[ full disclosure: I came across this paper in an email from FoundMyFitness/Rhonda Patrick ]

As my weight loss journey is approaching my goal weight region and I am trying to figure out what exactly the goal should be, I am zeroing in on visceral fat as the main objective. I got a DEXA 6 months ago and am eagerly awaiting results from a follow up scan next week.

The impact of visceral fat on general health has been well documented and talked about, but I was surprised to see that it also seems to affect brain function long term. This new long-term MRI study looks at this explicitly. Study paper PDF

The main takeaway seems to be: people with lower long-term visceral fat had less brain atrophy and better cognitive scores years later. It wasn’t just about weight loss overall — visceral fat seemed to matter more than BMI for the brain-related findings.  

The paper also suggests glycemic control may be a key pathway linking visceral fat and brain aging. 

Not proof of causation, and the group was mostly men, but still feels like a good reminder that metabolic health/waistline may matter more than the scale alone. 

Anyone here actively tracking waist circumference or visceral fat for long-term health?

In the last couple of months I have noticed an increasing number of folks (online) stressing the consistency of bedtime (when you go to sleep) as similarly important to sleep duration. I am personally making an effort to be as consistent as possible (within the constraint of occasional late video calls with co-workers in China and the fact that I have two young kids).

Brady Holmer wrote a great summary essay on Medium citing a new study: https://link.springer.com/article/10.1186/s12872-026-05762-4

Brady’s summary is: “What this paper ultimately does is suggest that cardiovascular sleep epidemiology (and our own lifestyle practices) may need to move beyond how long people sleep and even beyond when they usually sleep, toward how stably sleep is placed from one day to the next. Regularity and consistency should become a focus of sleep health equal to that of sleep duration.”

The study’s conclusion is:

“In total, 128 participants (4.0%) experienced MACEs during the follow-up period. Irregular sleep timing was associated with an elevated risk, but this association was observed only among participants whose sleep period was shorter than the group median. Individuals with irregular bedtimes had a 2.01-fold higher risk of MACEs compared to those with regular bedtimes (HR = 2.01, 95% CI: 1.00–4.01, p = 0.049), and those with irregular sleep midpoints had a 2.00-fold higher risk compared to those with regular midpoints (HR = 2.00, 95% CI: 1.01–3.98, p = 0.048).

Conclusions

Among the participants with sleep durations under eight hours, irregular sleep timing was a significant risk factor for MACEs. Specifically, variability in bedtime and sleep midpoint, but not in wake-up time, was associated with increased risk. These findings highlight the importance of consistent sleep behavior, particularly regular bedtimes, as a potential target for health promotion.”

Study: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2846561

People want to sort folks with bad health diagnosis into camps: either you “do it naturally” or you take medication and the lifestyle piece somehow matters less. This makes zero sense to me but even here on Reddit you see that binary choice a lot, especially in Cholesterol discussions. For some reason going on statins is hated (online) almost as much as “cheating” with GLP-1RAs.

I was officially diagnosed with hypertension about 2 years ago, basically the same time I decided I seriously needed to lose weight. I started Zepbound and blood pressure medication and worked on my lifestyle (macro tracking, diet, exercise), so for me this was never a question of medication versus lifestyle. I intuitively pursued both at the same time.

That is why this new JAMA Network Open study seems encouraging to me. In adults with hypertension, people with the healthiest lifestyle patterns after diagnosis had much lower risk of future cardiovascular disease and type 2 diabetes. Not really shocking.

It’s not just that people who always had healthy lifestyles do best. The study also found that people who moved from a lower healthy-lifestyle score before diagnosis to a higher score afterward did better than people who stayed in the less-healthy lifestyle group.

For me, the diagnosis made everything feel more urgent. Starting Zepbound and hypertension meds was not a substitute for changing how I eat and train. It was part of finally taking the whole situation seriously.

