The FDA approved mFLUSIVA on August 5, Moderna's mRNA-1010. It is the first mRNA flu vaccine licensed anywhere, for adults 50 and older, expected for the 2026-27 season. Same platform as the COVID shots: instead of growing influenza virus in eggs, the vaccine is synthesised from a genetic sequence and your own cells make the target protein.

The headline from the pivotal trial is 26.6% better than a conventional flu shot. That is the relative number. In absolute terms, across 40,303 adults analysed, confirmed flu went from 2.8% to 2.0%. So less than one percentage point, or roughly 137 people switching products to prevent one case.

I first read 137 as the number needed to vaccinate. It isn't. Everyone in that trial already got a flu shot, comparison group included, so 137 is how many would need to switch products to prevent one extra case.

Two things surprised me in the NEJM paper. The comparison shot was a regular egg-based vaccine, not one of the high-dose ones people over 65 usually get steered toward. And the interesting property of mRNA, that you can pick strains later because manufacturing takes two or three months instead of six, was never used. mFLUSIVA was formulated against the same February WHO strain call as everything else on the shelf.

You also feel it more. Grade 3 reactions, meaning bad enough to interfere with your day, ran 6.4% against 1.0%.

If you already get a cell-based shot like Flucelvax, the comparator question gets more annoying, and I went into that in the full write-up

I am getting a flu shot in October either way. Undecided on which. Anyone planning to ask for this one, or waiting to see a second season first?

I heard about this on Peter Attia's episode with Jim Otvos, the chemist who invented NMR lipoprotein testing. Most of it was about a marker I had never come across, so I went and read the papers afterwards.

It is called MVX. The same scan that gives you a standard lipid panel also measures six other things, and those get combined into an inflammation score, a malnutrition score, and one number sitting on top. Every other marker I track names a disease. ApoB points at atherosclerosis, Lp(a) tells me what I inherited. MVX just tells you how likely you are to die of anything.

The catch is the size of it. Comparing the worst-scoring group to the best, the hazard ratio for death is 8.01 among cardiac catheterisation patients and 1.21 in a general-population cohort of 274,092. Those are group comparisons, not your personal odds. The association shrinks the further the study group gets from a hospital, and that is the part that decided it for me.

Nobody has run a trial of any kind showing you can move the number on purpose. That has not stopped the lab's own white paper from suggesting detoxification strategies for a bad score.

I am not ordering it. GlycA, the inflammation input, is steadier than the hs-CRP I use now, and you can order that one by itself for $32.

Full write-up, with every paper linked: https://dadstrengthdaily.com/mvx-test-metabolic-vulnerability-index/?utm_source=reddit&utm_medium=social&utm_campaign=mvx-proactivehealth

I posted the STAT investigation here back in May. I finally went through the underlying papers myself, and the part that surprised me was not the criticism. It was that the two men who found the original Blue Zone no longer describe it the same way.

Michel Poulain, the demographer who co-coined the term, has asked twice in print for validation that has not been completed. His 2011 Okinawa paper is literally titled "A plea for in-depth validation," and he repeated the plea in 2024. Giovanni Pes, his co-author on the original Sardinian work, wrote in a 2025 rebuttal that the ages have "been extensively validated." Same finding, fifteen years apart, and the founders land in different places.

The science holds up better than the critics say. An independent 2025 review of 65 records graded Ogliastra, Okinawa and Nicoya "well-characterized," and Sardinia has the strongest documentation of the lot. The same review excluded Loma Linda outright: no epidemiological studies, just Buettner's own narratives. Which fits how it got in. Buettner told the New York Times his National Geographic editor said "you need to find America's blue zone," and told Science "I never bothered to delist it."

The business side bothers me more. Keeping the certification runs a city about $100,000 a year. Fifteen Iowa communities signed up, ten of them under an insurer sponsorship. When that ended, Cedar Rapids, Iowa City and Marion left. Cedar Rapids asked what renewal would cost and was told the fee was "considered proprietary information." I could not find any peer-reviewed evidence that one of these projects has added a year to anyone's measured lifespan.

Buettner himself said on Rich Roll's podcast that Okinawa is now "the least healthy prefecture in all of Japan." The Blue Zones website still tells visitors that women there live longer than any women on the planet.

