapists, and functional medicine practitioners.

That’s the education problem. There’s a financial problem layered on top. Nearly half of these influencers describe themselves as coaches or entrepreneurs. Their business model is selling a program, a supplement, a course, or an affiliate link. Platforms reward whoever monetizes hardest, and everyone drifts toward something to sell.

A 2025 JAMA Network Open study made the mechanism concrete. Researchers at the University of Sydney analyzed 982 Instagram and TikTok posts about five popular medical tests: full-body MRI, multi-cancer early detection, AMH “egg timer,” gut microbiome, and testosterone. Sixty-eight percent of posts came from accounts with a direct financial interest in the test. Eighty-seven percent mentioned benefits. Fifteen percent mentioned harms. Six percent mentioned overdiagnosis risk. Six percent cited any scientific evidence at all.

Accounts with a financial interest were about six times more likely to take a promotional tone, and far less likely to mention harms or overdiagnosis. The selling shapes what gets said. You won’t hear that the AMH test isn’t a reliable measure of fertility from someone selling fertility consults, and you won’t hear that BPC-157 has barely any human evidence from someone selling peptide stacks.

Rachel Moran, a health misinformation researcher at UW, put it best in the NYT writeup (gift link): “They offer certainty: ‘Buy this product, take agency over your life in this way, sign up for this program of mine.’ Medicine can’t always offer you that.”

The credential problem and the financial problem are the same problem. An audience that can’t tell evidence from anecdote also can’t tell sponsored content from sincere advice. The bar should be both: does the person actually know what they’re talking about, and would they say the same thing if there were no money in it? Almost nothing online passes both.

pewresearch.org
u/DadStrengthDaily — 5 days ago

I wanted this “art slows aging” study to be fake. It’s more annoying than that.

I have basically no hobbies outside of working out, so I went into this paper ready to dismiss it.

The study looked at 3,556 adults in the UK Household Longitudinal Study and asked whether arts/cultural engagement and physical activity were associated with seven epigenetic aging clocks. Arts/cultural engagement meant things like music, dancing, painting, photography, crafts, museums, galleries, libraries, archives, historic sites, and cultural events. Physical activity was measured separately.

The results were not “art makes you live longer.” The older first-generation clocks showed basically nothing. But the newer clocks — PhenoAge, DunedinPoAm, and DunedinPACE — did show slower epigenetic aging in people who were more engaged in arts/culture and in people who were more physically active. The effect sizes were apparently similar enough that the authors compare arts/cultural engagement to physical activity.

This is where my skepticism kicks in hard.

People who go to museums, sing in choirs, take classes, dance, do photography, make things, or visit historic sites are probably different in a thousand ways from people who do none of that. They may have more money, more free time, better mobility, better mental health, stronger social ties, more education, less loneliness, and fewer life constraints. The authors adjusted for a lot, including socioeconomic factors, smoking, drinking, BMI, and health status, but this is still observational. You cannot model your way into certainty.

Also, epigenetic clocks are not the same thing as hard outcomes. I care much more about whether people avoid heart attacks, dementia, falls, frailty, disability, and early death than whether a methylation algorithm moves a little. Interesting signal, not proof.

But the annoying part is that the result is still plausible.

A lot of “longevity” culture collapses into exercise, sleep, diet, lipids, glucose, supplements, wearables, and lab work. I’m guilty of this too. My default leisure activity is just more training. This paper is a reminder that a healthy life might need something less measurable: hobbies, culture, creativity, social identity, novelty, and reasons to leave the house that are not just zone 2 or errands.

I do not think anyone should read this and force themselves into museum optimization mode. But I am taking it as a nudge that “I lift and do cardio” may not be a complete adult life.

For those of you who actually have hobbies: what has felt health-giving in a way that is not just another workout?

ucl.ac.uk
u/DadStrengthDaily — 6 days ago

Stop telling your doctor you drink “socially.” Give them the number.

STAT’s new alcohol series is brutal, but the most useful part is not the giant public-health argument. It is the tiny moment in a 15-minute physical where everyone pretends “socially” is a medical answer.