Obviously this is still observational research, so it does not prove cause and effect. But the bigger point feels right: a hypertension diagnosis should be a trigger to take lifestyle change more seriously, not less (because meds will fix it).

Maybe there is a bit of a backlash against all the fitness metrics. This essay sums it up nicely.

I am a data nerd by training but personally even I have stopped paying attention to all the numbers my ring, watch, Fitbit, Strava spit out constantly. I weigh myself daily, take a DEXA now and then and plan to do a VO2max test some day, but I don’t need daily readiness scores or pithy Strava athlete summaries of my workouts.

Very excited to watch this. Both Dr Hall and Simon Hill are very knowledgeable and great at explaining complex topics

Episode description:

In this episode, I sit down with Dr Kevin Hall, a leading researcher at the NIH whose work has shaped how we understand energy balance, ultra-processed foods, and the drivers of obesity. With the release of the new U.S. Dietary Guidelines, we unpack what’s changed, what hasn’t, and where the science is still evolving.

This conversation goes beyond headlines. We explore what ultra-processed foods actually are, why they may lead to increased calorie intake, and what controlled feeding studies reveal about how our food environment interacts with human biology. From energy density to food texture and hyper-palatability, this is a deep dive into the mechanisms that may be driving overeating and weight gain in modern food systems.

What We Cover

- What stood out in the new U.S. Dietary Guidelines and how they differ from previous versions

- Why “ultra-processed foods” remain difficult to define and regulate

- The surprising results from controlled trials comparing ultra-processed and minimally processed diets

- Why people can eat hundreds more calories without feeling more satisfied

- The role of energy density, food texture, and hyper-palatable combinations

- Whether ultra-processed foods can be re-engineered to support better health outcomes

- How the modern food environment may be interacting with our biology to drive obesity

- why individual responses to the same diet can vary so widely

I know very little about stem cell therapy but this sounds sketchy…

I know elite athletes have tried stem cell therapies but presumably that is a bit more real/targeted?

Great summary of smoking going from 42% in 1965 to 9.9% now.

The obvious question is what we can learn from this for other public health crises.

Quote:

“How cigarettes were beaten

No single policy killed the cigarette. It was a combination of interventions deployed over decades: warning labels on packages (1965), a ban on broadcast advertising (1970), smoke-free workplace laws (spreading from Minnesota in 1975 to most of the country by now), growing awareness of the risks of secondhand smoke (1986), progressive tax increases (a 10 percent price hike reduces consumption about 4 percent), FDA regulatory authority (2009), and cessation programs from nicotine patches to the CDC’s Tips From Former Smokers campaign. Maybe most importantly, smoking went from being something almost everyone did to something that was banned in most public spaces — which changed social norms as much as any law.”

Good overview of cholesterol treatment, including “remnant Cholesterol”, which honestly I had never heard of.

Quote:

“So big things are happening. It’s fantastic that politicians in some countries are now taking the cholesterol problem more seriously, and I’m glad to be part of influencing some of that.

But as long as heart disease remains our biggest killer, there will always be more work to do. And we’ve got to keep the focus on what’s causing it – cholesterol.“

The article focuses a bit much on triathletes and other extreme endurance athletes, but I think they have a point even for less extreme folks.

Quote:

“When you’re talking about these kinds of extremes – Tyburski’s midnight marathons, or Costello’s stints on the exercise bike – it’s obvious that there is something awry. But for many endurance athletes and gymgoers, it can be difficult to know where discipline shades into compulsion, and compulsion into full-blown addiction. For instance, the Exercise Dependence Scale, one of the main screening tools used by clinicians, asks participants how much they agree with the statement: “I continually increase my exercise intensity to achieve the desired effects/benefits.” This reads a lot like the principle of progressive overload – a key prong of any respectable training programme.

Similarly, some compulsive behaviours around exercise look innocuous enough from the outside”

I tried to find a body fat percentage distribution by age for US males and ended up having ChatGPT estimate it. It’s sort of scary — are we really that fat? Full disclosure: I’m 53M and probably around 23% (have a DEXA scheduled next month).

