This is personal for me as an Alaska Native physician, and someone exposed to hepatitis B as a medical student before we had vaccinations.

A friend of mine’s son died a few years ago. He was 23 years old, and had a liver transplant when he was in his late teens because of hepatitis B infection he did not get from his mother. He was in and out of the hospital multiple times, both in Alaska and in the lower 48. His death reminds us that even in an era where we have liver transplants, preventing the disease is much easier than dealing with the consequences.

You see in Alaska, we did not debate hepatitis B in theory. We lived it. We studied it. We saw it in our friends, families, and villages. And over the last four decades, we helped eliminate it in children. References are at the end for those who wish to follow this.

What Alaska Looked Like Before Vaccination

Before the vaccine program began in the early 1970s, hepatitis B was endemic in many Alaska Native communities. This was before I was a physician. I was a graduate student in virology at The University of Chicago, and was sent off to the CDC to collect some viral samples. In the middle of that work, we discussed the hepatitis B problem that caused:

• Over 13% of the population showed evidence of infection

• About 3% were chronic carriers

• In some regions, that number climbed far higher

But numbers alone do not tell the story.

This was not a disease of needles, drugs, or sex in these communities. It spread in homes. Infants and children acquired hepatitis B from caregivers and siblings through everyday contact:

• saliva

• shared utensils

• premastication of food

• skin infections like impetigo

• small breaks in the skin

The virus was found in saliva and even on environmental surfaces in homes. It could live outside the body for days.

This meant something critical:

You did not need “risk behavior” to get hepatitis B. You needed proximity

Why Newborn Infection Matters

Here is the piece critics consistently miss.

Hepatitis B behaves differently depending on when you get it.

• Adults: less than 5% become chronically infected

• Newborns: up to 90% become chronically infected

And chronic infection is not benign.

It is a decades-long setup for:

• cirrhosis

• liver failure

• hepatocellular carcinoma

In Alaska, we saw liver cancer in young adults. In some cases, even in children.

This is not a hypothetical risk. It is observed reality. Imagine the young lady, first in her village, to go to college, having to have an operation because she had developed liver cancer at age 18. The first one in her community to ever go to college.

“But the Mother Tested Negative” — Why That Doesn’t End the Conversation

This sounds reassuring. It isn’t sufficient.

A negative maternal test is a snapshot, not a guarantee of safety over the next hours, days, and months when transmission can still occur.

Here is why relying on that alone fails in the real world:

1. Testing Is Good — Not Perfect

Screening can be missed, delayed, or improperly documented

Infection can occur late in pregnancy after testing

Lab error, while uncommon, is not zero

Public health decisions are not built on perfect conditions. They are built on what actually happens across millions of births.

The birth dose exists to close that gap.

2. Infants Do Not Play by Adult Rules

Adults typically acquire hepatitis B through:

blood exposure

sexual contact

shared needles

Infants do not need any of those.

Because their immune systems are immature, they are uniquely vulnerable to low-level, everyday exposure:

saliva from caregivers

shared utensils or pre-chewed food

contact with skin infections or small abrasions

contaminated household surfaces

In Alaska, hepatitis B was not primarily a disease of “risk behavior.” It was a disease of proximity.

3. The Immune System Changes the Outcome

This is the most important difference.

Adults: strong immune response → virus cleared in >95%

Newborns: tolerant immune response → virus persists in up to 90%

The infant immune system is designed to avoid overreaction. That is helpful for survival at birth. It is disastrous for hepatitis B.

Instead of clearing the virus, the infant often accepts it.

And that sets up decades of silent infection.

4. Early Infection Is the Dangerous Infection

When hepatitis B is acquired in infancy:

it is usually asymptomatic

it becomes chronic

it quietly increases the risk of cirrhosis and liver cancer

By the time it “matters” clinically, it is often too late to undo.

5. Vaccination Is About Timing, Not Just Exposure

The goal of the birth dose is simple:

Protect the infant before the first exposure occurs. Because in real life, exposure does not wait for adolescence, and does not ask permission.

A negative maternal test lowers risk. It does not eliminate it.

And in a newborn, even a small missed exposure is not a minor event — it is a lifelong infection waiting to happen. That is why we vaccinate at birth.

Not because we are careless with interventions, but because we have learned, over decades, what happens when we wait.

The Alaska Hepatitis B Study: One of the Longest in the World

The Alaska Hepatitis B cohort is one of the longest-running population studies of any infectious disease.

We followed over a thousand chronic carriers for decades.

What we learned:

• HBeAg clearance occurred in ~72% within 10 years

• Chronic infection persisted in many, with ongoing cancer risk

• Liver cancer incidence was measurable and real

• Certain viral genotypes dramatically increased cancer risk

With extended follow-up over 35 years, genotype F — common in Alaska Native populations — showed some of the highest liver cancer rates ever recorded for hepatitis B.

This is not a mild infection that you “deal with later.”

This is a virus that sets the stage for cancer early in life.

Then We Vaccinated

Beginning in 1983–1984, Alaska implemented one of the most comprehensive hepatitis B vaccination programs in the world:

• universal newborn vaccination

• catch-up vaccination for children and adults

• aggressive screening programs

The results were not subtle. They were extraordinary.

• Acute hepatitis B incidence dropped from 215 to 14 per 100,000

• No new cases of acute hepatitis B in children since 1992

• No liver cancer cases in people under 20 since 1999

• HBsAg-positive children fell from 657 to 2 over two decades

Read that again.

We eliminated a cancer in children.

This inspired me to become a physician. I liked people better than Petri dishes, but I wanted to be a doctor who helped directly. Oddly, I ended up in surgery, far from virology - or so I thought.

The Long-Term Question: Does the Vaccine Last?

This is the second claim often made: that immunity “wears off.”

We did not guess at this.

We followed vaccinated individuals for 30 to 35 years.

• About 47–51% still had measurable antibodies decades later

• 74–88% mounted a strong response to a booster

• ~86% showed ongoing protection overall

• No breakthrough chronic infections were observed

Immunity is not just a number on a lab test.

It is immune memory.

And in this case, it works.

Why Give It on Day One?

Because the window we are trying to close is immediate.

Even if a mother tests negative:

• testing is not perfect

• infection can occur late in pregnancy

• household transmission begins early

In a place like Alaska, we learned the hard way that waiting is not neutral.

Waiting means risk.

And risk in a newborn carries lifelong consequences.

This Is What Long-Term Science Looks Like

There are many things in medicine where we argue from short-term data.

This is not one of them.

We have:

• 40 years of follow-up

• population-level data

• cancer outcomes

• real-world elimination of disease

This is not pharma marketing.

This is epidemiology, public health, and time.

The Autism Claim — Let’s Deal With It Directly

Now we get to the part that always shows up.

It doesn’t matter if we are talking about measles, hepatitis B, or anything else. The word “autism” gets dropped like a trump card.

So let’s deal with it.

Because in Alaska, we did not just track hepatitis B.

We tracked outcomes. Long-term. Carefully. Repeatedly.

And here is what we found.

There is no increase in autism, developmental delay, or neurologic disease in children who received the hepatitis B vaccine — including in the Alaska Native population that has been followed for over 35 years.

None.

What the Large Data Actually Show

When you step away from anecdotes and look at actual population data:

A meta-analysis of over 1.2 million children shows no association between vaccines and autism

No signal for thimerosal. No signal for mercury

No signal for hepatitis B vaccination specifically

Multiple independent reviews — including large systematic analyses — come to the same conclusion:

If there were a link, we would have seen it by now.

We have not.

The Alaska Data Matters Here

This is not theoretical.

We vaccinated entire populations of Alaska Native children starting in the early 1980s.

We followed them for decades.

We published about infection rates, antibody persistence, liver cancer outcomes. And if there had been a signal for neurodevelopmental harm, it would have shown up in one of the most closely studied public health cohorts in the world. It did not.

What About the “Studies” That Say Otherwise?

Yes, a few small papers get circulated online.

They share a pattern:

small sample sizes

parental self-report of autism

poorly defined control groups

selection bias

results that cannot be reproduced

And most importantly:

They collapse when tested against large, well-designed studies.

That is how science works.

Not by finding one paper you like, but by seeing what holds up when the sample size hits a million.

The Real Tradeoff

This is the part that gets lost in the noise.

We are not choosing between:

vaccine vs nothing

We are choosing between:

vaccination against a virus that causes lifelong infection and liver cancer when acquired in infancy. In Alaska, we watched what happened before and after.

Before: chronic infection, cirrhosis, cancer

After: elimination of hepatitis B in children, elimination of liver cancer in children

And no increase in autism.

FINALLY

The autism claim persists not because the evidence supports it, but because it is emotionally powerful and endlessly repeated.

But repetition is not evidence.

And after decades of data, across millions of children, in one of the longest-running cohorts we have:

The hepatitis B vaccine prevents disease. It prevents cancer. And it does not cause autism.

That is what the data say.

The Bottom Line

The idea that the hepatitis B vaccine at birth is unnecessary is not a bold new insight. It is a dismissal of one of the most successful long-term public health interventions ever conducted.

We did not theorize this in Alaska. We measured it. And we watched a generation grow up without a virus that once defined entire communities.

And that mother whose child died–I see her two or three times a year. And every time we talk about her son. She is thankful for the care he received, and works hard in healthcare to ensure that no other mom has to suffer as she did, and no other child has to suffer as her son did.

And that story, and many others, inspired me to become a physician.

References

1. 1. McMahon BJ, Holck P, Bulkow L, Snowball M. Serologic and clinical outcomes of Alaska Native patients with chronic hepatitis B virus infection. Ann Intern Med. 2001.

   2. McMahon BJ, Nolen LD, Snowball M, et al. Hepatitis B virus genotype and risk of hepatocellular carcinoma. Hepatology. 2021.

   3. Gounder PP, Bulkow LR, Snowball M, et al. Hepatocellular carcinoma risk in Alaska Native children and young adults with hepatitis B. J Pediatr. 2016.

   4. Hayashi S, Khan A, Simons BC, et al. Core mutations and hepatocellular carcinoma in hepatitis B genotype F1b. Hepatology. 2019.

   5. McMahon BJ, Rhoades ER, Heyward WL, et al. A comprehensive program to reduce hepatitis B virus infection in Alaska Natives. Lancet. 1987.