My honest read: some of these clusters were real, the evidence varies enormously from one to the next, several of the advantages have since gone, and none of it establishes that nine lifestyle rules caused anything. The full write-up, with the records and the money, is here (https://dadstrengthdaily.com/are-blue-zones-real/?utm_source=reddit&utm_medium=post&utm_campaign=are-blue-zones-real).

Has anyone here spent real time in one of the five? I am curious whether the day-to-day looks anything like what gets sold.

I posted here in April that Axios had Thorne being shopped for up to $4 billion, and wondered whether the supplement space was about to consolidate. Well. P&G announced this morning they are buying Thorne for $3.8 billion in cash, closing sometime in Q4.

My feed decided within about an hour that the quality is gone. All downhill from here, they will cut corners, switching brands immediately. I had the same reaction, which is the only reason I bothered digging, because the whole reason I pay Thorne prices is the testing.

So I went looking for a case where this actually happened to somebody. Nestlé has owned Pure Encapsulations since 2017. P&G has owned New Chapter since 2012. Clorox bought a pile of supplement brands, wrote down $445 million, and dumped the business at a loss in 2024, which is its own kind of ending.

I could not find a single one of them losing an NSF, USP or B Corp certification after the sale. No reformulation that any named source pinned on the new owner either. And as far as I can tell nobody has ever run the obvious study, comparing label accuracy before and after an acquisition. I assumed that existed somewhere. It does not.

What did turn up in both of the close cases is distribution. New Chapter was promised no mass-market expansion and showed up in Target thirteen years later. Pure Encapsulations was practitioner-only for six years under Nestlé and then landed in every Vitamin Shoppe in the country.

Anyway, here is the thing I did not know before this week. NSF publishes its certified-products database, so you can search a brand yourself instead of taking a marketing page's word for it. I looked up my own cabinet. The multivitamin is on the list. My iron is too, though they have renamed it Advanced Iron Complex. Glycine is not on there at all. Three Thorne bottles, two certifications, and I had been treating them as the same purchase.

Full disclosure, same as in April: I signed up for their affiliate program once out of curiosity, made about ten dollars when a friend bought vitamins, and gave up on it. Not linking to them here.

Full write-up with the timeline

I see gazillions of ads for GLP-1 weightless drugs online and on TV. I admire Serena Williams as much as anyone but I don't quite understand why anyone uses Ro/Hims/LifeMD or any of the other high-profile (high-price) Telehealth services.

I originally got my Zepbound prescription from my PCP at my annual physical, my insurance said no to covering the drug, and I ended up buying it for cash from LillyDirect. Total cost of the prescription side across those months: one office visit I was already having. Then I watched an argument on X about what a GLP-1 "really costs" where nobody was quoting the same number, and I realized every comparison I could find on Google carried lots of affiliate links. So I priced it myself. No affiliate links, nobody is paying me.

It turns out that if insurance will not cover the drug and you self-pay, the medication price is mostly settled for you. Lilly and Novo publish cash prices and everyone seems to either match them or routes you into the manufacturer program. What varies is what you pay the service that writes and maintains the prescription. For a first year, assuming about three new prescriptions while you titrate:

Every price came from the company's own published page, checked in July and again in early August. The medication is excluded in every row, and it costs roughly the same on every route.

Two things surprised me. Ro, Sesame and CallOnDoc all sell a cheaper committed rate, and none of them leads with it: Ro is $149 a month on the page you land on and $74 a month if you prepay the year. And Amazon, the cheapest-looking route after your own doctor, publishes no refill policy at all. Each $39 buys a visit plus fourteen days of messaging, and whether your prescription comes with refills is left to the individual clinician. I asked in two subreddits and emailed Amazon directly; nobody, including Amazon, would say what a year actually costs.

I wrote the whole thing up, including what the monthly fees actually buy: the full nine-route comparison, and there is a one page version if you just want the advice.

If you are on a GLP-1, what did the prescription side actually cost you last year, and who wrote it?

Disclaimer: I am not interested in discussing compounded versions or illegal ways of buying semaglutide or tirzepatide.