Alcohol kills nearly 500 Americans a day, according to STAT. Their chart on page 7 puts alcohol-attributable deaths at 178,000 a year — more than opioid-related causes — with deaths from heart disease and stroke, alcoholic liver disease, cancer, alcohol poisoning, crashes, and other causes all stacked together. The page 3 chart shows alcohol-specific ER visits climbing to 5.4 million.
And yet at a normal checkup, alcohol often gets handled like small talk.

“How much do you drink?”

“Socially.”

Box checked. Move on.

That is insane if you think about how we treat everything else. Nobody says their LDL is “social.” Nobody says their blood pressure is “weekend-ish.” Nobody tells their doctor their A1c is “mostly with dinner.”

STAT’s second piece is about this exact failure. Alcohol screening and counseling are often rushed or skipped, even though there are evidence-backed tools that can fit into a short primary-care visit. STAT reports that in one study, 30% of people with alcohol use disorder were not asked by their clinician about drinking at all. In another example from recorded VA visits, a patient said they drank six to eight beers at a time and the clinician just changed the subject.

The fix is not complicated. AUDIT-C is three questions: how often you drink, how many drinks you usually have, and how often you have six or more in one sitting. STAT says it can identify unhealthy drinking patterns quickly, including people who do not meet criteria for alcohol use disorder but are still drinking enough to affect long-term health.

The part I would actually use: at your next physical, don’t say “socially.” Say the boring number.

“I average 8 drinks a week.”

“I have 2 most nights.”

“I usually don’t drink during the week, but I’ll have 6–8 on Saturday.”

“I use it to fall asleep.”

“I’ve tried to cut back and it was harder than I expected.”

That gives your doctor something real to work with. Blood pressure, sleep, liver enzymes, cancer risk, anxiety, depression, weight, reflux, AFib, medication interactions — alcohol touches a lot more than people want to admit.

STAT also shows this can work at scale. Kaiser Permanente Northern California built alcohol screening into primary-care workflows in 2013. Now more than 90% of patients are asked specific alcohol questions at primary-care visits. They have done over 24 million screenings and 1.4 million brief interventions. Patients who got a brief intervention had larger reductions in health care costs, including ER costs, and some analyses found fewer drinks and heavy-drinking days among people with hypertension.

This is the part of “preventive health” that does not look sexy on a podcast. No wearable. No peptide. No supplement stack. Just asking a direct question and giving a direct answer.

How much do you actually drink? Not your identity. Not your story. The number.

statnews.com
u/DadStrengthDaily — 9 days ago

I finally understand why getting caught didn’t kill Liver King’s career

I didn’t really follow Liver King. He was just everywhere — hard to miss a shirtless guy gnawing on raw bull testicles — but he wasn’t my thing and I mostly scrolled past. What I couldn’t figure out was why getting completely exposed as a fraud in 2022 didn’t end his career. His supplement businesses reportedly do $100M a year. The $25M class action from his own fans got dropped. He got a Netflix documentary.

A paper just came out in Television & New Media — Alison Miller and Lee McGuigan at UNC — that gave me the framework I was missing.

Some details I didn’t know: his flagship supplement lists testicle and prostate first among its ingredients, based on the “doctrine of signatures” — a medieval and thoroughly debunked idea that consuming something resembling a body part will benefit that body part. He also sells “Barbarian Water,” laced with bull blood. His website has a section titled “Net Worth” that reads like a startup pitch deck, including this line: “You are never enough… you are never enough, and the minute you think you are, you coast, you rest, you decay, you die, you suck at life.”

The paper’s key concept is borrowed from professional wrestling: kayfabe. In wrestling, everyone knows the match is scripted but the performers maintain the fiction and the audience participates knowingly. The paper argues Liver King was running kayfabe from day one — a “porous identity” where he was never fully committed to the “100% natural” claim, and his audience was never fully credulous. They were in on a performance.

So when the leaked emails came out — $11,000 a month on steroids and HGH — it didn’t shatter a belief system so much as shift the terms of the show. He cried on camera, admitted it, came back as “Liver King 2.0” with cigars, firearms, a cowboy hat, and a golden knife he sells on his website. He admitted in August 2023 he’d resumed steroids, then turned that into content too. A heel turn, in wrestling terms.