   6. McMahon BJ, Bulkow LR, Singleton RJ, et al. Elimination of hepatocellular carcinoma and acute hepatitis B in children 25 years after immunization. Hepatology. 2011.

   7. Harpaz R, McMahon BJ, Margolis HS, et al. Elimination of new chronic hepatitis B virus infections in Alaska. J Infect Dis. 2000.

   8. Bruce MG, Bruden D, Hurlburt D, et al. Antibody levels and protection after hepatitis B vaccination: 30-year follow-up. J Infect Dis. 2016.

   9. Bruce MG, Bruden D, Hurlburt D, et al. Protection and antibody levels 35 years after hepatitis B vaccination. Hepatology. 2022.

   10. McMahon BJ, Schoenberg S, Bulkow L, et al. Seroprevalence of hepatitis B virus markers in Alaska Natives. Am J Epidemiol. 1993.

   11. Taylor LE, Swerdfeger AL, Eslick GD. Vaccines are not associated with autism: an evidence-based meta-analysis. Vaccine. 2014.

   12. Dudley MZ, Halsey NA, Omer SB, et al. The state of vaccine safety science: systematic reviews of the evidence. Lancet Infect Dis. 2020.

   13. Larson HJ, Gakidou E, Murray CJL. The vaccine-hesitant moment. N Engl J Med. 2022.

   14. Schillie S, Vellozzi C, Reingold A, et al. Prevention of hepatitis B virus infection in the United States: ACIP recommendations. MMWR Recomm Rep. 2018.

   15. Haber P, Moro PL, Ng C, et al. Safety of hepatitis B vaccines in the United States (VAERS 2005–2015). Vaccine. 2018.

   16. McMahon BJ, Bulkow LR, Singleton RJ, et al. Elimination of hepatocellular carcinoma and acute hepatitis B in children after immunization. Hepatology. 2011.

   17. Dentinger CM, McMahon BJ, Butler JC, et al. Persistence of antibody and protection after hepatitis B vaccination in Alaska Natives. Pediatr Infect Dis J. 2005.

   18. Bruce MG, Bruden D, Hurlburt D, et al. Protection and antibody levels 35 years after hepatitis B vaccination. Hepatology. 2022.

   19. Ulrich AK, Fleming DF, Smith EA, et al. Hepatitis B vaccination at birth: safety and effectiveness. Pediatrics. 2026.

   20. Gallagher CM, Goodman MS. Hepatitis B vaccination of male neonates and autism diagnosis. J Toxicol Environ Health A. 2010.

   21. Geier DA, Kern JK, Homme KG, Geier MR. Hepatitis B vaccine exposure and special education services. Int J Environ Res Public Health. 2018.

   22. Yang J, Qi F, Yang Y, et al. Neonatal hepatitis B vaccination and transient neurobehavioral effects in mice. Psychoneuroendocrinology. 2016.

If you are going to argue against a vaccine, at least argue against the data.

Because in this case, the data are not subtle — they are definitive.

A new set of cancer numbers dropped, and for about a day and a half the internet did what it does best — found a number, stripped it of context, and declared the case closed.

Cancers in people under 50 were “up 6.4%.” Must be the turbo-cancer of the vaccines.

That was enough. No pause. No curiosity. Just a straight line drawn from that number to the conclusion: vaccines.

And then, just as quickly, the story faded. Not because the data disappeared — but because once you actually look at it, the conclusion doesn’t hold up.

Share

Because here’s the part that never makes it into the viral posts: some of these cancers have been rising for decades.

Early-onset colorectal cancer didn’t begin in 2021. It didn’t begin in 2020. The curve starts bending upward long before COVID, long before mRNA vaccines, long before any of the current talking points. In fact, it started rising in the mid 1980’s.

So if the explanation you’re offering requires a starting point in 2021, but the data clearly start in the 1980s, that’s not a bold hypothesis, or some new discovery. That is inconvienient data that is best ignored.

COVID and lack of Cancer Screening

Then there’s the pandemic itself — another variable that gets conveniently skipped. Remember during the pre-vaccine times in the pandemic, when you couldn’t go to the hospital because it was overwhelmed?

During COVID, cancer screenings dropped. Colonoscopies were delayed. People stayed home. Health systems were strained. When that happens, diagnoses don’t disappear — they get pushed forward.

So when normal care resumes, you see a rebound. Not because cancer suddenly appeared, not because cancer burst out from vaccines, but because it’s being found after a delay. The mammogram that wasn’t done because they were sheltering in place, or the colonoscopy cancelled, and now we find a tumor.

What We’ve Actually Won — And It Matters

It’s easy to miss this part because it doesn’t trend, but it should.

We are better at preventing and treating cancer than we’ve ever been.

Lung cancer deaths have fallen — not because of a miracle drug, but because fewer people smoke. That’s public health working exactly as intended.

Cervical cancer has dropped dramatically in screened populations and continues to fall with HPV vaccination. That’s prevention layered on top of early detection.

Colon cancer deaths in older adults have declined, largely because we find and remove precancerous polyps before they ever become cancer. That’s not treatment — that’s interruption of the disease itself.

And across multiple cancers, survival has improved with better surgery, targeted therapies, and immunotherapy. Not perfect. Not evenly distributed. But real progress.

So when someone tells you “nothing is working,” they ignore decades of measurable, repeatable gains.

Early Detection — Why the Numbers Can Look Worse Before They Look Better

Screening complicates the story, and that’s where many people get lost.

When you look harder, you find more. This is the story of breast cancer. When I was a surgical resident, we found breast cancers by examinations. As technology of mammography improved, we started finding smaller breast cancers with mammograms. Smaller cancers, earlier detection, earlier treatment, and we went from 75% five year survival to 99% five year survival and cures.

That means:

• More early-stage cancers were detected

• More “cases” counted

• Sometimes a temporary rise in incidence

But catching cancer earlier is exactly what reduces death.

A colonoscopy doesn’t just detect cancer — it prevents it. A mammogram finds tumors before they spread. HPV testing identifies risk before cancer develops.

So yes, better detection can make the numbers look worse on the surface. But underneath, it’s shifting cancers into stages where we can actually do something about them.

If you only look at case counts without understanding detection, you can convince yourself that things are getting worse when, in fact, outcomes are improving.

Cancer deaths, by the way, with one glaring exception, are going down.

Smoking, Public Health, and What Actually Works

If you want a clean example of medicine and public health getting it right, look at smoking.

In the mid-20th century, smoking was everywhere — culturally accepted, heavily advertised, even wrapped in a kind of manufactured credibility. You’ll still see people drag out those old Camel ads with physicians in white coats, as if that somehow indicts modern medicine. It doesn’t. It shows how marketing worked.

What changed wasn’t a grassroots epiphany or sudden shift in personal responsibility. It was leadership. It was data. And it was institutions willing to act on both.

The turning point came with the 1964 Surgeon General’s Report on Smoking and Health — a moment when the evidence became impossible to ignore, and the federal government said so clearly and publicly. From there came warning labels, advertising restrictions, public campaigns, and eventually indoor smoking bans.

And here’s the part that gets conveniently left out: no major medical organization endorsed smoking once the evidence was clear. Quite the opposite. The entire weight of public health moved in one direction.

The result? Smoking rates fell. And with them, lung cancer deaths began to decline. Not overnight, not perfectly, but steadily and measurably.

That’s what success looks like in medicine — not perfection, but progress that shows up in real populations over time.

There’s still work to do. Smoking hasn’t disappeared, and lung cancer hasn’t either. But the next frontier isn’t pretending cigarettes were harmless — it’s recognizing that air quality matters more than ever.

Wildfire smoke, urban pollution, fine particulate matter — these are not trivial exposures. They increase the risk of lung cancer, even in people who have never smoked, and likely contribute to other cancers.

So the lesson isn’t that public health got it wrong.

The lesson is that when we identify a real risk, measure it carefully, and act on it consistently — we reduce disease.

What Is Rising — And Why We’re Paying Attention

Now here’s the part that deserves concern.

Some cancers, particularly in younger adults, are rising. Early-onset colorectal cancer is the one that has everyone’s attention, and it should.

But again, this didn’t start in 2021. It started in the 1980’s, and perhaps even earlier.

This has been building for decades, and the likely drivers are not mysterious:

• Increasing obesity

• Changes in diet, especially ultra-processed foods

• Microbiome alterations

• Sedentary behavior

• Metabolic dysfunction

None of these flipped on overnight. None of them align with a single event.

This is what a real public health problem looks like — gradual, multifactorial, and frustratingly resistant to simple answers.

Which is exactly why it gets replaced online with a simple answer. Cancers don’t happen overnight, they happen when they are in an environment that leads to progressive damage to a person’s DNA.

This is why we are now focusing on cancers due to the other lifestyles - food, metabolic disorders, and obesity. This will be the GLP-1 shift, as obesity drops, so will these cancers. As fiber is incorporated into the diet, so will these tumors decrease.

Turbo Cancer

And then there is this term. Turbo cancer. It is not a real term. But sometimes it seems like cancer goes fast.

Find a cancer that is widespread, which we do all too often, and it kills quickly. This is nothing new, this is cancer. This is why we focus on early detection, because if we detect early, we prevent a cancer from widespread metastasis.

Still, the anti-vax crowd took this term and is running with it. And every person with a friend or relative with widespread cancer adopts it. It isn’t from the vaccine, it is the nature of cancer.

Vaccines are Easy to Blame

Blaming vaccines works because it’s simple. One cause. One villain. No need to wrestle with decades of shifting diet patterns, metabolic disease, or screening behavior.

The one “cause” is the mark of a huckster. Today it is vaccines, yesterday it was a parasite, who knows what one thing it will be tomorrow.

Complex problems are frustrating. Simple answers are comforting.

Even when they’re wrong. And there is an industry based on cancer caused by the COVID vaccines. Charlatans are already selling detoxification (there is no such thing). It is in an enema form, god knows why these people love their enemas. From coffee to god knows what.

And if there were a real signal — something meaningful, something large enough to move population-level cancer rates — it wouldn’t show up as a selective, inconsistent pattern that appears in one age group, one time window, and nowhere else.

It would be obvious. It would be reproducible. It would be everywhere.

That’s how epidemiology works. Signals don’t whisper.

So what happened to the story?

Nothing mysterious. It just didn’t survive contact with the full dataset.