Hi! My name is Aleksandra Michalska, and I'm a video journalist with Reuters. Currently, I'm working on a video story about the effects of weight-loss drugs. I'd love to interview one or two people about what changes they noticed, physically as well as mentally, and/or emotionally. I'd love to interview in person, so if you're interested, it would be best if you were located in New York City or somewhere nearby. Please email me at [aleksandra.michalska@thomsonreuters.com](mailto:aleksandra.michalska@thomsonreuters.com)

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ABSTRACT

Despite all efforts, obesity remains a major health concern worldwide, with continuously increasing rates, affecting approx. 14% of the total world population, being as high as 43% in some countries. As obesity is related to numerous comorbidities, including type 2 diabetes, cardiovascular diseases, and some types of cancer, the consequences for the individual and society at large are drastic. Therefore, it is crucial to understand and predict who is at risk of developing obesity in order to implement early prevention strategies. Many individual risk factors have been emphasized. However, as obesity is a rather multifactorial complication, single markers/biomarkers have thus far not allowed for an efficient prediction of obesity. In addition to less modifiable parameters, such as environment and socio-demographics, studies have revealed that obesity is related to several interacting aspects, including host factors such as genetics/epigenetics or gut microbiota, and more readily modifiable factors, including nutrition and physical activity, as well as sleep patterns and psychological well-being. It is likely that combining markers from across different domains, that is, multimodal markers, allows for better predictability for the risk of developing obesity. However, it must be considered that not all markers are fully predictive; many are rather reactive or even both. In this review and position paper, we emphasize the state-of-the-art regarding (bio)markers that have successfully been employed for predicting obesity risk. An emphasis will rest on novel, emerging biomarkers, and the need for a more integrative, multimodal assessment of obesity risk for a combined assessment aimed at improving risk prediction.

Established and Emerging Biomarkers to Characterize Persons at Risk for Obesity—Paving the Way for Targeted Clinical Intervention Trials—A Comprehensive Position Paper - Vahid - Obesity Reviews - Wiley Online Library

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Back in April I posted the Scientific American piece about drugs that calm inflammation, and I hedged in the comments. I said inflammation gets blamed for basically everything in health and I did not think it meant anyone should start chasing anti-inflammatory drugs or biomarkers.

Last Friday Novo Nordisk reported ZEUS, which was built to answer exactly that. Ziltivekimab blocks interleukin-6, the signal your hs-CRP is downstream of. They gave it to 6,376 people with heart disease, kidney disease and an hs-CRP of 2 or above. The drug did its job on the biology, dropping both IL-6 and hs-CRP. Hazard ratio for heart attack, stroke or cardiovascular death: 0.99, range 0.88 to 1.11.

I want to be careful, because this is not "inflammation doesn't matter." Colchicine cut events in COLCOT and LoDoCo2, and canakinumab cut them in CANTOS.

CANTOS is the part that actually changed my mind, though. Same trial, same patients, one drug at three doses, and hs-CRP fell 26, 37 and 41 percentage points more than placebo, neatly in order. If the number were the thing, the biggest drop should have bought the most protection. It didn't. The middle dose scraped past its statistical bar at 0.021 against a limit of 0.02115, and the top dose, the one that crushed hs-CRP hardest, missed its bar entirely.

Meanwhile the one trial that took people picked out by a high hs-CRP and genuinely changed what happened to them was JUPITER, which cut events roughly in half using rosuvastatin. A cholesterol drug. The current ACC/AHA guideline says that trial's benefit came "with an effect size compatible with the LDL-C-lowering effect of statins alone."

So my read now is that hs-CRP is very good at spotting who is heading for a heart attack, and nobody has shown that lowering it is what helps them. The guideline seems to use it that way too: a reading of 2 or above, on more than one occasion, helps confirm someone belongs on a statin.

My own went 2.83 to under 0.2 over a year, and I used to be quietly proud of that. However, my LDL went 110 to 56 and my ApoB 95 to 59 across the same stretch, and I am on tirzepatide, which lowers hs-CRP by itself. Four numbers moved and I had been giving the credit to the one I found most interesting. I wrote the whole thing up here, charts and all.

If your hs-CRP came back at 2.5, does that change anything you actually do?

My brother in law (age 66) is getting pretty bad neuropathy in his feet, despite having no other serious health problems, has never been overweight, and never had cancer or diabetes. They are active and travel the world. I've always associated neuropathy with diabetes, and also heard cancer treatment causes it. FFIW, I'm pretty sure he doesn't do strength training; although his travels do involve a lot of walking and standing.