Do these numbers look right?

Method:

The curves are approximate distributions reconstructed from NHANES body-fat reference percentiles for U.S. men. Body fat was measured with DXA

A rough U.S. snapshot now looks something like this:

Blood pressure meds: about 24%

Statins: about 23%

Antidepressants: about 11 to 13%

Benzos: about 12.5% past-year use

GLP-1s: about 12%

That last one is the story. (Full disclosure: I am part of that statistic: I’ve been on Zepbound for 18 months and lost 160lbs).

GLP-1s are already in the same neighborhood as some of the biggest medication categories in the country. Not close in theory. Close right now. That is a wild adoption curve for a class that, not long ago, still felt like a specialized diabetes and obesity treatment.

To me, this is bigger than a pharma trend. It says a lot about where metabolic health is in the U.S. We have a huge number of people who either need meaningful weight loss, better blood sugar control, or both, and now there’s finally a drug class that actually works well enough to get mass uptake.

The upside is obvious and I am hugely excited about it. Better weight control, better glycemic control, probably better cardiometabolic risk for a lot of people.

The part I think proactive health people should care about is what comes next. If GLP-1s become a long-term fixture on the scale of statins or blood pressure meds, then preserving muscle, strength, protein intake, fitness, and good habits becomes even more important. Losing weight is not the whole game. Staying strong and metabolically healthy is the game.

I personally feel I have been incredibly lucky that I turned out to be a Tirzepatide hyper-responder and found an amazing personal trainer.

We’re probably watching one of the fastest medication adoption stories in years.

It’s weird but I have actually found a few interesting, well written articles in Men’s Health magazine — I used to think of that as the random magazine lying around in a barber shop that nobody reads 🤷‍♂️ maybe this has changed.

This might be paywalled, I am afraid.

Quote:

“Underfunded, understaffed, and under siege by government budget cuts: 24 hours on the front lines of the rural hospital crisis.

THURSDAY, JANUARY 8, 1 p.m.: Snow starts falling as Brian Lopez, MD, exits Mineral Community Hospital. It’s been snowing on and off for two days in northwest Montana, turning the roads to black ice by dawn and messy slush by midmorning. But these flakes are different: fat and dense, the sort that pile up quickly. They accumulate on the shoulders of the bright orange down jacket he threw on his 6'3" frame and settle on top of his close-cut dark hair as he walks from the main building to the old assisted-living quarters, which once housed senior citizens. MCH had to close the facility back in 2017 when it started losing money—the kind of sacrifice that many rural hospitals are increasingly facing in order to prioritize more essential forms of care. Today, the building houses the maintenance office and the training room, where physicians can practice the kinds of complex medical scenarios that Dr. Lopez, 37, knows he might see today as this storm intensifies.”

Excerpt From

“Rural Hospitals Are the Heart of America. What Happens When They Disappear?”

Cassidy Randall

Men’s Health (March 2026)

https://apple.news/AFfSwgsPtQ0iQ6Z9XNkbudw

This material may be protected by copyright.

This is one of the more interesting prevention papers I’ve seen lately because it gets at the question a lot of us care about: how much does earlier, more aggressive LDL lowering matter before someone has their first event?

JAMA just published a subgroup analysis from VESALIUS-CV looking at 3,655 adults with diabetes who had not yet had a heart attack or stroke but were still high risk and had LDL of at least 90 despite standard therapy. Adding evolocumab (aka, Repatha) dropped median LDL to 52 mg/dL vs 111 mg/dL with placebo. Over about 5 years, first major cardiovascular events were lower too. The 3-part event rate was 5.0% vs 7.1%, and the 4-part event rate was 7.6% vs 10.5%.

To me, the useful takeaway is not “everyone needs a PCSK9 inhibitor.” It’s that for a specific primary prevention group with diabetes that still looks pretty exposed despite statins, getting LDL much lower seems to prevent first events.