The headline traveled. The correction didn’t.

Closing

What we’re watching isn’t the emergence of a new truth. It’s the recycling of an old habit — start with a conclusion, find a number that sounds alarming, and ignore everything that complicates it.

The data didn’t go anywhere. They’re still there, doing what data do — quietly resisting oversimplification.

My love of great food has not changed with Zepbound—in fact, it may have sharpened it.

There’s a persistent worry I hear from patients and readers:

“If I start a GLP-1, will I still enjoy food?”

Sometimes it’s framed more personally—“I’m a foodie. I don’t want to lose that.”

Fair concern. Wrong conclusion.

Because what most people fear losing isn’t food—it’s excess. And those are not the same thing. What you gain, is the ability to enoy food.

For those who don’t know, I have been on Zepbound for over a year and a half and have maintained my 50 pound weight loss — and I still enjoy going to great restaurants - see more to follow.

What Actually Changes

I’ve eaten at some remarkable places—restaurants where the view competes with the plate, where timing is as precise as a surgical incision, where a single bite tells you more than a full plate at a mediocre restaurant ever could.

And I still seek those places out. In a recent trip to Italy, I sought the great places to eat, not only Michelin Star, but the places the locals love.

What has changed is not my love of food—but my relationship to it.

I eat more slowly now. Not because I’m forcing myself to, but because I can. The urgency is gone. That background pull—the one that says keep going—quiets down.

And in that quiet, something interesting happens.

Taste, Finally Heard

You start to notice things. The acidity that cuts through richness. The balance of fat and salt. The texture—crisp, soft, structured, fleeting. The intention behind the dish.

You realize something important:

Great restaurants were never about portion size.

They were about precision, restraint, and execution.

In other words, they were always designed for the version of you that Zepbound allows you to be.

The Moment Most People Miss

Before, I could appreciate a great meal—but I was also fighting something. Speed. Habit. That subtle pressure to keep eating past the point where the experience was actually improving.

Now?

I stop when the experience peaks. I enjoy each bite, the flavor bursts through and develops in my palate.

Because the best meals don’t get better after the third or fourth bite—they just get bigger. You taste more precisely, you get the message from the chef.

And bigger isn’t better.

Better is better.

Discernment Over Volume

There’s a shift that’s harder to describe but easy to feel: discernment.

When you’re not driven by hunger or food noise, you choose differently. Not less joyfully—but more selectively.

You don’t want more food. You want better food.

And that aligns perfectly with what the best chefs in the world are trying to do anyway—deliver something thoughtful, balanced, and intentional in a few bites, not overwhelm you with quantity.

I want you to think of Zepbound as the perfect date. Ever go to a restaurant with a bad date? The experience isn’t quite the same. Then you find someone who enjoys that food as much as you do, be it a date or a friend, and you find going with them is amazing.

Tell me the places you’ve enjoyed since you started this journey?

🔒 Paid Section: What’s Actually Happening in Your Brain and Body

Let’s move this out of philosophy and into physiology.

Read more

Red meat does not prevent Alzheimer’s disease. It does not “normalize” genetic risk. And it certainly doesn’t cure dementia.

What we have is a single observational study—interesting, limited, and now badly overinterpreted—being turned into dietary dogma. Parts of the low-carb and carnivore community have taken a subgroup signal and promoted it as if it were a prescription.

It isn’t.

And if we’re going to talk about diet and dementia honestly, we also have to talk about what does have real evidence behind it.

Of course, Gary Taubs and the entire low-carb group are grabbing this study as some proof - it isn’t. In fact it almost shows the opposite of what they state.

What the Swedish Study Actually Showed

The study followed about 2,100 older adults and looked at meat intake and cognitive outcomes.

In people carrying the APOE4 allele, those eating more meat had less observed excess risk of dementia compared to those eating less.

That’s the finding.

Not prevention.
Not reversal.
Not treatment.

An association.

How It Became “Meat Slashes Alzheimer’s Risk”

This is how nutrition misinformation evolves:

1. A subgroup association appears

2. “No excess risk” becomes “risk normalized”

3. “Associated with” becomes “slashed risk”

4. A headline becomes a belief system

By the end, we’ve gone from a signal to a slogan.

What Everyone Missed

This wasn’t a high-meat diet

Even the highest meat consumers in the study were eating:

• about 1–2 pounds per week

That’s moderate intake—not a carnivore diet. In fact the average American eats 3.6 pounds of meat per week. This is, by American standards, small. But oddly, it does fit into one of the Mediterranean groups - which allows 4 ounces of meat per day.

This was observational

No randomization. No intervention.

Which means:

• healthier people cluster together

• diet tracks with lifestyle

• causation is not established

Even the authors acknowledge this. Does that mean eating more red meat is healthy - absolutely not.

Subgroup findings are fragile

The effect appears:

• in one genetic group

• in one cohort

• under specific conditions

That’s hypothesis-generating—not practice-changing. We also call this p hacking - find something significant by going through every group and every permutation until we grab onto some statistic that hits a p value and publish it.

This is how they published chocolate is good for you. A deliberate attempt to prove that chocolate was more than dessert - and yet even though they admitted they did this, it lives on in American lore. This will live on in the Twitter wars of the meat eaters, and Gary Taubs.

Now Let’s Talk About What Actually Works

This is the part that gets ignored in the excitement.

Because while one small study is being amplified, we already have decades of data on dietary patterns and brain health.

The diets that consistently show benefit:

Mediterranean Diet

• Lower rates of cognitive decline

• Reduced risk of Alzheimer’s disease

• Benefits seen across large populations

People who adhere more to the Mediterranean diet (see terrysimpson.com for a description of this) live longer and have less cognitive decline. More fruits, more vegetables, fish, olive oil, whole grains, and allow about 4 ounces of meat a day (that would fit into this study).

DASH Diet (Dietary Approaches to Stop Hypertension)

• Originally for blood pressure

• Also associated with better cognitive outcomes

We also call this the American version of the Mediterranean diet.

MIND Diet (Mediterranean + DASH hybrid)

• Specifically designed for brain health

• Associated with slower cognitive decline equivalent to ~7.5 years of aging delay in some cohorts

These are not fringe findings.

They come from:

• large prospective cohorts

• repeated analyses - two different studies one from Chicago and one from New York (Columbia) showed delay in cognitive decline. So, put off losing your keys for seven years.

• consistent directional results

What Do These Diets Have in Common?

They don’t rely on a single food.

They emphasize:

• vegetables

• fruits

• whole grains

• legumes

• nuts

• fish

• olive oil

And they consistently limit:

• ultra-processed foods

• refined carbohydrates

• excessive saturated fat

Notice what’s missing?

There is no:

“eat more steak to prevent dementia” - but they still can eat the amount listed on here and make it.

The Gene Question

The APOE4 allele increases risk through complex pathways:

• lipid transport

• amyloid metabolism

• inflammation

Diet may influence these.

But the idea that:

one food cancels genetic risk

…would require randomized trials showing exactly that.

We don’t have those. And having the gene does not DETERMINE destiny, it increases risk.

Common Questions

“Should APOE4 carriers eat more meat?”

We don’t know.

One observational signal is not enough to guide clinical advice. They should eat a Mediterranean/DASH/MIND diet.

“Does avoiding meat increase dementia risk?”

No credible evidence supports that claim.

That’s an inference—not a finding. In fact, plenty of studies show increasing saturated fat increases dementia and colon cancer might give one pause.

Vascular dementia is clearly related to higher levels of saturated fat.

“Does this overturn everything we know?”

No.

It adds a small, interesting piece to a much larger body of evidence.

“Were we wrong about red meat?”

Sometimes, yes—nutrition messaging has oversimplified.

But correcting that mistake by declaring:

“red meat protects your brain”

…isn’t science.

It’s a pendulum swing. But the details are important - it isn’t a heavy meat diet, and it is eating better. Honestly we have better diets for the brain.

The Bigger Issue

This isn’t really about meat.

It’s about how we handle uncertainty in nutrition science.

Weak signals get turned into strong claims.
Subgroups become universal truths.
Headlines outrun the data.

And patients are left trying to make sense of it.

What You Should Actually Do

If you care about brain health:

• Focus on dietary patterns, not single foods

• Follow evidence-based approaches like Mediterranean or MIND

• Exercise

• Sleep

• Manage vascular risk factors

Because dementia is not caused—or prevented—by one ingredient.

Final Word

This study is interesting. It may lead to better research on gene–diet interactions.

But it is not a breakthrough.

And it is certainly not a reason to tell patients:

“Eat more red meat to prevent Alzheimer’s.”

One Line, Because It Bears Repeating

This isn’t a cure—it’s a correlation, dressed up as certainty by people who were already convinced of the answer.

🔒 Paid Member Section: What the MIND Diet Actually Is—and Why It Still Matters

Let’s slow this down a bit and talk like adults for a moment.

Because while everyone is arguing about whether red meat is secretly a brain-saving superfood, we already have something far more useful sitting in plain sight: dietary patterns that have been studied over and over again, in large groups of people, for years.

Not perfect studies. Not randomized in the way we’d like. But consistent.

And the most “brain-specific” version of that work is the MIND diet.

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The X Files - Food noise Is Just Hunger

Some of you follow me on Twitter (now called X) and there I am often faced with people who don’t understand how GLP-1 works, and think that food noise is nothing more than a hunger/satiety problem.

They sneer and say - if it isn’t the food, then what is obesity? Often these folks are people selling a low-carb diet along with a workout program. They think all a person needs is discipline - usually to eat nothing but steak and work out in the gym hours a day. I am sorry, but I do have a life, and it isn’t flexing my muscles and eating steak. But more important, food noise that drives obesity is not due to a lack of working out, or from eating “carbs.”

So today we will dive into food noise, because it is an important driver of obesity, and something I didn’t know I had until 12 hours after my first Zepbound shot nearly 18 months ago.

It’s Not Hunger. I Know Because I’ve Heard Both.

I once sat at a medical conference across from another weight loss surgeon. Thin. Unremarkable lunch. The kind of hotel dessert that looks better than it tastes.

He took one bite of the cake, paused, made a face—not dramatic, just…dismissive—and put the fork down.

Done.

I remember watching that like it was a magic trick.

So I tried it. Took a bite myself.

Now, in the old days, I would have finished that cake in six bites. Not because I was hungry. Not because it was good. Just because it was there—and because something in my brain said, keep going.