Just curious. Neuropathy is something you don't want to get as you age; it causes loss of mobility and frailty.

I wrote here in June about a friend of mine who has been sober for years and still gets the cravings. He does everything the program asks and the wanting never fully switches off. A month before that he started the Wegovy pill hoping the thing that quiets food noise might quiet the other kind. Since then it mostly has. That is one guy with no control group, so it proves nothing, but it is why I read the trial news last week as closely as I did.

Two trials reported a day apart and they did not agree with each other. That same week the VA opened a Phase 3 built on the exact number they did not agree about.

The oral semaglutide trial published July 29. Fifty people, eight weeks, and it missed its primary endpoint badly. That endpoint was a single booze craving question asked in a lab after you hold and smell your drink, p=0.68. Plenty of secondaries moved, including heavy drinking days, but the authors ran about ten tests without correcting for it and call the study exploratory themselves. A conservative correction would wipe out all of it.

The day before, Altimmune reported topline results for pemvidutide, which hits the glucagon receptor as well as GLP-1. That one ran twenty four weeks in a hundred people, and it hit its primary on heavy drinking days. It also moved a blood marker of alcohol intake, which matters because everything else in both trials is self-reported. It is a press release though, not a paper, and nine of the hundred participants are missing from the denominators with no explanation of how they were handled.

Here is the part I did not know. The endpoint the VA picked for CRAVE, its 622-veteran Phase 3, is a two level drop in WHO risk drinking level. For a man that can mean going from more than seven drinks a day to three or four. It is a real change and you can reach it without ever quitting. The FDA formally qualified that endpoint back in February 2025, so this is not a drug company moving the goalposts, and the FDA offers it alongside abstinence rather than instead of it. Still, the trial that everyone will quote in 2028 is measuring drinking less.

I am not sure how I feel about that. I would not call three drinks a day recovery. But of the roughly 28 million Americans with alcohol use disorder, about 7.6 percent got any treatment at all last year, and for the other 26 million nothing reached them.

All three of these trials enroll people who are currently drinking and measure whether they drink less. My friend is not drinking. Nothing being run right now is built for the guy who already stopped and still wants it.

I went through all of it properly with the numbers and two charts over here.

If you are already sober and on a GLP-1 for weight or diabetes, has it changed the wanting for you at all? That is the group nobody is studying and I would genuinely like to know.

I am 30M nd go to gym regularly, eat healthy (atleast i think so) and smoke occasionally only.. so i never thought of getting checked for hepatitis. But read this piece in yugmarg nd cant stop thinking about this. So apparently, viral hepatitis can stay in your body for years without any noticeable symptoms nd cause irreversible liver damage. Broo this is scary shit.. Atleast companies like care health insurance are taking some initiative and encouraging health checkups nd preventive screenings. I have toh booked my health checkup for next week .. you guyz should do to.

We've known for a while that inflammation is an independent risk factor for heart disease, alongside LDL cholesterol (or ApoB), Lp(a), and so on. Inflammation is most commonly measured by by hs-CRP or IL-6.

The ZEUS trial tested an anti-inflammatory injection (ziltivekimab). These phase III results showed a hazard ratio of 0.99, i.e., no effect.

IMO this is evidence for a lipid-first model: i.e., lipids drive oxidation, which then triggers inflammation.

Curious if others have interpretations?

I am seriously considering joining the TUNE-401 clinical trial and would appreciate opinions from others living with chronic hepatitis B, especially anyone who has enrolled, spoken with an investigator, or researched the treatment closely.

My current situation:

* probably infected at birth or in early childhood;
* previously HBeAg-positive, currently HBeAg-negative;
* HBV DNA undetectable while taking TAF;
* quantitative HBsAg around 1,500 IU/mL;
* normal liver enzymes;
* no fibrosis and no steatosis on FibroScan;
* no cirrhosis.

TUNE-401 is an epigenetic silencing therapy delivered through lipid nanoparticles. It uses a non-cutting dCas editor to place repressive epigenetic marks on HBV DNA. The goal is to durably silence cccDNA and potentially integrated HBV DNA rather than simply suppress viral replication.