The Peterson connection is more direct than I realized. There’s an actual TikTok in the paper captioned “Liver king eating eyeballs to pregame Jordan Peterson tonight.” The paper’s argument is that the recovery of “authentic masculinity” is the central product across all three acts — Liver King, Tate, Peterson — sold to the same audience, with different packaging.

There’s also a body horror coda: the paper notes injuries to his eye, arm, and internal organs. Growth at all costs turns out to have costs.

The reason this matters here: you can’t debunk a kayfabe act with evidence, because the audience was never operating on the assumption of literal truth. That’s why the “but the science says” response to these figures consistently fails. You can’t debunk a wrestling match.

doi.org
u/DadStrengthDaily — 11 days ago

Sam Neill is cancer-free after a CAR-T trial. The science behind it is more interesting than the celebrity story.

Sam Neill announced last month that his stage 3 blood cancer is in complete remission after a CAR-T clinical trial in Sydney. The Guardian followed up this weekend with a piece on what the science means and why researchers describe it as a major step forward for cancer treatment more broadly.

CAR-T therapy takes a patient’s own immune cells, engineers them in a lab to recognize cancer, and puts them back in. It’s been around for about a decade and has produced real cures, but every approved CAR-T drug works on the same family of blood cancers, the kind that come from B-cells. Seven approved in the US, four in Australia, all for B-cell cancers or multiple myeloma. None of them work for what Sam Neill has.

Neill has angioimmunoblastic T-cell lymphoma, AITL. It’s a cancer of T-cells, the other major branch of the immune system. CAR-T didn’t work on T-cell cancers for a long time because CAR-T cells are themselves T-cells. Engineer them to kill T-cell cancer and they kill each other in the manufacturing tank, and they wipe out the patient’s healthy T-cells too, leaving them with no immune system. Researchers worked on this problem for thirty years.
AITL is brutal. Five-year survival on standard chemo is about 30 percent. When chemo stops working, which it did for Neill after three years, most patients are out of options. He told 7News he thought he was on the way out.

The trick the trial pulled off was finding a marker on the cancer that’s only on half of healthy T-cells. T-cell receptors come in two versions. Normal people have a mix. But each cancer is a clone of one cell, so every cancer cell carries the same version. Target only that version and you kill the cancer while sparing the other half of the patient’s healthy T-cells. That’s enough to keep the immune system working.

The published trial using this approach reported encouraging results in Nature Medicine in November 2024. Of ten patients with relapsed T-cell lymphoma, six responded. At the highest dose, all four patients responded. The two longest remissions, both still going past 18 months, were patients with AITL, Neill’s exact diagnosis. Small trial, early data, but for a disease with no standard treatment after first-line failure, that matters.

I can’t confirm Neill was in this exact trial. The news coverage hasn’t named his protocol, and the published trial’s sites were UK and Spain, not Australia. Several T-cell CAR-T trials are running with different targets. The point is the whole category is moving.

This is what actual cancer progress looks like, and it’s a useful contrast to the wellness internet. Thirty years of immunology to find a tiny biological difference that lets you treat a brutal cancer without destroying the patient. No supplement stack does anything close.

The Guardian piece closes with one of the researchers saying “hope is warranted, but so is impatience.” Neill got a trial slot in Australia. Most patients with relapsed AITL won’t. That gap is the part of this story that doesn’t make the entertainment pages.

theguardian.com
u/DadStrengthDaily — 12 days ago

Sort of depressing that this doctor needs to buy a bus and bring PSA screening to the people but at the same time inspiring that he is making a difference.

u/DadStrengthDaily — 14 days ago

I knew statins worked. I did not know the origin story.

The first statin came from Akira Endo, a Japanese biochemist who grew up fascinated by fungi and was inspired by the discovery of penicillin. In the 1960s, he spent time in New York and was struck by how common heart attacks seemed compared with rural Japan. Cholesterol was becoming a serious suspect in heart disease, and Endo wondered whether a mold might contain a compound that could block the body’s cholesterol production.

He screened thousands of mold samples and eventually found compactin, later called mevastatin, in blue-green mold from rice collected at a Kyoto grain shop. That discovery led to lovastatin, FDA-approved in 1987, and then the statin class. Endo never got the Nobel Prize and did not get rich from the drugs that followed, but his work almost certainly prevented a staggering number of heart attacks.