But this time I paid attention. It wasn’t good. It wasn’t worth it. And for once, I stopped.

Not willpower. Observation.

That distinction matters more than people think.

The Lie: “Food Noise Is Just Hunger”

People who have never experienced food noise say this with confidence.

They shouldn’t.

Because hunger is quiet, logical, and surprisingly polite. You feel it, you eat, it goes away.

Food noise doesn’t behave like that.

Food noise is:

• thinking about food when you’re not hungry

• continuing to eat after you’re satisfied

• wanting something specific, not just calories

In medical terms, we call it hedonic hunger—a drive that comes from reward pathways, not energy need.

But that clinical language misses the lived experience.

Food noise is not a signal from your stomach.

It’s a conversation in your brain that doesn’t know when to end.

The Change Wasn’t Discipline

There’s this idea that the difference between people is discipline.

It isn’t.

Here’s another example.

Today, if I order a glass of wine and don’t like it, I stop. One sip, maybe two. That’s it.

Before? I would have finished the glass. Maybe had another. Not because it was good—because it was there.

No internal discussion. No pause.

Just completion.

Now I’ll sit on a plane and skip the wine altogether and have tea instead. Not as a moral victory. Just because it’s the better choice in the moment.

Something changed—but it wasn’t a lecture I gave myself.

It was the volume of the signal.

This Isn’t Coming From Your Stomach

One of the biggest mistakes people make is assuming food noise starts in the gut. It doesn’t. It starts in the brain—and not the part that measures hunger.

It comes from the reward centers.

When you see food, smell it, or even just think about it, a different set of regions gets involved. The ventral tegmental area flags something as important. The nucleus accumbens generates that quiet push to get it. The orbitofrontal cortex weighs whether it’s worth it. None of those counting calories. None of them ask if you’ve eaten enough.

They’re asking a different question: is this worth repeating?

That’s a very different conversation than hunger.

Why Full Doesn’t Mean Finished

This is where people get tripped up. They assume that once you’re full, the signal should shut off. That would be true if everything ran through the same system—but it doesn’t.

The hypothalamus handles hunger and satiety. It’s the part that says, “you’ve had enough.” But the reward system sits alongside it, connected to it, and at times capable of overruling it .

So you can finish a meal, feel physically satisfied, and still find your brain circling back to food. Not because your body needs more, but because something in the reward system is still active. It hasn’t gotten the memo that the meal is over—or more accurately, it doesn’t care.

That’s the difference. Hunger stops. Food noise lingers.

The Brain Learns What to Want

What makes this more complicated is that the reward system is trainable. It learns quickly, and it doesn’t forget much.

Highly palatable foods—especially ultra-processed ones—are very good at teaching it. They deliver a strong, fast reward: sugar hits quickly, fat carries flavor, salt enhances everything. The brain notices. Then it remembers.

After enough repetition, you don’t even need the food itself. The cue is enough. You walk past a bakery, see a commercial, or just remember a taste, and the system activates. It’s not responding to hunger. It’s responding to expectation.

That’s why someone can say, “I’m not even that hungry, but I want something.” They’re not confused. They’re describing two different signals.

This Is Why the Advice Falls Flat

If you think food noise is hunger, the advice seems obvious: eat less, wait it out, use discipline. But that advice assumes the signal will behave.

It often doesn’t.

Because this isn’t a simple input-output loop. It’s a learned, reinforced, cue-driven system that can keep firing even when the biological need has been met.

Once you see it that way, the experience makes more sense. You’re not failing to control hunger. You’re dealing with a system that was designed to notice reward and repeat it—and in the modern food environment, it has plenty of opportunities to practice.

Eating Slower Isn’t a Trick—It’s a Symptom

This morning at breakfast, I ordered two poached eggs with avocado and pico de gallo. The waitress asked if I wanted a biscuit.

“Sure,” I said.

The biscuit never came.

And here’s the part that would have been impossible before: I didn’t care.

I finished the meal. I was full. I paid and left.

No reminder. No irritation. No sense that something was missing.

Before, I would have noticed. Asked. Waited. Wanted it.

Not because I needed it.

Because the system that says “complete the meal” used to run the show.

Now it doesn’t.

Why This Happens

We like simple explanations, but this one isn’t simple.

There are two systems involved in eating:

• one that regulates hunger (the hypothalamus)

• one that drives reward (dopamine pathways)

They are not the same.

And importantly, the reward system can override the hunger system .

That’s how you end up:

• full, but still thinking about food

• satisfied, but still reaching for more

That’s food noise.

Ultra-Processed Food Turns Up the Volume

Here’s where modern life complicates things.

Ultra-processed foods are engineered to hit reward pathways hard:

• sugar, salt, fat combinations

• texture that dissolves quickly

• flavors that linger

They don’t just feed you. They stimulate you.

And for some people—not all, but enough—the brain learns this quickly.

It starts to anticipate.
Then it starts to seek.
Then it starts to repeat.

That’s when food stops being about hunger and becomes about response.

Alcohol: The Quiet Amplifier

Alcohol makes this worse in a way people underestimate.

It lowers the part of your brain that says, “that’s enough.”
At the same time, it makes food more rewarding.

So now you have:

• less inhibition

• more reward

That’s not a fair fight.

Which is why the same person who can skip dessert at lunch suddenly finds themselves ordering it after a glass or two of wine.

We’ve Seen This Before

Long before we had a name for any of this, we saw it play out in history.

Henry VIII

A man who went from controlled and athletic to impulsive and excessive after a head injury that likely affected central appetite regulation.

Different era. Same principle.

When the brain changes, behavior follows.

What People Get Wrong

People who don’t experience food noise think this is all semantics.

They think:

“You’re just hungry.”
“You just need discipline.”

But those explanations don’t survive contact with reality.

Because if it were hunger, it would stop when you ate.

And if it were discipline, it would be consistent.

Neither is true.

The Difference

The difference is this:

Hunger asks.
Food noise insists.

And once you’ve experienced both, you never confuse them again.

Paid Section Preview

In the paid section, we’ll go deeper into what’s actually happening in the brain:

• the reward centers involved

• why “wanting” and “liking” separate

• and why some treatments quiet food noise instead of just fighting hunger

Because once you understand that, you stop blaming behavior—and start understanding biology.

A Tour Through the Circuits (Not the Sermons)

If the free section is the experience, this is the wiring.

Because once you understand where food noise lives, the conversation changes from “why can’t I control this?” to “what system is talking right now?”

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Somewhere along the way, the em dash went from a mark of confident writing to a supposed tell of artificial intelligence. That’s backwards. The em dash didn’t come from AI—AI rediscovered what good writers have been doing for centuries.

And now, oddly, some writers are afraid to use it.

That’s a mistake.

I like to write, and am currently writing a book about GLP-1 from the perspective not only of a doctor — but a patient. And if anyone follows my Twitter (X) account, they will see me dismantle pseudoscience with abandon. But then someone decides to check grok to see if I am using AI? What does grok do- it looks for the em dash.

The Three Dashes (They Are Not the Same)

Let’s get the basics out of the way—because most people lump these together, and they shouldn’t.

Hyphen (-)
This is the workhorse. It connects words.

• evidence-based

• well-known

• GLP-1

It’s glue. Nothing fancy.

En dash (–)
Slightly longer. Quietly useful.

• 1990–2025

• dose–response relationship

• New York–London flight

It means “to” or “between.” Most people ignore it—good writers don’t.

I love the en dash because it is in the en dash that we have life. Life is not the day you were born, or the day you die, life is the en dash.

Em dash (—)
Longer. Stronger. This is where voice lives.

• The argument—confidently stated—falls apart under scrutiny.

• GLP-1 drugs don’t just reduce appetite—they change physiology.

It interrupts, pivots, emphasizes. It lets you think on the page.

Why Writers Have Always Used It

The em dash isn’t new. It’s not trendy. It’s not algorithmic.

It shows up everywhere once you know to look:

• Emily Dickinson used it as breath itself

• Herman Melville used it to layer ideas mid-sentence

• Virginia Woolf used it to mirror thought

• James Joyce used it to fracture and flow at the same time

• Mark Twain used it for timing—especially comedic timing

The common thread isn’t style. It’s control.

The em dash lets you move faster than a comma and more flexibly than a period. It captures interruption—the way people actually think.

What AI Actually Did

AI didn’t invent the em dash. It just uses it a lot.

Why?

Because it’s trained on good writing—and good writing uses em dashes.

So now we have this odd moment where:

• People notice em dashes more

• They associate them with AI

• And they start avoiding them

That’s like avoiding verbs because AI uses verbs.

The Real Problem

The problem isn’t the em dash.

It’s bad writing using the em dash badly.

You’ve seen it:

• Overused—every sentence fractured

• Forced—where a comma would do

• Decorative—rather than functional

That’s not a punctuation problem. That’s a thinking problem.

Where to Find It (So You Actually Use It)

On iPhone / iPad

• Press and hold the hyphen (-) key

• Slide to:

  • – (en dash)

  • — (em dash)

Or type two hyphens (--) → autocorrect often converts to an em dash.

On Mac

• Em dash: Option + Shift + -

• En dash: Option + -

On Windows

• Em dash: Alt + 0151 (numeric keypad)

• En dash: Alt + 0150

Or in Word:

• Type -- → autoformats to em dash (if enabled)

In Google Docs / Word

• Type -- → usually converts automatically

• Or go to: Insert → Special Characters → search “dash”

Should You Use It?

Yes—with intent.

Use it when:

• You want to interrupt a thought

• You want to add emphasis without starting a new sentence

• You want your writing to sound like a person thinking—not a report being filed

Don’t use it:

• Because it “looks smart”

• Because you saw it on Twitter

• Because you’re trying to imitate a style you don’t understand

The Bottom Line

The em dash isn’t an AI tell. It’s a writer’s tool.

Good writers have always used it—confidently, deliberately, and sparingly.

If anything, AI has just reminded people it exists.

And now, instead of fearing it, you should do what good writers have always done:

Use it when it makes the sentence better—and don’t apologize for it.

And if someone says that you used AI, and you didn’t — do this, put a bit of Mark Twain’s writing in and show that his was all AI.