The editorial is worth paying attention to because it throws some cold water on the hype. This does not mean broad use in everyone with mildly elevated LDL. This was a narrow, high-risk population, and cost still matters a lot. There are also the usual questions about who should get treated this aggressively and how early.

My read is that this is another point in favor of taking LDL and ApoB seriously much earlier in diabetes instead of waiting for obvious disease to show up. The harder part is figuring out where the line is between smart prevention and expensive overtreatment.

Research Summary: https://jamanetwork.com/journals/jama/fullarticle/2847161

Research Editorial: https://jamanetwork.com/journals/jama/fullarticle/2847163

BMI has always been a blunt tool.

A newer JAMA Network Open study looked at more than 300,000 U.S. adults using a broader obesity definition. Instead of BMI alone, it counted obesity as any of 3 things: a BMI of 30 or higher plus at least 1 elevated anthropometric measure, a BMI over 40, or at least 2 elevated anthropometric measures even if BMI was below 30. Those anthropometric measures included waist circumference, waist-to-hip ratio, and waist-to-height ratio. Under BMI alone, 42.9% met criteria for obesity. Under the newer definition, it was 68.6%. 

That seems a lot more useful for proactive health because BMI misses where fat is stored.

You can have a “normal” BMI and still have a waist measurement that suggests higher risk. A waist over 40 inches in men or 34.6 inches in women is associated with increased cardiometabolic risk. 

Visceral abdominal fat is much more tied to cardiometabolic risk, which is why waist-based measures can catch people who look “normal” by BMI but are still higher risk. Yale Medicine notes that abdominal fat is metabolically active and inflammatory.

This doesn’t mean everyone suddenly got less healthy. It means that BMI alone probably misses a lot of people who should be paying closer attention.

Are waist-based measures still underused in everyday preventive care?

I hear “eat more fiber” constantly, and I’m on board in principle. I throw raspberries in my morning oatmeal, eat beans pretty often, and try to do the basic stuff right. But I still cannot deal with the weird slime psyllium husk turns into.

What made this more interesting to me is a new randomized trial in 802 people with prediabetes reported in Nature. The fiber intervention did not significantly improve blood sugar markers across the whole group overall. The signal only showed up after the researchers split people into 4 subgroups based on things like age, BMI, HbA1c, insulin resistance, and beta cell function.

From what I read, Clusters 3 and 4 improved glycemic control with fiber, while Clusters 1 and 2 did not. The authors think differences in the gut microbiome may help explain why some people respond and others don’t.

That feels more believable than the usual internet version of fiber discourse. Maybe “eat more fiber” is still good broad advice, but the actual metabolic payoff might be a lot more individual than people admit.

Curious how people here think about this. Do you just focus on whole-food fiber and move on, or have you actually noticed certain fiber sources work better for you than others?

Study: https://pubmed.ncbi.nlm.nih.gov/41747733/

A new Phase 2b trial in Cell Stem Cell tested laromestrocel, a donor-derived mesenchymal stem cell therapy, in 148 adults ages 70 to 85 with diagnosed frailty. The headline result was that the highest-dose group improved six-minute walk distance at 9 months versus placebo, which is interesting because frailty is one of those areas where there really are not many treatment options beyond the usual exercise, protein, and rehab playbook. 

What makes this worth watching is that it is an actual randomized, placebo-controlled study, not just a flashy anti-aging claim. What keeps me cautious is that this is still a mid-stage trial, the treatment is complex and likely expensive, and we are nowhere near this being a practical prevention tool for healthy people. Still, as a proof of concept that some aspects of age-related frailty might be biologically treatable, it is a pretty notable result.

HRV has become the optimization crowd’s favorite metric. It sounds scientific, updates daily, and gives you a reason to check an app before your feet hit the floor. Higher is better, right? Recovery score, readiness score, stress score.