I also did not know statin fear had its own origin story. In the early 1990s, Danish physician Uffe Ravnskov published The Cholesterol Myths, arguing that the cholesterol-heart disease link was fraudulent and statins were unnecessary or harmful. That movement never really disappeared. It just moved from books and fringe circles into Facebook groups, YouTube comments, podcasts, and family group chats.

The fears usually have a grain of truth. Muscle symptoms happen. Serious muscle injury can happen, though it is rare. Statins modestly increase diabetes risk. Some people really do not tolerate a specific statin.

But the online version often blows this out of proportion. Muscle pain is the best example. In normal life, lots of people report aches on statins. In blinded trials, where people do not know whether they are taking a statin or placebo, much of that difference disappears.

The SAMSON trial is the one that stuck with me. It enrolled people who had already quit statins because of side effects, then rotated them through months of atorvastatin, placebo, and no pills. Their symptom burden was almost the same on placebo as on the statin. The researchers calculated a 0.90 nocebo ratio, meaning about 90% of the symptoms people attributed to the statin were also triggered by placebo.

That does not mean symptoms are fake. It means bodies are noisy, expectations matter, and aging/training aches can get misattributed to a pill.

The practical question is not “statins good or bad?” It is: what is my actual cardiovascular risk, what LDL or apoB target makes sense, and what is the least annoying way to get there?

Sometimes that is diet. Sometimes it is low-dose statin plus Ezetimibe. The worst version is quietly stopping because a comment section made every ache feel like a warning sign.

u/DadStrengthDaily — 15 days ago

The NYT has a piece from Meatstock, a carnivore diet convention where people are not just talking about eating meat. They are talking about meat as medicine, meat as identity, meat as community, and in some cases meat as a replacement for the health system they no longer trust.

I’ll admit my bias up front: I’m suspicious of a lot of diet fads. Carnivore, keto, OMAD, juice cleanses, whatever the next thing is — once a diet starts sounding like it has all the answers, I start backing away.

But I also think it is a mistake to dismiss why these things work for some people. Rules help. A lot. “Don’t snack.” “Only eat in this window.” “Avoid ultra-processed food.” “Build meals around protein.” “Cut out the foods that make you overeat.” Whether that shows up as OMAD, keto, carnivore, Mediterranean, or something else, the structure itself can be powerful. Some people do better with clear lines than with vague advice like “eat in moderation.”

That is probably part of the appeal here. A lot of people do not end up at something like carnivore because they read a perfect randomized trial. They end up there because they were tired, heavy, inflamed, anxious, in pain, or frustrated with advice that did not seem to help. Then they try something simple and strict, they lose weight, they feel better, and suddenly the whole thing feels obvious.

But that is exactly where proactive health has to stay boring in the best possible way.

Feeling better matters. Weight loss matters. Less joint pain, better glucose, fewer cravings, better sleep — all of that matters. But if the diet also drives LDL or ApoB way up, wipes out fiber, makes constipation normal, removes most plant micronutrients, or nudges someone toward raw dairy and anti-medical thinking, then the story is not as simple as “it healed me.”

The current evidence on carnivore is still thin. A 2026 scoping review found only nine human studies, mostly small, short, uncontrolled, or self-reported. Some people reported real improvements, especially around weight and metabolic markers. The same review also flagged nutrient deficiencies, very low fiber, higher LDL and total cholesterol, and unknown long-term safety.

So I do not think the useful response is to mock people eating steak with butter. The useful response is: keep score.

If someone is going to experiment with an extreme diet, the minimum should be baseline and follow-up labs: LDL-C, ApoB if available, triglycerides, HDL, A1c, blood pressure, kidney markers, maybe hs-CRP depending on the situation. Track bowel habits, sleep, training, mood, and whether the diet is making life bigger or smaller. And raw milk is not a wellness hack; it is a food-safety risk with real outbreak history.

The more interesting question is not whether meat can be part of a healthy diet. Of course it can. The question is when a diet stops being a tool and turns into a belief system that makes every bad marker feel like a conspiracy and every good feeling feel like proof.