Oh, here is what I found about AI writing— it just isn’t that great. When someone says AI will replace people, I don’t see it. Let me give you an example:

AI vs Me

After gastric bypass, GLP-1 levels surge dramatically. Ghrelin falls after sleeve gastrectomy. Insulin sensitivity improves long before meaningful weight loss occurs. The metabolic machinery begins shifting almost immediately.
We thought we were carpenters rearranging plumbing.
We were endocrine surgeons with staplers.
Eventually the field acknowledged what the data had been quietly telling us. Bariatric surgery became bariatric and metabolic surgery. The name changed because the science demanded it.

Here is when I asked AI to redo it:

After gastric bypass, GLP-1 levels surge. Ghrelin falls after sleeve gastrectomy. Insulin sensitivity improves well before meaningful weight loss appears—the metabolic machinery begins shifting almost immediately.
We thought we were carpenters, rearranging plumbing.
We were something else entirely—endocrine surgeons with staplers.
In time, the field caught up to what the data had been saying all along. Bariatric surgery became bariatric and metabolic surgery, not by preference but by necessity. The name changed because the science refused to be ignored.

— Anyway, I prefer me. AI can write for you, but you have a unique voice. Use it. And learn to use the em dash

In this episode, Dr. Terry Simpson breaks down what really happens to lean body mass during weight loss—whether it’s diet, surgery, or medications like semaglutide. He explains why glycogen and water get mislabeled as “muscle loss,” why severe protein deficiency is actually rare, and why most people naturally move more—and get stronger—after losing weight.

Then we tackle bone: why some bone loss is a normal adaptation to carrying less weight, what actually causes osteoporosis, and why staying active matters far more than clinging to excess pounds out of fear.

And yes—we take on the “gym bro” narrative that GLP-1s are dangerous unless you follow their program. (Spoiler: that’s not evidence, that’s marketing.)

If you’ve heard the panic, this is the episode that puts it back into physiology.

The Claim That Sounds Scarier Than It Is

Every few months, a new version of the same warning circulates: GLP-1 drugs like semaglutide cause you to lose muscle. It’s usually delivered with a number—“up to 40%”—and a tone suggesting something important is being quietly taken from you.

The problem isn’t that there’s no truth there. The problem is that the truth is being told badly. And usually being told by some gym-bro who wants to sell you their brand of protein powder with their workout program. Arg.

Weight Loss Always Includes Lean Mass

If you lose weight, you will lose some lean body mass. That’s not controversial. It’s not new. It’s not drug-specific. It’s what the human body does in a calorie deficit.

We saw this every day in bariatric surgery. Patients lost fat, yes—but also lean mass. Not because surgery was uniquely harmful, but because weight loss itself carries that feature.

Lean Mass Is Not Just Muscle

Here’s where the internet takes a wrong turn.

Lean body mass includes:

• Muscle

• Glycogen

• Water

• Organs and connective tissue

That matters, because the first thing you lose when you cut calories is glycogen—and the water that comes with it. Glycogen lives in muscle, so when it leaves, the scan reads that as “lean mass loss.”

That is not the same thing as losing contractile muscle.

And just as importantly, glycogen and water are meant to come back. That early drop is reversible. It’s not your body dismantling itself—it’s your metabolism adjusting.

Surgery vs GLP-1: Not the Same Physiology

After surgery, there’s a period of recovery. People are less active. There is stress, healing, and temporary catabolism. That contributes to lean mass loss.

With GLP-1 therapy, you don’t have that.

You can move. You can function. And when people lose weight without the burden of recovery, they usually do more, not less.

That’s the part the panic misses.

The Reality No One Mentions: You Move More

Lose a meaningful amount of weight and the world feels different.

Walking is easier. Getting up is easier. Exercise becomes something you might actually want to do.

In my own case, I didn’t join a gym or reinvent myself as a fitness influencer. I just did more of what I already liked. Yoga went from once a week to several times a week. I walk more. I enjoy it more.

That matters more than any theoretical loss on a scan.

What I Actually Measure

I’m not guessing.

I use a Withings Body Scan scale daily, and I use the segmental features weekly to look at arms and legs. Not obsessively—just enough to follow trends.

What I’ve seen is straightforward: despite losing weight, my lean body mass has increased.

No gym membership. No elaborate lifting routine. Just more movement and feeling better.

I’ve lost 50 pounds, and my muscle mass has increased. Makes me happy because I try not to sweat too much - hard on my hair.

The Protein Panic

Yes, protein matters.

No, you do not need to eat like a competitive bodybuilder to preserve muscle during weight loss.

If you are truly protein deficient, you can lose more lean mass than you should. But the leap from that to “you need massive protein intake and structured resistance training or you’ll waste away” is more marketing than medicine.

Most people need adequacy, not excess.

The “40%” Statistic

You will see it everywhere.

Sometimes up to ~40% of weight loss is labeled lean mass. That can happen depending on how and when it’s measured—but it is not universal, and it includes glycogen and water.

More importantly, it is not unique to GLP-1 drugs. Similar proportions show up with other forms of weight loss.

The number sounds dramatic. The biology is not.

Bone Mass: The Part No One Explains Well

Now let’s talk about something even more misunderstood: bone.

When you lose weight, you will often see a reduction in bone mass. That alone is enough to send people into a tailspin, as if their skeleton is quietly dissolving.

It isn’t.

Bone is living tissue. It remodels constantly. It responds to load. When you carry more weight, your bones adapt to that load. When you carry less, they adapt again.

So yes—lose weight and you may see some reduction in bone density. That is not automatically pathology. It is, in part, normal adaptation.

Where it becomes a problem is not weight loss itself, but deficiency or disease.

True bone loss of concern—osteoporosis—is about changes in bone quality and structure, not simply calcium leaving the body. It involves the bone matrix, the architecture, and the balance between formation and resorption. Genetics plays a large role. Age, hormonal status, and certain medications matter far more than whether someone lost weight on a GLP-1.

Deficiencies can contribute—particularly vitamin D and, to a lesser extent, inadequate calcium intake—but in most people eating a normal diet, severe deficiencies are not common drivers.

And just like muscle, bone responds to stimulus.

Weight-bearing activity and resistance matter. You don’t need a barbell to do that. A well-executed chaturanga—repeated, controlled, weight-bearing through the upper body—is resistance work. Walking is load. Daily life is load.

The skeleton is not passive. It adapts to what you ask of it.

What Actually Matters

Not the scan in isolation.

Not the percentage of “lean mass.”

Not the influencer warning you about invisible losses.

What matters is whether you are:

• Moving more

• Functioning better

• Maintaining strength

• Improving metabolic health

GLP-1 therapies do that for many people.

Final Thought

The internet loves a good warning. It loves to take a piece of physiology and turn it into a threat.

But the reality is quieter.

You lose weight. Some lean mass goes with it. Your body adapts. You feel better. You move more. And in many cases, you end up stronger where it counts.

If someone wants to turn that into a crisis, they are welcome to it.

I’ll be at yoga.

Paid Section: What to Actually Do (Without Losing Your Mind)

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I Just Got Back From Italy. That’s not the Mediterranean Diet.

Yes, I ate the pasta. The bread. The gelato. The cured meats. Wine at lunch, wine at dinner. Late meals, long walks, repeat.

And like clockwork, I can already hear it:

“See? Mediterranean diet. Pasta, bread, wine.”

No. That’s not what we mean. Not even close.

The Mediterranean diet isn’t what people in Italy eat today. It’s not a travel experience. It’s not “they eat carbs and live long.” It’s a score.

A score that we actually measure. Roughly nine components. Vegetables, fruits, legumes, whole grains, nuts. Olive oil as the main fat. Some fish. Moderate alcohol. Less red meat. Less processed food.

You get points for hitting those targets. Add it up. Higher score, lower risk.

That’s the diet. Not Rome in 2026.

And this is where people get sideways, because they want the story to be cultural. It’s easier that way. “They eat this, we should eat that.”

But the whole thing only makes sense if you understand where it came from.

Ancel Keys wasn’t studying restaurants.

One of my heroes is Ancel Keys, widely credited with the Mediterranean Diet. He studied people.

The story goes like this. In the 1950’s there was an epidemic of middle aged men suddenly dying of heart disease. Sudden cardiac death - grab the chest, keel over and die. Eisenhower had a heart attack, LBJ had a heart attack - they survived those.

He was in Cambridge doing a sabbatical when someone told Keys that in the village in Italy hardly anyone had a heart attack. He had to investigate, so he and his wife went to that small village and looked over things. It was true, there were fewer heart attacks in this village.

By the way, if you think heart disease is bad now, in the 1950’s there were five times as many deaths from heart disease as today. Think about that - five times. And this was something new. Prior to the 1950’s the main cause of heart disease was not “coronary artery disease”, it was valvular heart disease due to rheumatic fever. Antibiotics changed that. As people lived longer, ate better, smoked more, there was more atherosclerotic heart disease.

So to study this, Keys decided to do a comprehensive study following a group of men over time, what they ate, lab values and etc. Specific groups. Villages. Cohorts. People he could measure and then follow for years inside what was ultimately called “The Seven Countries Study.”

And this matters, because we keep retelling it like he looked at countries on a map and picked the ones he liked. That’s the “22 countries, picked 7” line. You’ve heard it. It’s wrong, but it sticks because it sounds simple.

Here’s what actually happened.

Early on, there were rough country-level comparisons. Food supply data. Mortality stats. Big, messy, indirect stuff. Even at the time, people pointed out that those data could only suggest associations, not prove anything. This is the preliminary work done for epidemiology.

Keys decided to study what we call cohorts. Built studies where he could measure what people actually ate, track risk factors, and follow outcomes over time.

Not countries. People. That’s the difference everyone keeps missing.

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Now zoom out.

This was the 1950s and 60s. No statins. No stents. No modern cardiology safety net. You had some blood pressure meds. You had surgery if things got bad enough.

Mostly, you had a diet. That was the tool.

And what showed up, over and over, was a pattern. Not perfection, not a single cause, but a pattern.

Populations eating diets lower in saturated fat, higher in plant foods, had less heart disease. Then we followed them. Not for five years. For decades. Fifty-plus years of follow-up.

To be clear: some of the villages had diets rich in fats (like Finland and the United States). They had more heart disease than those places that ate less saturated fat, more olive oil, more vegetables, whole grains, fruits, and fish. So when people claim Keys didn’t study villages that ate a high fat diet, they are simply wrong. They probably never read Keys work (I did, so you don’t have to).