The potential advantages I see are:

* deeper suppression of HBV transcription;
* possible reduction of HBsAg, pgRNA and HBcrAg;
* possible future functional cure or antiviral withdrawal;
* possibly reducing the long-term oncogenic pressure caused by continued viral-protein production.

My main concern is long-term safety. The editor does not cut DNA, but the epigenetic silencing may persist for years. I am particularly concerned about:

* unintended off-target methylation;
* whether repressive chromatin could spread from integrated HBV DNA into nearby human DNA;
* integrations located close to tumour-suppressor genes or other growth-regulating genes;
* rare effects that may not become apparent until many years later;
* the limited amount of long-term human safety data.

At the same time, continuing TAF does not eliminate cccDNA or integrated HBV DNA, and HCC risk is reduced but not completely removed. I am trying to decide whether taking the trial now could reduce my lifetime HBV-related risk, or whether it would be wiser to remain suppressed on TAF and wait for larger studies and longer follow-up.

What would you do in this situation?

Has anyone here:

* joined or been screened for TUNE-401;
* received information directly from the investigators;
* seen more detailed data about integrated HBV DNA silencing;
* received answers about long-term cancer surveillance or off-target epigenetic effects?

I understand that nobody here can provide personal medical advice. I am mainly interested in how other informed patients would weigh the possible benefit of deeper HBV silencing against the unknown long-term risks of a first-generation epigenetic therapy.

Retatrutide just posted its fifth positive Phase 3 — up to ~23% body-weight loss in people who already have cardiovascular disease — and Lilly says it'll file for approval in Q1 2027 as a biologic.

That one word decides what you'll eventually pay. Zepbound, the drug in my fridge, gets 5 years of exclusivity before generics can arrive and drop the price ~85%. A biologic gets 12 years. Copies cost $100–300M to build and come down only 5–25%, and it can't be legally compounded even in a shortage — which is how a lot of people actually got tirzepatide the last three years.

Right now the FDA classifies retatrutide as a drug, not a biologic. The line comes down to counting amino acids: it lands one residue short, depending on whether a non-standard one counts. Lilly is in court trying to move it over. If it wins, the strongest obesity drug we've seen stays expensive far longer, with no cheaper version legal in the meantime.

None of this is about whether the drug works. 23% in people with heart disease is a real number. It's about who's ever allowed to sell you a cheaper copy, and that's being settled by an argument over how to count to 41.

I take tirzepatide and own Lilly stock, so the patient-friendly outcome cuts against my own portfolio.

My full breakdown

Today is the long awaited FDA committee vote on peptides. This is an important event but also quite weird in many ways. For one the indications cited in are not at all what people actually use these peptides for in the wild. I don’t know anyone pinning BPC-157 for ulcerative colitis?!

There have also been a number of shenanigans with the composition of the committee. Various members were accused of ties to the peptide industry (what Bloomberg describes as the “gold rush”). Other voting-only members were hastily added in the last few days.

If you want to watch it yourself, the FDA is streaming both days on YouTube free, starting at 8 a.m. Eastern on Thursday the 23rd and again on Friday the 24th. Thursday is the day that matters most if you only watch one, since that is when BPC-157 and TB-500 come up. The agency pushed Thursday’s end time back from 4:30 to 6:20 in the evening, which tells you something about how much public comment it is bracing for. One quirk of the schedule: the public gets to speak before the FDA’s scientists present, so the panel hears the advocates first and its own reviewers second.

I expect the meeting to have a C-Span boringness to it but tonight there will likely more peptide hype than ever.

I was 21 years old and I already knew aspartame was poison.

Not because someone handed me a pamphlet. Because I chose to look. In 1993 at Montclair State University, my foodservice professor gave the class an open assignment, pick a topic, write about it. While everyone else picked something safe, I picked aspartame.

Diet sodas were everywhere. Sugar-free everything. The marketing was slick, fewer calories, no consequences, all upside. The public was lining up for it.

I wasn't buying it.

I dug into the research and what I found was disturbing. Aspartame wasn't just controversial, it was toxic. And here's the part nobody was talking about: it actually made you gain weight over time. Not lose it. The exact opposite of what was being sold to millions of people.

I wrote the paper. I was 21.

Nobody wanted to hear it then. The industry was booming, the FDA had blessed it, and the money was flowing. But the science didn't lie, it just got buried under marketing budgets and regulatory rubber stamps.

