I thought the USA Today story on biohacking was pretty solid because it gets at something real: a lot of people are building their own mini health system now with wearables, self-ordered labs, biological-age tests, AI, full-body MRIs, longevity clinics, all of it.

What bothers me is that “biohacking” now covers two totally different kinds of people.

One person is basically just trying to be more on top of their health. They lift, do cardio, track blood pressure, try to sleep better, maybe use a wearable, maybe get a few extra labs here and there. Fine. Nothing wrong with that.

The other person is basically just buying the feeling of being proactive.

That’s the version I’m a lot more skeptical of.

At some point it stops being about health and starts being about consumption. More tests, more scans, more supplements, more numbers, more subscriptions, more stuff to fuss over.

And I think that’s what a lot of this industry quietly feeds on. Not better outcomes. Just the feeling that you’re being unusually serious about your health because you have access to more data than the average person.

But most people are not stuck because they lack information.

They’re stuck because the basics are hard to do over and over.

Sleep on time. Exercise regularly. Keep your weight in a decent place. Don’t smoke or drink. Get stronger. Go for walks. Get your screenings done. Keep your blood pressure under control.

That stuff is not exciting, and nobody is getting rich selling it to you in a sleek box every month.

So I’m not anti-data. I just think a lot of people use data to avoid the boring work. It feels productive to stare at numbers. It feels way less fun to admit you’d probably get more out of walking every day and going to bed earlier than from another panel or another gadget.

That’s kind of where I land on this whole thing:

Good “biohacking” helps you follow through on basic healthy behavior.

Bad “biohacking” is just health anxiety with nicer branding.

I quit drinking after getting headaches, looking at the evidence and deciding it wasn’t worth it. Most people with alcohol use disorder can’t just decide. Fewer than 2% of them ever get medication for it, and the drugs we do have (naltrexone, acamprosate, disulfiram) produce small effects and get almost no uptake.

This drug could be different and have big impact.

Lilly has a drug [Brenipatide](https://en.wikipedia.org/wiki/Brenipatide) in late-stage trials called brenipatide. Same class as tirzepatide (Mounjaro/Zepbound), but engineered with a much longer half-life. Dosed once a month, subcutaneous. That schedule alone is a big deal for addiction medicine, where adherence is half the battle. Vivitrol, the monthly depot of naltrexone, outperforms the daily pill for exactly that reason.

Two Phase 3 AUD trials are actively enrolling ([RENEW-ALC-1](https://clinicaltrials.ucsf.edu/trial/NCT07219966) and [RENEW-ALC-2](https://clinicaltrials.gov/study/NCT07219953)), 1,100 patients each. Separate trials are running for smoking relapse, opioid use disorder, bipolar disorder, and asthma. Readouts start landing in 2027.

Here’s why Lilly is going hard at this. The signal in the existing data is almost hard to believe.

A [BMJ study published last month](https://pmc.ncbi.nlm.nih.gov/articles/PMC12958796/) followed 606,000 veterans on GLP-1s vs. SGLT2 inhibitors. In people with no prior substance use disorder, GLP-1 users had 18% less alcohol use disorder, 20% less nicotine, and 25% less opioid use disorder. In people with an existing SUD, GLP-1 use was associated with 39% fewer overdoses and 50% fewer substance-related deaths over three years.

A [JAMA Psychiatry Phase 2 trial of semaglutide in AUD](https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2829811) (48 people, 9 weeks) showed medium-to-large effect sizes on drinking outcomes and reduced cravings. That matters because approved AUD meds like naltrexone typically show only small effect sizes. And the semaglutide group hit those numbers at the two lowest clinical doses.

So here’s the case. A drug class that wasn’t designed for addiction is already outperforming drugs that were. Lilly is now testing a molecule engineered for it, with a dosing schedule that solves the adherence problem, in the largest randomized AUD trials ever run.

If these trials turn out positive, it’s the biggest thing to happen to addiction medicine in a generation.

I’m not necessarily a huge fan of all the health “scores” but must admit this is nifty marketing.

San Millán is the exercise physiologist behind a lot of the Zone 2 and mitochondrial work this world cites. He trained Tadej Pogačar. He has been on every major health podcast in the space.

He just published a funny, sharp critique of where the longevity industry has ended up. Worth a read.

Good piece on something that feels very real now: GLP-1s are escaping the obesity/diabetes box fast.