And the signal didn’t flip. It didn’t disappear. It stayed. Meaning those places that ate more saturated fat had more heart attacks and strokes. Keys measured total blood cholesterol, they didn’t start to measure LDL or Apo(b) until much later.

You can argue mechanisms. You can argue edge cases. But the direction has been boringly consistent.

What’s interesting is how the biology caught up later.

Back then, Keys didn’t have genetics directly. He did have some interesting observations among families. Those families who moved out of the villages and into the city, eating a higher fat diet, had more heart attacks.

Today we can look at a gene called PCSK9. Most people have never heard of it, but it matters. It’s a protein that helps regulate LDL cholesterol. Some people are born with variants that reduce its activity. Technically, LDL cholesterol is a measurement of a particle that carries cholesterol around. That little bag of cholesterol is covered by a protein, called Apo(B) and that is the causative agent in atherosclerosis.

Lower cholesterol from less saturated fat in your diet over a lifetime, and dramatically lower your risk of heart disease.

Different lens, same story: lower LDL over time, lower risk. Higher LDL over time, higher risk.

This biology has been shown again and again. Today we have drugs like statins - I take Crestor because my LDL was high (190), and now with statins it is in the 40’s. So my risk of heart disease, which runs in my family, has dramatically lowered.

And then there’s the modern rewrite.

Writers like Gary Taubes or books like The Big Fat Surprise take that early ecological data and treat it like it was the whole story. It wasn’t.

They blur the line between rough observations and actual cohort studies.

Once you do that, it looks like Keys was picking data.

But if you keep the designs separate, it looks like what it was: early hypothesis, then better studies.

Back to Italy.

If you walk around today and try to “see” the Mediterranean diet, you’ll miss it.

Because it’s not a place. It’s a pattern we built from data. Defined, scored, tested. Over and over again.

And yes, people will still tell me, “But they eat pasta.” They do.

That’s just not the part that predicts anything.

Italy was great, because it has a rich history, lots of cool stuff, and I got to spend time with my son, JJ, and show him the parts of Italy that I love.

If there’s a takeaway, it’s this.

The Mediterranean diet isn’t Italy. Ancel Keys didn’t pick seven countries out of twenty-two. And after more than half a century, with cohorts, trials, and now genetics all pointing in the same direction, the core signal hasn’t gone away.

We’ve just gotten better at explaining why it was there in the first place.

References

• Yerushalmy J, Hilleboe HE. Fat in the Diet and Mortality from Heart Disease

• Aboul-Enein BH et al. Ancel Benjamin Keys (1904–2004): His early works and the legacy of the modern Mediterranean diet

• Mitrou PN et al. Mediterranean Dietary Pattern and Prediction of All-Cause Mortality

• Widmer RJ et al. The Mediterranean Diet and Cardiovascular Disease

• Lyon Diet Heart Study

• Morze J et al. Mediterranean Diet and Cancer Risk

• Wise Nutrition Coaching. “Ancel Keys did not manipulate his data”

• Your Doctor’s Orders. “Ancel Keys and revisionist history”

• Seven Countries Study website

• terrysimpson.com Mediterranean diet scoring system

🔒 Paid Section: The Actual Mediterranean Diet Score (Not the Instagram Version)

Alright, this is the part most people skip.

They like the idea of the Mediterranean diet. They like the photos. They like saying “olive oil” and “Italy.”

They don’t actually want to score it.

But this is the whole thing.

This is how we turned observation into something measurable.

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If you have ever had even a few pounds to lose, you probably felt it, that quiet, creeping sense that something about you has gone wrong, that you have slipped in a way that is not merely physical but moral, that you have somehow failed a test you were supposed to pass without thinking. It does not arrive announced. It seeps in, through comments, through glances, through that ever-present cultural hum that insists this is all within your control, that if you were just a little more disciplined, a little more careful, a little more committed, you would not be here.

I know that feeling, not as an observer, but as someone who lived it.

Because I felt the shame, and what I realized slowly and somewhat uncomfortably, is that while I never blamed my patients, I absolutely blamed myself. I ran support groups for years, sat with people carrying that same burden, and helped them see that this was not a moral failure, that this was biology, that they deserved treatment and not judgment. I could say that clearly, convincingly, even compassionately. I just never extended that same reasoning to myself. I assumed, quietly but persistently, that I should do this on my own, that if anyone could will their way through it, it would be me.

Just Try Harder

And so I did what many of my patients did. I went on the diets. I tightened things up. I ate vegetables, cut out foods, added others back in, adjusted, refined, optimized. And like many of those approaches, they worked, at least for a while. Weight came off, enough to reinforce the idea that I had found the answer, that this time it would stick.

But it never did.

And if there is a profession built on stubbornness and willpower, it is surgery. We train ourselves to push through fatigue, override discomfort, stay focused when everything in the body says stop. If this were simply a matter of discipline, then I should have been the success story that proves the rule.

I was not.

Because the problem was never simply discipline. It was the constant, low-grade insistence of hunger, the persistent signaling beneath awareness, shaping decisions, narrowing attention, creating a friction that accumulates over time. You can manage it for a while, but management is not resolution, and eventually the system reasserts itself in ways that feel, and are often described as, failure.

And the truth, the part that took me longer than it should have to accept, is that I never did it on my own.

Then I started Zepbound

I am down fifty pounds now.

Not because I suddenly discovered a deeper reserve of willpower, but because the biology changed, and once it did, the behaviors followed in a way that finally felt sustainable rather than forced.

When you look at the data, the personal experience aligns with what has been observed again and again. Long-term weight loss with lifestyle alone is not just difficult, it is uncommon to the point of rarity. We see early success, often meaningful, followed by gradual regain, as metabolic adaptation lowers energy expenditure and increases hunger. The Diabetes Prevention Program, Look AHEAD, and numerous observational cohorts all tell the same story in different ways. A small percentage of people maintain significant weight loss at five years, often cited in that narrow band of three to five percent, and the rest, through no lack of effort, drift back toward where they began.

Which is why the advice to simply try harder has always rung hollow, even when I told it to myself.

The Cycle Where Your World Shrinks

Because weight gain is not just a number on a scale, it is a loop. Sleep worsens, appetite rises, movement becomes uncomfortable, so it decreases, and food becomes more rewarding because it is one of the few reliable sources of comfort. The loop feeds itself quietly and effectively. And when that loop is interrupted, everything begins to change.

With GLP-1–based therapies, as I saw with surgery and now experienced myself, the first thing that goes quiet is the noise. That persistent signaling softens, and with it the cascade begins to reverse. My sleep improved almost immediately. My snoring stopped. My sleep scores shifted in a way that was not subtle, and that alone alters appetite, energy, and capacity to engage with the day. Movement followed, not as a prescription, but as a possibility. Where I had avoided the yoga studio, attending occasionally out of obligation, I now go several times a week because I want to, because the body I am in responds differently, because movement feels like something I can do rather than something I must force.

And that is the part that is so often misunderstood when people say this is the “easy way out.”

There was nothing easy about fighting biology for years. What is different now is that I am no longer fighting it.

The People Who Shame Want You To Think a Pill or Surgery is the Easy Way

And the people who matter in that space, the ones who actually help, do not shame you. But too often on social media I see these coaches fat shaming people who take GLP-1. Saying they will regain if they stop (yes, we will, and if we stop exercising with you we regain too).

My yoga instructor never shamed me. He was simply glad I was back. He helped me find better alignment, better movement, better balance. He met me where I was and helped me improve from there. I have not lost muscle mass in the 19 months I have been on a GLP-1. It is easier to go to yoga, I feel better I want to go.

That, I suspect, is what the future looks like. Not coaches who insist there is one way, their way, delivered with the certainty of an evangelist.

But coaches who understand the biology, who are not threatened by medication, who can take someone using a GLP-1 and help them build strength, improve movement, add muscle if they want it, refine nutrition without turning it into a moral exercise.

Because the truth is, the old model is already breaking.

The idea that you must suffer through restriction, that you must prove your worth through discipline, that there is a single dietary truth that will save you if only you adhere hard enough, that model depends on failure. It depends on people cycling through attempts, blaming themselves, and trying again.

And it depends, above all, on a lack of empathy.

Because it is very easy to prescribe discipline when you have never had to fight your own biology to achieve it.

So if you think you should sign on with a coach who thinks a pill or short or surgery is the easy way out - I would advise you not to.

We want you to exercise, to eat better, to move more. Not because of maintaining your loss, but because it is opening the world for you. It will help you live better, live longer, live healthier.

Eli Lilly’s New Oral Medicine

It is also worth noting that this field is moving quickly, and the medications we are talking about today are not the endpoint. Recently, Eli Lilly announced results for a new oral GLP-1–based therapy, orforglipron, being developed under the brand name often referred to as Foundayo, which represents a meaningful shift in how these treatments may be delivered. Unlike current injectable GLP-1 receptor agonists, this is a non-peptide oral agent, designed to activate the same pathways without the need for injections, and early trial data suggest weight loss in the range that begins to approach what we have seen with established agents.

That matters, not because it replaces what we have, but because it expands access and normalizes treatment. The more options we have, the less this becomes a niche therapy and the more it becomes what it should have been all along, a standard part of treating a common, chronic, biologically driven disease.

And perhaps that is the thread that ties all of this together, the part I wish I had understood earlier, the part I tried to teach my patients but failed to apply to myself, which is that this was never about proving something.

You do not have to earn the right to treatment.

You do not have to demonstrate sufficient suffering to deserve help.

You do not have to win a battle against your own biology to be taken seriously.

What you need, and what I needed, was the recognition that the system itself could be changed, and that once it was, everything else became not effortless, but finally possible.

And that is not failure.

That is medicine catching up to reality.

Paid Section: The Biology We Ignored

What we have been calling “willpower” is, in large part, a negotiation with reward circuitry that was never designed for the modern food environment. The brain regions involved, particularly the hypothalamus and the mesolimbic dopamine system, constantly integrate signals about energy status, nutrient availability, and reward. In a natural environment, this system works elegantly. Food is scarce, effort is required, and reward reinforces behaviors that keep you alive.

You can no more will yourself to not have food noise than you can will your blood pressure, heart rate, or breathing rate to change. It is a program.

In the paid section, we will talk about hyper-processed food and how it triggers this.