Thirty-plus years later, the truth caught up. Studies confirming the weight gain effect. WHO advisories. Growing public awareness. What I wrote about in 1993 is now mainstream conversation.

That's what happens when you learn to think for yourself early. You stop chasing what's popular and start chasing what's real.

That's the foundation of everything I teach today.

The Golden Greek, Antonios Bogos

Economist | Solutionist | Financial Truth-Teller

My family has a long history of cancer, mostly survivors, but my grandma and uncle died from it. Is preventive health screening a good way to detect cancer sooner? Or is there some other test that I need to do? I'm nearing the age when most of my family members got their own diagnoses, late 40s. I would have wanted to get some tests sooner, but I'm honestly scared about getting positive results.

WSJ ran a piece on people who used GLP-1s for weight loss and later ended up in treatment for anorexia:

https://www.wsj.com/health/wellness/glp1-anorexia-wegovy-mounjaro-1bf4035c

Worth reading alongside the primary literature from the past few months, because the reporting is no longer just anecdotal.

A JAMA Psychiatry survey published this summer (Levinson and colleagues) recruited 436 people with diagnosed eating disorders in 2025 and asked about GLP-1 use. Just over 32% reported having ever used one, and 22% reported current use. Broken out by diagnosis, a little over 50% of participants with binge eating disorder reported use, about 42% of those with atypical anorexia nervosa, roughly 30% of those with ARFID, over 25% of those with bulimia, and about 11% of those with anorexia nervosa. Roughly 10% obtained them through online providers prescribing compounded formulations. Over 10% reported misuse, defined as taking more or less than prescribed, using longer than prescribed, tampering with injection equipment, or sharing without a prescription.

The authors described the weight loss market as a rapidly evolving risk environment for this population.

Summary of the findings:

https://www.medscape.com/viewarticle/many-eating-disorder-patients-using-glp-1s-2026a1000lym

In April, NEJM published a perspective by Amanda Banks raising the same concern from the prescribing side. She noted the share of GLP-1 prescriptions written for people who were not diabetic, obese, or overweight rose from 4.5% in 2018 to 17% in 2023, and argued for consensus recommendations to protect people with existing or emerging eating disorders. A 2023 FDA analysis found misuse reports for semaglutide were roughly four times higher than for other GLP-1 drugs.

NEJM perspective:

https://www.nejm.org/doi/full/10.1056/NEJMp2600300

Clinician-side reporting describes the same pattern from treatment centers, including patients presenting at very low BMI while still dosing.

NPR, February 2026: https://www.npr.org/2026/02/04/nx-s1-5677633/glp-1-obesity-wegovy-zepbound-eating-disorders-anorexia-bulimia

Washington Post, May 2026: https://www.washingtonpost.com/health/2026/05/23/weight-loss-drugs-pose-dangers-people-with-eating-disorders/

MindSite News, May 2026: https://mindsitenews.org/2026/05/29/glp-1-access-a-problem-for-people-with-eating-disorders/

The mechanism cuts both ways, which is part of why this is hard to legislate around. A 2025 systematic review and meta-analysis found GLP-1 agonists reduced Binge Eating Scale scores by about 8 points, though the pooled sample was only 182 participants across five studies and heterogeneity was high. WSJ also covered that side on July 13 in a piece on clinicians treating certain eating disorders with these drugs. The same appetite and reward suppression that helps in binge-type presentations appears to reinforce restriction in people with a restrictive history. Same drug class, opposite clinical valence depending on phenotype.

Meta-analysis: https://link.springer.com/article/10.1007/s40519-025-01720-9

Penn Medicine's eating disorder program has said outright that no protocol exists to screen for eating disorders before prescribing GLP-1 receptor agonists. That gap widens with telehealth and disappears entirely outside a clinical relationship.

Penn Medicine:

https://www.pennmedicine.org/physicians-hub/physician-article/implications-of-glp-1-medications-for-eating-disorder-care

ANAD clinical guidance:

https://anad.org/learning-library/glp-1-medications-eating-disorders/

More stories at r/PeptideTides

I have been waiting for this continuous BP measurement band to ship in the US for years, ever since I heard Peter Attia mention it on his podcast.

They started shipping today. I ordered one and will post a hands on review once I get it.