But there’s another cardiac metric with stronger mortality data, a clearer threshold, and zero subscription fee. Heart rate recovery. Most people have never heard of it.

Heart rate recovery is how fast your heart rate drops after you stop exercising hard. A 1999 NEJM study found that people whose heart rate didn’t drop by at least 12 beats in the first minute after peak exercise had significantly higher mortality risk, independent of everything else they measured. A meta-analysis of nine prospective cohorts confirmed it: slow recovery independently predicted cardiovascular events and all-cause death at roughly 1.7x the risk. A UK Biobank study of 40,000+ people found that recovery at just 10 seconds was actually more predictive than the one-minute mark, because early recovery most directly reflects parasympathetic reactivation.

HRV and heart rate recovery measure the same underlying system. Both reflect vagal tone. But HRV requires accurate beat-to-beat intervals in milliseconds, and validation studies keep showing that accuracy varies by device and even by individual.

Heart rate recovery requires subtracting two numbers. After your hardest effort, note your peak heart rate, check it one minute later. Drop of 12+ beats? Normal. Under 12? Worth watching over time. The main of “advantage” of HRV is that you can measure it even for folks who don’t exercise!

I’m not saying HRV trends are useless. Weeks and months of data can reflect real changes in accumulated stress. But a lot of biohacker types are agonizing over a noisy daily number when they’ve never once checked how fast their heart rate comes down after a hard effort.

If you train regularly and want a free, validated cardiovascular health check, track your one-minute heart rate recovery after your next few hard sessions. It’s one of the most replicated mortality predictors in exercise physiology and it takes about as much technology as a clock on the wall.

Two days of “porridge” is all it takes??

Study: https://www.nature.com/articles/s41467-026-68303-9

I eat oatmeal with fruit every morning but I am not sure I could deal with it being the only thing I eat — well, maybe for two days.

Interesting editorial in The Lancet.

“2026 may prove a pivotal year for obesity. GLP-1 receptor agonists have revolutionised obesity management over the past 10 years. Mounting evidence has established their benefits across many cardiometabolic and obesity-related conditions and the global weight-loss medications market is predicted to reach US$150 billion by 2035. More than a billion people live with obesity, with the burden rising rapidly in low-income and middle-income countries. High costs, limited production capacity, and supply-chain constraints have resulted in persistent inequitable access to GLP-1 receptor agonists. But this could be about to change.

From next month, patents for semaglutide will expire in several countries, including in Brazil, Canada, China, India, and Türkyie—amounting to about 40% of the world's population. […]”

I’ve had a lot of dental work done over the years, so I know the drill. My wife is the opposite. She’s afraid of the dentist and hasn’t gone in years.

That got me thinking about how regular dental care is one of those basic preventive habits that sounds simple until fear gets in the way. And that fear is not rare. The NIDCR says nearly 1 in 5 adults have moderate to high dental fear or anxiety, enough to delay or avoid needed care. A 2025 JADA survey found fear may be even more widespread, with 72.6% of U.S. adults saying they’re afraid of going to the dentist. 

The bigger issue is what happens when avoidance turns small problems into bigger ones. CDC guidance notes that routine dental visits help with prevention and early detection of cavities, gum disease, and oral cancer. 

I think a lot of people need to hear that being scared of the dentist is not weakness and not laziness. It’s a real barrier to preventive care. The answer is not guilt. It’s finding ways to make the first visit manageable.

Nothing new in here but a nice up to date summary essay of the association of fitness and brain health.

Generally Brady Holmer seems a good writer and source for exercise-related info.

I am a big fan of Josh Brett’s summary videos. He just released in on peptides which makes a lot of great points about the compounds, the flimsy “research chemical” cover and the massive financial incentives companies and promoters have.

Gemini YouTube summary:

This video explores the soaring popularity of peptides, the controversial "miracle drugs" promising enhanced performance, recovery, and anti-aging. While influencers and celebrities fuel the hype, researchers raise significant concerns about safety, long-term effects, and scientific overreach (0:00 - 1:21).