People are trying them for everything from addiction and brain fog to menopause symptoms, bodybuilding, and “longevity” use, while the actual evidence is still much thinner than the online hype. The interesting part is that some benefits may be partly weight-independent, which helps explain why the drugs seem to be doing more than just making people eat less. But the article also makes clear that some promising uses have already flopped in trials, and a lot of this experimentation is happening through telehealth, compounded products, and gray-market sources.

My take: this looks less like a miracle and more like a powerful tool some people are already overextending. Big upside for some people, but a huge gap between what’s being claimed online and what’s actually been tested. However, I remain optimistic that many of the (currently off-label) uses will work out with the right dosing regime and show so in studies.

I have been on Zepbound for weight loss for a year and a half and saw a lot of improvements but in my case I believe they were almost all related to significant weight loss.

For the last few years, the obesity-drug story has sounded pretty simple: find better ways to hit GLP-1 harder.

This new STAT piece suggests that may be too simple.

Richard DiMarchi and Matthias Tschöp’s group has published preclinical (i.e. not human) work on a GIP + glucagon co-agonist that does not directly target GLP-1. In rodents and monkeys, they argue it can still drive major weight loss, and possibly with less of the nausea/vomiting baggage that comes with current drugs.

The most useful way to read this is not “GLP-1 was a mistake.”

It is more like this: weight loss and side effects may be more separable than current drugs make them look.

That idea is not crazy. GLP-1 drugs seem to do a lot of their work by reducing energy intake. Glucagon may add something different by pushing energy expenditure and catabolism. And GIP may help soften some of the aversive GI effects that make dose escalation miserable for a lot of people.

This is still animal data. The approved and most advanced obesity drugs with the best human evidence still include GLP-1 signaling. And GLP-1 may be doing more than just helping with weight loss. The current class already has real outcome data in areas like cardiovascular and kidney disease. A future drug that matches the scale loss but drops GLP-1 would still have to prove it is not giving up benefits we already know matter.

No one should read this and come away thinking the GLP-1 era was built on the wrong target. What this paper does suggest is that the next big leap may not be “more weight loss at any cost.” It may be finding ways to keep strong efficacy while making fewer people feel awful.

I am not an expert by any stretch of the imagination but I keep reading that vague “inflammation” is behind basically every bad thing in health, so I’m a little skeptical of how this gets discussed.

That said, the Scientific American piece seems directionally right: heart disease probably isn’t just a cholesterol story. Inflammation seems to play some role in how plaques behave and how risky they become.

What I don’t think this means is that LDL suddenly matters less, or that everyone should start chasing anti-inflammatory drugs or biomarkers.

My cautious takeaway is:

inflammation may be a useful extra layer in cardiovascular risk, especially in some higher-risk people, but it still seems easy to oversell because the word is so broad and often used sloppily.

Curious how others here think about it.

Does this feel like a meaningful shift in prevention, or just another case of a real idea getting stretched too far?

What I liked about this interview is that the practical message is a lot less delicate than the usual bone-health advice people get. The conversation is basically a pushback against the idea that once bone density slips, your best option is to become timid. The argument here is that bone needs a real training signal: progressive resistance training, impact where appropriate, and actual coaching instead of a permanent “be careful” mindset. The episode title itself leans on a reported 78% fracture reduction, which is what made me click in the first place.

This one landed for me because I had a DEXA in October. My total body BMD was 1.327 g/cm² with a T-score of 1.3, which was normal, and my left femoral neck BMD was 0.905 g/cm² with a T-score of -1.0.

My FRAX from that same scan was 4.1% for major osteoporotic fracture and 0.3% for hip fracture over 10 years, based on left femoral neck BMD, with no listed risk factors.

So I’m in that annoying zone where the overall picture is reassuring, but there is still a pretty obvious message hiding in the details: don’t act fragile, but also don’t pretend bone health is automatic just because you are a male who lifts. My report specifically called out the left femoral neck result and recommended continuing to load the hips and legs with weight-bearing resistance work.

A lot of people here talk about longevity training as cardio zones, steps, or staying “active.” But once you actually look at a scan, it gets more specific. Are you giving your skeleton a reason to stick around?

Something that increasingly bothers me in health media is how often research universities now sound like wellness marketers. This week’s Keck/USC headline said fruits, vegetables, and whole grains “may increase” early-onset lung cancer risk. But the underlying work was a conference abstract, not a full peer-reviewed paper, and the comparison was basically young lung-cancer patients versus broad U.S. reference data, not matched cancer-free controls.