That is where proactive health should live: curious, self-experimenting, but not allergic to data.

u/DadStrengthDaily — 15 days ago

I’ve never really trusted the genre of papers that seem to tell us coffee, red wine, chocolate, or whatever else we already like is secretly medicine.

But this coffee paper is a special one.

The study starts with 62 people: 31 coffee drinkers and 31 non-coffee drinkers. Then the actual intervention is only the coffee-drinking group, split into 15 people drinking decaf and 16 drinking caffeinated coffee. The paper has 23 authors. There are more authors than people in either intervention arm, which feels like something you should not be able to say with a straight face.

And then they measure everything. Gut microbiome, fecal metabolites, urine metabolites, cytokines, cortisol, blood pressure, stool charts, cognitive tests, mood scales, impulsivity, emotional reactivity, caffeine cravings, food diaries. It reads less like a coffee study and more like someone backed a grant-funded truck over 31 people and sequenced whatever fell out.

My favorite detail is Table 1 noting that “most participants were born per vaginum.” I understand why birth mode gets included in microbiome research, but these are ~39-year-old adults. At some point, blaming your adult coffee microbiome on how you exited the womb starts to feel like the field parodying itself.

The paper’s story is that coffee drinkers had different gut bacteria, different metabolites, and different scores on some behavioral measures. They were more impulsive and emotionally reactive than non-coffee drinkers. Then after abstaining from coffee, some of those scores improved. Then after coffee came back, more things shifted again. Decaf and caffeinated coffee sometimes appeared to do different things.

But with 15 and 16 people in the intervention arms, and this many outcomes, something was always going to sparkle. Add enough microbiome, metabolomics, immune markers, cognition tests, and self-report questionnaires, and eventually you can build a gorgeous little cathedral out of noise.

The boring version is probably true: coffee leaves a detectable biochemical signature, and caffeine withdrawal/reintroduction changes how people feel. Fine. Interesting.

Instead, we get sweeping language about the microbiota–gut–brain axis and “modifying cognition,” and then media runs with it. Wired already turned this into a full “science has found even more ways coffee is good for you” story.

All from a study where the key intervention group fits in two minivans.

u/DadStrengthDaily — 17 days ago

Cold tubs had a run. Still kind of are.

Every gym is installing one, every “optimization” podcast covered it, and people like Andrew Huberman pushed pretty specific protocols — how cold, how long, when to use it.

The pitch was simple:

- reduces inflammation
- speeds recovery
- helps you perform better next session

With the usual caveat: yeah it might blunt muscle growth but I do it for performance and recovery.

A newer meta-analysis throws a wrench into that second part. This one pooled 30 randomized controlled trials (527 participants) across lifting, HIIT, endurance work, and team sports:

Effects of cold-water immersion at different body regions on performance recovery after exercise: a systematic review and meta-analysis

What it found:
- People felt less sore after cold immersion
- Objective performance (strength, jump height) did not meaningfully recover faster
- Even muscle damage markers weren’t consistently reduced once you correct for bias

So the updated picture looks like:
less soreness (subjective)
no clear performance benefit (objective)

That’s basically the argument Mike Israetel is making in his breakdown of the paper (the video that’s been circulating).

Where this gets interesting is the disconnect with real-world use.

Teams in the NFL still use cold tubs constantly. Not because they’re chasing a better vertical jump in a lab test, but because:

- players feel less beat up
- it helps with heat
- it makes back-to-back sessions more tolerable

Those aren’t well captured by “jump height 24 hours later.”

So the more grounded take now:
- If your goal is hypertrophy → don’t cold plunge right after lifting
- If your goal is just to feel less sore → it probably works
- If your goal is measurable recovery/performance → evidence is a lot weaker than it was sold

Feels like another case where something got very popular for one reason, but the best evidence supports a much narrower use case.

u/DadStrengthDaily — 17 days ago

A new JAMA piece on GLP-1s and exercise hit close to home for me.

I get annoyed when people act like GLP-1s are just “take a shot, get healthy.” That is not how it felt from the inside.

Yes, the drug helped. A lot. It quieted the food noise and made it easier to eat less. I’m not going to pretend that part was willpower.