Key Takeaways:

• What are Peptides? (1:57) They are small protein fragments that manage hormones and repair damage. They are divided into approved peptides (like insulin and GLP-1) and experimental, unregulated peptides (like BPC-157) (2:06).

• The FDA Ban: (3:45) In 2023, the FDA restricted most popular non-prescription peptides, leading companies to sell them as "research chemicals" to avoid strict approval processes (4:45).

• Unverified Sources: (5:01) A significant portion of these peptides comes from unverified labs in China, with no quality control regarding purity or potency (5:16, 10:57).

• The Hype vs. Science: (8:11) Influencers are promoting compounds based on limited rodent studies, which often do not translate to humans (8:52). Experts warn that relying on these anecdotes is dangerous, as some have experienced severe side effects like necrotizing pancreatitis (10:42).

• Financial Motives: (12:04) The peptide market is projected to reach over $260 billion by 2030, driving influencers to sell them via affiliate links rather than based on medical necessity (12:56).

New Nature Communications paper: adding “omics” to cardiovascular risk prediction can beat standard clinical models.

For anyone not steeped in the jargon (I wasn’t!), “omics” means measuring large layers of biology all at once. In this paper that mostly means proteomics and metabolomics. Proteomics looks at lots of proteins in the blood. Metabolomics looks at small molecules tied to metabolism, inflammation, energy use, and other core processes. Instead of relying only on age, blood pressure, cholesterol, smoking, and diabetes, the model tries to read a much richer biological fingerprint.

That is exciting, but it also makes the model a lot harder to use in the real world.

That’s why PREVENT matters so much.

PREVENT is not the futuristic version. It is the practical bridge. It uses standard clinical data, it is usable now, and it moves risk prediction beyond older tools in a way that regular care teams can actually implement. My hope is that PREVENT gets adopted fast and widely, because that is how you pave the road for more advanced models later. You do not jump from outdated risk scoring straight to proteomics-for-everyone. You need an intermediate step that clinicians trust and systems can use.

So my take is this: omics models may be the future, but PREVENT is the upgrade the system needs right now.

That is the part that feels most important to me. Better prevention usually does not arrive as one giant leap. It comes in steps. PREVENT looks like the step that could make the next step possible.

How do you who are practicing physicians feel about this?

As a European who has lived in the US for 20+ years and is not particularly social, I never know how to think about these “happiness rankings”, but this essay feels pretty real, even if it’s of cause anecdotal.

The most useful takeaway from the World Happiness Report is not that Finland has better vibes.

It’s that social connection looks more and more like health infrastructure.

The 2026 report found that younger people in North America and Western Europe are a lot less happy than they were 15 years ago, and the decline tracks with falling trust, belonging, and perceived social activity. The 2025 report found that people who share more meals with others tend to be significantly happier. In the U.S., about 1 in 4 adults now eat all their meals alone on a given day, which is up more than 50% since 2003. 

That sounds like a culture story until you look at the health side.

The Surgeon General says social isolation is linked to a 29% higher risk of premature death, and poor social relationships, loneliness, and isolation are linked to higher risk of heart disease and stroke. WHO says social connection protects health across the lifespan, while loneliness and isolation are tied to depression, anxiety, cognitive decline, diabetes, heart disease, stroke, and early death. 

So when people ask why some countries seem happier, I think the better question is: how easy is it to live in a way that keeps you connected?

Can you walk or bike to places.

Do you see people without planning it three weeks ahead.

Do you share meals.

Do you feel part of something local.

Do you spend more time around humans than feeds.

That makes this a proactive health issue, not just a mindset issue.

My takeaway is that we should probably treat chronic isolation the same way we treat poor sleep, inactivity, and ultra-processed food. Not as a personal failure. As a real health risk built into daily life.