Read more

There were many stories I heard, but there was one that repeated itself with such consistency that you couldn’t ignore it. When menopause—or even perimenopause—arrived, weight would follow. Not gently. Not politely. It would accumulate in a way that felt unfamiliar, almost unfair.

Some of these women had struggled with weight before. Others had never given it much thought. They had lived their lives, eaten reasonably well, stayed active, raised families, built careers. Then something shifted.

Not overnight—but steadily enough to feel unmistakable.

And the explanation they were given was always the same.

“Your metabolism is slowing down.”

It sounded scientific. It sounded final.

It just wasn’t the whole story.

What We Missed

What we know now is more interesting—and far more useful.

Estrogen does not just affect hair, hot flashes, or the vaginal epithelium. It has a quiet but powerful role in the brain. Specifically, it acts on the hypothalamus, that small but commanding region that helps regulate hunger, satiety, and energy balance.

When estrogen is present, it helps keep the system in tune.

When it declines, the signal changes.

And when the signal changes, something women often describe as food noise begins to rise.

Not because they’ve changed.

Because the system has.

The Brain Before and After Menopause

Here is the simplest way to understand it.

You don’t need to memorize the names—but they tell a story.

On one side, you have POMC—the signal that says, you’ve had enough. It promotes satiety, helps you feel full, and allows you to walk away from the table without negotiation.

On the other side, you have NPY—the signal that says, eat now. It increases hunger, sharpens attention toward food, and makes eating feel more urgent.

Estrogen, quietly and effectively, helps keep these in balance.

It supports the fullness signal.
It restrains the hunger signal.

When estrogen declines, that balance shifts.

The “eat” signal grows louder.
The “stop” signal becomes less convincing.

And the experience of eating changes.

Why It Feels Different Before It Looks Different

One of the most striking things women tell me is this:

“I don’t think I’m eating that much more—but I’m thinking about food all the time.”

That matters.

Because appetite isn’t just behavior—it’s perception. It’s the internal conversation that happens before you ever pick up a fork.

Studies have shown that hunger increases and fullness decreases during menopause—even when intake hasn’t yet changed. The system becomes less efficient.

And that’s when frustration begins.

Because from the outside, it looks the same.

But from the inside, it feels completely different.

The Part We Should Have Said Sooner

There is a part of this conversation that deserves some honesty.

For years, women were told to endure menopause. To manage symptoms. To tolerate the changes.

And when weight increased, when hunger changed, when the body felt unfamiliar—they were told to try harder.

Eat less. Move more. But we were missing something fundamental.

Estrogen is part of the system that regulates appetite. So when that system changes, the experience changes. And instead of acknowledging that—we blamed the patient.

That wasn’t just incomplete. It was unfair.

What Estrogen Replacement Really Does

When we talk about estrogen replacement, the conversation is often limited to hot flashes and sleep. But there is another layer.

Estrogen helps restore some signaling in the brain that menopause disrupts. It supports the pathways that promote satiety and helps quiet the ones that drive hunger.

It doesn’t turn the clock back. But it can help the system function more like it used to. And importantly—it does not cause weight gain.

That idea has lingered far longer than it should have.

How This Fits Into Modern Treatment

Now, medicine evolves. What we once treated as symptoms, we now understand as systems. Hormone therapy is no longer just about symptom relief. It is part of a broader understanding of how hormones influence the brain, metabolism, and long-term health.

We are beginning to see menopause not as something to endure—but as something to manage thoughtfully. Not aggressively. Not reactively. But intelligently.

And Then There Is GLP-1

There is another piece to this story, and it is impossible to ignore.

GLP-1 medications act on the same appetite centers in the brain. They enhance the fullness signal and quiet the hunger signal.

But here’s the part that matters:

Estrogen appears to improve how well GLP-1 works.

That includes both:

• the GLP-1 your body naturally produces

• and the medications we now use clinically

So menopause may not only reduce estrogen—it may also reduce the brain’s responsiveness to satiety itself. Which helps explain why things feel harder.

And why, for some women, restoring part of that system—through hormones, through GLP-1, or both—can feel like turning the volume down on something that had been getting louder for years.

Where This Leaves Us

This isn’t about telling every woman what she should do.

It’s about giving her the right explanation.

Menopause is not a failure of willpower.
It is not simply a slowing metabolism.

It is a shift in how the brain regulates hunger.

And once you understand that—you stop blaming yourself. You start asking better questions. And you realize something important: The system changed. Not you.

1.mTOR Signaling in the Arcuate Nucleus of the Hypothalamus Mediates the Anorectic Action of Estradiol.The Journal of Endocrinology. 2018. González-García I, Martínez de Morentin PB, Estévez-Salguero Á, et al.

2.Hypothalamic Actions of Estrogens in the Regulation of Energy and Glucose Homeostasis.Reviews in Endocrine & Metabolic Disorders. 2025. González-García I, Xu Y.

3.Estrogen as a Key Regulator of Energy Homeostasis and Metabolic Health.Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie. 2022. Mahboobifard F, Pourgholami MH, Jorjani M, et al.

4.Metabolism Regulation by Estrogens and Their Receptors in the Central Nervous System Before and After Menopause.Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme. 2016. Coyoy A, Guerra-Araiza C, Camacho-Arroyo I.

5.Estrogen Synthesized in the Central Nervous System Enhances Mc4r Expression and Reduces Food Intake.The FEBS Journal. 2025. Hayashi T, Kumamoto K, Kobayashi T, et al.

6.Estrogen in the Brain - Neuroestrogens Can Regulate Appetite and Influence Body Weight.The FEBS Journal. 2025. Nguyen TT, Kanemoto Y, Kurokawa T, Kato S.New

7.Menopause: A Cardiometabolic Transition.The Lancet. Diabetes & Endocrinology. 2022. Nappi RE, Chedraui P, Lambrinoudaki I, Simoncini T.

8.Weight Gain in Women at Midlife: A Concise Review of the Pathophysiology and Strategies for Management.Mayo Clinic Proceedings. 2017. Kapoor E, Collazo-Clavell ML, Faubion SS.

9.Mechanisms of GLP-1 Receptor Agonist-Induced Weight Loss: A Review of Central and Peripheral Pathways in Appetite and Energy Regulation.The American Journal of Medicine. 2025. Moiz A, Filion KB, Tsoukas MA, et al.New

10.Glucagon-Like Peptide 1 (GLP-1) Action on Hypothalamic Feeding Circuits.Endocrinology. 2025. Hwang E, Portillo B, Williams KW.New

11.Direct and Indirect Effects of Liraglutide on Hypothalamic POMC and NPY/­AgRP Neurons - Implications for Energy Balance and Glucose Control.Molecular Metabolism. 2019. He Z, Gao Y, Lieu L, et al.

12.GLP-1 Physiology and Pharmacology Along the Gut-Brain Axis.The Journal of Clinical Investigation. 2026. Beutler LR.New

13.Liraglutide Prevents Body and Fat Mass Gain in Ovariectomized Wistar Rats.Molecular and Cellular Endocrinology. 2024. Rossetti CL, Andrade IS, Fonte Boa LF, et al.

14.Estradiol Modulates the Anorexic Response to Central Glucagon-Like Peptide 1.Hormones and Behavior. 2017. Maske CB, Jackson CM, Terrill SJ, Eckel LA, Williams DL.

15.GLP-1 and Its Analogs: Does Sex Matter?.Endocrinology. 2025. Börchers S, Skibicka KP.

16.Interactions Between Glucagon Like Peptide 1 (GLP-1) and Estrogens Regulates Lipid Metabolism.Biochemical Pharmacology. 2024. Model JFA, Normann RS, Vogt ÉL, et al.

17.GLP-1 Receptor Agonists for Weight Loss for Perimenopausal and Postmenopausal Women: Current Evidence.Current Opinion in Obstetrics & Gynecology. 2025. Mikdachi H, Dunsmoor-Su R.New

18.Impact of GLP1 Agonists on Reproduction.The Journal of Clinical Endocrinology and Metabolism. 2025. Couldwell M, Tidwell AJ, Taylor AE.New

19.GLP-1 Increases Preovulatory LH Source and the Number of Mature Follicles, as Well as Synchronizing the Onset of Puberty in Female Rats.Endocrinology. 2015. Outeiriño-Iglesias V, Romaní-Pérez M, González-Matías LC, Vigo E, Mallo F.

What I Tell My Patients, Family and Friends About Menopause and Hunger

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I am on Zepbound for weight loss, one of the newer GLP-1 drugs, and I often get asked what to do about constipation—which is one of the most common issues people run into on these medications.

One of the reasons I love Substack is that I can take the time to actually walk through this. Not just a quick answer—but something useful. And frankly, even if you’re not on a GLP-1, a lot of this will still apply.

Weight loss surgery patients have this same issue - and these are many of the same strategies that worked for them.

Let’s start with definitions.

The official definition of constipation is fewer than three bowel movements per week. You may also notice hard stools, straining, or that frustrating feeling that you’re not quite finished.

Now—we need to adjust that definition a bit.

Because if you’re on a GLP-1, you’re eating less. Sometimes a lot less. So your bowel frequency will naturally decrease.

But here’s the key point:

Constipation on GLP-1s isn’t just about how often you go—it’s about how difficult it is to go, and what the stool is like when you do.

And yes—this is common.

Constipation occurs in up to about 24% of patients on a GLP-1. Roughly one in five.

I’ve had it myself.

And like most patients, the cause wasn’t mysterious. It was hydration.

So Why Does This Happen?

Let’s do the quick science before we fix it.

GLP-1 drugs slow down your gut. That’s the point.

They:

• Slow gastric emptying

• Reduce appetite

• Reduce overall intake

But downstream, that means:

• Less food → less stool

• Less fluid → drier stool

• Slower motility → slower transit

And then patients unintentionally make it worse:

• Eating mostly protein

• Skipping vegetables

• Drinking less (because they’re not thirsty)

So the colon ends up with less volume, less water, and slower movement.

That’s constipation.

And the job of the colon - reabsorb water. So if you are not drinking enough water, the colon absorbs more and you will spend time on the toilet with your phone.

Let’s Talk About Hydration

This is where most people get into trouble.

Hydration is more than just “drink some water,” although that’s a perfectly good place to start. The issue on a GLP-1 is that you have to be intentional—because your body isn’t giving you the usual signals.