But the injection didn’t make me train every day. It didn’t fix my diet. It didn’t make me prioritize protein, go to bed earlier, or keep showing up when I didn’t feel like it.

It gave me room to do those things.

The JAMA authors make a useful distinction: exercise has strong “efficacy,” meaning it works under ideal conditions. The problem is “effectiveness,” meaning what happens in real life when people are tired, busy, sore, discouraged, or just don’t stick with it.

That feels right. Exercise works. But only if you actually do it.

The same goes for GLP-1s. They can move the scale, but they don’t build muscle, fitness, or a routine for you. And since a lot of people stop these drugs and regain weight, the habits underneath matter.

So yes, the medication helped me lose weight.

But the habits are what made me healthier.

jamanetwork.com
u/DadStrengthDaily — 17 days ago

There’s something irritating about seeing serious research packaged in the exact style that made people distrust health media in the first place.

The researcher here, Dr. Andrea Glenn, appears to be a respected nutrition scientist: RD, PhD, assistant professor at NYU, visiting scientist at Harvard, and someone publishing in the actual peer-reviewed literature. I’ll link to her faculty/profile page and the underlying paper directly so people can judge the work without the YouTube wrapper.

The study itself is not quackery. It’s mainstream nutrition epidemiology: large cohorts, long follow-up, careful adjustment, and a finding that fits with a lot of prior evidence. More plant protein relative to animal protein, especially when that means more legumes, nuts, and whole grains instead of red or processed meat, tends to track with lower cardiovascular risk.

Fine. Useful. Not magic.

But then the packaging turns it into another culture-war food fight: seed oils, carnivore people, “nutrition epidemiology is junk,” serious scientists versus online cranks. I get why creators do it. Conflict gets clicks. But it also makes the work feel cheaper than it is.

This is becoming a pattern. Good studies get pushed through the same attention machine as bad influencer content, so everything starts to sound like a sales pitch. Even careful findings get flattened into team sports. Then the audience either overreacts or tunes out.

The actual lesson here is boring and probably right: eat more minimally processed plant foods, do not build your protein intake entirely around red meat, and stop pretending every nutrition question has to become a referendum on seed oils, vegans, or carnivores.

Good science does not need to be marketed like a YouTube fight.

u/DadStrengthDaily — 17 days ago
▲ 15 r/PeterAttia+1 crossposts

The Blue Zones idea has always been a great story: specific places, specific habits, unusually long lives. Personally I must admit that I have always been skeptical about some community having cracked some secret longevity hack.

What makes this STAT piece more interesting is that Eric Topol and Shelley Wood are not random skeptics. They write that both of them have written books about extreme longevity, so people regularly ask them about Blue Zones. Topol’s recent book is Super Agers, while Wood’s recent book is The Leap Year Gene of Kit McKinley.

Their point is not that all the lifestyle advice is garbage. It’s that the Blue Zones concept has gotten much fuzzier than the brand suggests.

The original term came from work in Sardinia in the early 2000s, later popularized by Dan Buettner through National Geographic, books, Netflix, consulting, retreats, and certified “Blue Zone” cities. STAT notes that Buettner has written nine bestselling Blue Zone books and built a business around the concept.

The skepticism centers on whether the extreme longevity data is as solid as advertised. Saul Newman has argued that clerical errors, natural disasters, and pension fraud may explain some supposed centenarian clusters, though STAT is careful to note his paper still has not been formally published in a peer-reviewed journal.

Other evidence is less easy to wave away: newer papers suggest some original Blue Zones are no longer producing the same longevity patterns. Nicoya’s advantage appears weaker for people born after 1930, and Okinawa shows major lifespan differences before and after World War II, with both lifestyle changes and reconstructed records possibly playing a role.

So the useful point is narrower than “Blue Zones were fake.”

Walking more, eating mostly plant-based/simple foods, managing stress, and having strong social ties are still reasonable health advice. STAT says many of those tenets have support from broader scientific literature.

But “these habits are healthy” is very different from “this place proves a formula for living to 100.”

Blue Zones may still be useful as lifestyle inspiration. They look weaker as a clean scientific explanation for extreme longevity — especially now that the definition, the data, and the business incentives are all being questioned.

u/DadStrengthDaily — 18 days ago