That matters because the press release runs way past what the study can actually show. It jumps from “this group reported healthier diets than the general population” to speculation about pesticides, despite not directly measuring pesticide exposure in food, blood, or urine. One outside expert put it perfectly: the headline could just as well have been that “non-smokers eat healthier diets than smoking Americans.”

And this is the bigger problem. A BMJ study found that 40% of university press releases contained exaggerated advice, 33% made causal claims from correlational data, and 36% presented animal findings as though they applied to humans. When the press release exaggerated, the news often followed.

We spend a lot of time mocking influencers for overselling shaky evidence. Fair enough. But universities deserve more scrutiny when they use institutional credibility to do the same thing. A conference abstract is not consumer advice. And a medical-school logo should not be enough to turn speculation into authority.

Give it a week and someone with a supplement code or an organic-only shopping list will be quoting this as proof that broccoli is dangerous unless you eat ribeye or shop at Erewhon.

I liked Dr. Michael Hunter’s recent essay on magnesium and sleep because it is representative of his writing at its best: thoughtful, grounded in real (albeit anecdotal) patient experience, and resistant to the usual supplement hype. He is not claiming magnesium is a miracle. He is trying to explain why it seems to help some people and does very little for others. That basic point fits the evidence pretty well.

Magnesium is an essential mineral involved in nerve and muscle function, so it is plausible that it could help when poor sleep is tied to things like cramps, physical restlessness, or low magnesium status. But the research on magnesium for insomnia is still limited, and reviews suggesting benefit have mostly relied on small, low-quality studies. (nccih.nih.gov)

What I found useful in Hunter’s essay is the distinction between sleep problems that feel more physically “wired” and sleep problems that are really about mental overload. That is not some settled law of sleep medicine, but it is a practical way to think about why magnesium helps one person and does almost nothing for another.

For what it’s worth, I have tried both magnesium glycinate and L-threonate. The L-threonate version seems to have some effect for me, but it definitely is not magic. That personal experience made the essay ring true. Sometimes these supplements seem to take the edge off a little without actually “solving” sleep.

One important evidence-based point to add: for chronic insomnia, the first-line treatment is CBT-I (cognitive behavioral therapy for insomnia). It is a structured, non-drug approach that helps people change the habits and thought patterns that keep insomnia going. It often includes things like a consistent sleep schedule, using the bed only for sleep, getting out of bed when you cannot sleep, and reducing the panic spiral around a bad night. The American Academy of Sleep Medicine recommends CBT-I as first-line treatment for chronic insomnia in adults. (aasm.org)

My practical read:

Magnesium seems like a reasonable thing to try when sleep problems come with cramps, tension, or bodily restlessness. But if your main issue is rumination, stress, or chronically bad sleep habits, the bigger payoff is probably not in supplement stacking. It is more likely to come from CBT-I style changes and better evening routines.

I volunteer at a local university wellness program and we have a high quality iDXA, VO2 setup up and lactic acid measurement system (though I’ve not seen this used allot)

I’m super interested in collecting anonymized data and doing some analysis. My first thought is validating some of the HRR (heart rate recovery) studies as a proxy for VO2. I’d also like to do some comparisons between bio-impedance devices and iDXA. Priority should be given to new studies, but replication could be valuable as well. Any reference to existing studies for ideas offered would be helpful.

Another thought was around the performance benefits of seeing real time data/feedback when doing VO2 measurements.

I’d love to hear other ideas. We have the potential of doing experimental paired before/after studies with some of the aligned programs at the university. I think the easiest population to do this with would be an older group ranging from 55-80+ with a mean age of 65.

Funding is always an issue - so using existing data or what would normally be gathered is helpful.

I welcome your ideas.

Thanks!!

Article might be paywalled. Apple News+ link

Joe Rogan is now talking up plasmapheresis / therapeutic plasma exchange as a way to remove “toxins,” inflammatory proteins, and maybe even microplastics. The problem is not that this procedure is fake. It’s real medicine.

The problem is that “real medical procedure” and “good idea for healthy people” are not the same thing.

Therapeutic plasma exchange is used in serious medical situations. That’s very different from using it as a longevity move, a recovery hack, or some vague detox upgrade for rich healthy people.

The microplastics angle is where this gets especially flimsy. Yes, there’s early discussion around whether apheresis might remove some particles from blood. But we are nowhere near “therefore healthy people should pay to do this.” Tiny studies, lots of uncertainty, and a giant gap between mechanistic curiosity and proven benefit.

And this is not harmless self-experimentation. We’re talking about an invasive procedure with real risks, not a fancy sauna or a supplement stack.

What bothers me most is the pattern: A legitimate treatment for genuinely sick patients gets turned into premium prevention content for people who want to feel like they have access to secret medicine.

Very interesting episode by the Barbell Medicine guys. Some of the stats are very surprising (to me). I had thought that two blood tests showing low T and symptoms were standard but apparently not. To be honest I did get a labcorp test in my own and then had one from the clinic that prescribed TRT. I don’t actually know whether they would have insisted on a second one.

I am sure that they are correct that often test levels are low (and symptoms are present) because of general bad health (in particular significant amounts of visceral fat). I was arguably in that position.

Also, I’m very interested in seeing the Book the guys are about to publish.

Gemini YouTube summary:

This video, the first in the Signal launch series by Barbell Medicine doctors Dr. Jordan Feigenbaum and Dr. Austin Baraki, explores the current "testosterone crisis" and the medical, social, and analytical problems surrounding it.

Key Problems in the Current System:

Inappropriate Prescribing: Approximately 25% of men start testosterone replacement therapy (TRT) without even a single preceding blood test, often driven by the "wellness clinic" business model (1:41-2:57).

Ineffective & Contaminated Supplements: Most "testosterone booster" supplements lack scientific evidence, with 62% having zero published data. Furthermore, 12% of muscle-building supplements are contaminated with undisclosed steroids, which can paradoxically suppress natural production (3:36-7:49).

The Unreliability of Single Tests: A single low testosterone reading is not a diagnosis. The body's hormone levels fluctuate significantly due to sleep, stress, and illness, and roughly 50% of initially "low" results normalize upon repeat testing (13:40-14:53).

Addressing the "Testosterone Decline" Headline:

The narrative that testosterone is crashing 1% per year across generations is largely overstated due to two main factors:

Testing Artifacts: Older research relied on immunoassays, which are less accurate and prone to cross-reactivity, leading to overestimation. Modern mass spectrometry (the gold standard) has largely corrected these readings, making it difficult to compare data across eras (22:02-23:38).

The BMI Blind Spot: Many studies rely on BMI to control for obesity, but BMI fails to account for visceral adipose tissue (VAT)—the hormonally active fat packed around organs that contains the enzyme aromatase, which lowers testosterone. When researchers account for both better testing and actual waist circumference, the "decline" largely vanishes (26:58-31:38).

Takeaways for Patients:

Metabolic Health is Key: Longitudinal data shows that men who stay lean, active, and free of chronic disease maintain stable testosterone levels well into their 70s and 80s (34:46-35:12).

Don't Treat the Number: If you are concerned about your testosterone, the first step is not a clinic or a supplement, but a thorough clinical evaluation to understand your lifestyle, symptoms, and health context (37:05-38:24).

I heard a claim on a podcast (The Drive) recently that we only don’t know the mechanism of action for about 3% of FDA-approved drugs. That sounded low to me, so I looked it up.

It seems it’s not just 3%. Depending on how you count, it’s somewhere between 7% and 18% of approved drugs where we don’t have a clear, confirmed mechanism of action. A 2020 review in iScience put it at 10 to 20%. Wikipedia maintains a list of 146 drugs with unknown mechanisms. These aren’t obscure veterinary compounds. They include Tylenol, Mucinex, lithium, metformin, ketamine, modafinil, and general anesthetics as a category.

Let that sink in. We don’t fully understand how general anesthesia works. We put people under every day in every hospital in the world, and the honest scientific answer to “how does this work?” is “we have some theories.”

Tylenol is the wildest example. It’s been in widespread use since 1950. Sixty million Americans take it every week. Researchers are still publishing new mechanism-of-action papers about it. The current best guess involves the endocannabinoid system, which nobody even knew existed when Tylenol hit the market. A new study came out just last year proposing yet another pathway.

Mucinex isn’t much better. One otolaryngology journal called guaifenesin “the ubiquitous orphan” and questioned whether the evidence supports its use at all.

This matters because we tend to assume FDA approval means we deeply understand a drug. It doesn’t. The FDA’s standard is safe and effective, not “we know exactly what this does at the molecular level.” That’s a reasonable standard for approval. But it should make all of us a little more humble about how much we actually understand about the medicines we take every day.

It should also make you skeptical of anyone who speaks with total confidence about the mechanism of every supplement and peptide they’re selling. At the same time we shouldn’t think we understand how our bodies work. I always felt a lot of medicine is just applied statistics!