You simply won’t feel as thirsty.

And there’s another piece people miss:

A large portion of the water you normally get comes from the food you eat.

So think about what happens on a GLP-1:

• You eat less

• You drink less

• You don’t feel thirsty

That’s a setup.

Less food means less water coming in. Less thirst means less drinking.

So we have to add liquid back in on purpose.

First—Kill the Coffee Myth

Coffee and tea do not dehydrate you.

They count toward your fluid intake. Full stop.

So if you like coffee in the morning—have it. I drink mine cold because I prefer it that way. If you like it hot, great. Same with tea.

That fluid still counts.

What I Actually Do

I make this very simple.

I take a small ceramic pitcher—about 2 liters—and put in four black tea bags. Fill it with water, leave it in the refrigerator overnight, and that’s my iced tea for the next day.

I carry it with me and drink from it throughout the day instead of plain water.

I don’t love most flavored waters—but if you do, enjoy. The goal is simple:

Find a way to drink more that you’ll actually stick with.

Let’s Talk Electrolytes (Briefly)

Electrolytes can help—especially if you’re not eating much.

But don’t get carried away with the “zero sugar, keto-friendly” obsession.

A small amount of glucose actually helps absorption. That’s basic physiology.

You don’t need a sports drink all day—but a little support is fine.

A Practical Tip (This One Matters)

If you’re increasing your GLP-1 dose, that day—and especially that morning—I recommend adding something like Pedialyte.

You can get it at any pharmacy. I keep this in the house all the time.

The liquid works, and the popsicles are great if you’re a bit nauseated.

And that’s the point—when you escalate the dose, nausea goes up, intake goes down, and hydration often drops when you need it most.

This is an easy way to stay ahead of it.

The Bottom Line on Hydration

Most constipation on GLP-1s comes down to this:

You are taking in less fluid than you think.

So don’t wait until you’re thirsty.

Drink early. Drink throughout the day. Make it easy.

Eat the Right Foods

Now let’s talk about what you’re eating—because this is the other half of the problem.

When people start GLP-1s, they often shift hard toward protein:

• Chicken

• Eggs

• Protein shakes

And they quietly drop:

• Vegetables

• Whole grains

• Legumes

That’s a mistake.

Foods to Choose

• Fruits: berries, apples, citrus, grapes

• Vegetables: leafy greens, broccoli, carrots, peas

• Whole grains: oats, quinoa, brown rice

• Legumes: lentils, chickpeas

• Yogurt

These add fiber, water, and bulk—the things your colon needs to function.

Foods to Ease Back On

• Highly processed foods

• Refined carbohydrates

• Very high-fat meals (they can slow things further)

Fiber—But Don’t Be a Hero

Fiber helps—but only if you do it right.

• Add it gradually

• Too much too fast → bloating and discomfort

And remember:

Fiber without water can actually worsen constipation. Trust me - think of hibernating bears - they stop drinking water - get a large mass of fiber in their gut and sleep for the winter. No wonder they are a bit grizzly when they wake up. That first movement would have to be rough.

Move Your Body

You don’t need a gym membership.

A simple 20–30 minute walk daily—especially after meals—helps stimulate bowel movement. Seriously - if you are not walking and have constipation, you are missing the movement for the movement.

I do yoga. I know, you move to California and take up yoga - but I did. It keeps me moving - in more ways than one.

Keep Some Meal Rhythm

Even small meals help trigger the gastrocolic reflex. You know, your stomach is right behind one part of the colon. And when the stomach stretches, the colon feels the bulge and moves. Some people think when they eat, they defecate it is what they just ate - it isn’t

In plain English: your gut needs reminders to move.

How to Treat It (If Prevention Isn’t Enough)

If you’re already constipated, here’s a simple approach.

First Line

Polyethylene glycol (Miralax)

• 17 grams daily in water

• Safe and effective

• Takes 2–3 days

Magnesium citrate (powder)

• Adjustable dose

• Helps draw water into stool

Add If Needed

Fiber supplements

• Psyllium (Metamucil), methylcellulose

• Start low, go slow

Stool softeners

• Docusate

• Helpful if straining

Rescue (Not Daily)

Stimulants

• Senna or bisacodyl

• Use as needed, not every day

When to Call Your Doctor

Call right away if you have:

• No bowel movement for more than 5–7 days

• Severe abdominal pain

• Vomiting

• Blood in stool or black stools

• Severe bloating

One More Thing Before We Get Practical

I start my day with a breakfast shake.

Why?

Because it solves multiple problems at once.

It gets fluid in early.
It gives me protein.
It gives me fiber.

And it’s easy when you’re not that hungry.

What I typically do:

• Oat milk

• About 1½ cups of berries

• Protein (Greek yogurt or powder)

• Sometimes oats—about ⅓ cup

If I’m using oats, I’ll soak them overnight in the oat milk so they soften up.

You don’t have to start with that much—start smaller if you want.

And if things are a bit slow, I’ll add chia, flax, or even supplemental fiber. Citrocele has a nice flavor and can easily work with the shakes.

It’s a simple way to start the day with hydration, fiber, and nutrition—before appetite has a chance to get in the way.

If you want to see my recipes for shakes, go to terrysimpson.com and look under Mediterranean Breakfasts.

Transition

Now—this is where most advice stops.

“Drink more water. Eat more fiber.”

That’s fine. It’s also not helpful when you’re standing in your kitchen wondering what to eat.

So in the paid section, I’ll walk you through exactly how I structure a day of eating to prevent constipation on a GLP-1—with real meals and recipes you can actually use.

Read more

The first time I realized something odd was happening in nutrition was not in a medical journal. It was on social media, where a man was explaining with complete certainty that every human disease could be solved with beef.

Just beef.

Not a pattern of eating. Not a cuisine. Not even a diet in the traditional sense. Simply beef, eaten daily and heroically, preferably from a cow that had lived a morally upright life on a grassy hillside.

Vegetables, he explained, were toxic. Fiber was unnecessary. Fruit was suspicious. And legumes — well, legumes were practically chemical warfare.

This was delivered with the sort of confidence that once belonged to televangelists and late-night gold dealers.

And as I listened, I realized something familiar was happening. Nutrition had once again stopped behaving like a science and started behaving like a religion.

Yes, there are real scientists studying nutrition. But out on the fringes — where the supplements are sold — a different strategy emerged. They found a religion to deliver the message. There were prophets. There were commandments. And there were heretics. The newest sacrament, it turns out, is beef.

The Prophets: The Case of the Liver King

Every movement needs prophets.

The carnivore world found one in a man who called himself Liver King.

If you missed this particular chapter of internet nutrition, Liver King was a bearded, shirtless evangelist for what he called “ancestral living.” He appeared on podcasts and social media surrounded by raw organs, axes, and the occasional animal carcass, proclaiming that modern men had become weak because they had abandoned the ways of their prehistoric ancestors.

The solution, he said, was simple.

Eat organs.
Eat raw liver.
Train like a caveman.
Reject modern foods.

And, conveniently, purchase the supplements he was selling to help you live this ancestral lifestyle.

The image was powerful. A muscular man with the physique of a comic-book barbarian, declaring that everything modern medicine had learned about nutrition was wrong and that the answer lay in returning to primal habits.

There was only one problem. He wasn’t telling the truth. Does this sound like some modern “prophets” in other religions?

In 2022, leaked emails revealed that the Liver King spent over $10,000 per month on performance-enhancing drugs, including anabolic steroids and human growth hormone. Shortly afterward, he released a video admitting what most physicians and exercise physiologists already suspected.

His physique was not built on raw liver. It was built with pharmacology. Yes he did a lot of working out, but it was enhanced or “jacked.” It was not made with liver.

None of this stopped the business. By the time the truth surfaced, the Liver King had already built a supplement empire reportedly generating tens of millions of dollars per year.

And that is the real lesson. The carnivore movement often presents itself as a rebellion against modern industry and pharmaceutical influence. But many of its loudest voices are not rebels against the system.

They are simply running a different version of the same business model.

Sell certainty. Sell identity. Sell supplements. And if that fails, sell a coaching program. The beauty of the movement is that as you bring more people in, more can grift. Then they become the defenders of the steak, because now they have their finances invested in it.

The prophets of dietary purity rarely live the lifestyle they preach. But they are good at selling it.

The Other High Priest: Paul Saladino

Every movement needs its theologians. If the Liver King was the circus barker of the carnivore movement — shirtless, roaring, waving a slab of liver like a medieval relic — then the movement’s more intellectual voice has been Paul Saladino.

Saladino is technically a physician. He trained as a psychiatrist, which means he spent a good deal of time learning about the mind, human behavior, and why people believe things strongly even when the evidence is less enthusiastic. Somewhere along the way, he pivoted away from psychiatry and toward nutrition evangelism, rebranding himself as Carnivore MD, a title that has the advantage of sounding both medical and vaguely medieval simultaneously.

For several years, his message was uncompromising. Plants, he argued, were full of toxins. Vegetables were chemical warfare. The safest diet for humans was meat, organs, animal fat, and little else. His book The Carnivore Code became something of a manifesto for the movement — a long argument that most human civilization had misunderstood food until the rediscovery of steak.

The difficulty with these sorts of absolute claims is that eventually the human body gets a vote.

After about two years of eating a strict carnivore diet, Saladino began describing many symptoms that were, shall we say, inconvenient for the theory. His sleep deteriorated. His heart would race unexpectedly. He developed muscle cramps. Testosterone levels reportedly fell. The body was sending a message that perhaps an all-meat diet was not the evolutionary triumph it had been advertised to be.

And so something interesting happened. Fruit appeared. Honey appeared. Raw dairy appeared.

The diet that had once condemned plants as toxins quietly evolved into what he now calls an “animal-based diet,” which in practice looks suspiciously like meat plus carbohydrates from fruit and honey. One might say the diet rediscovered sugar, but with better branding.

This sort of evolution is not uncommon in nutrition movements. The early phase is absolute — purity, certainty, doctrine. The later phase becomes more flexible once biology has made its objections clear.

From Psychiatry to Supplements

The other piece of the story is economic.

Saladino did not merely write books about carnivore diets. He also co-founded a supplement company that sells capsules made from freeze-dried animal organs and other “ancestral” ingredients. The marketing language is very clever. Modern food, we are told, is inadequate. The way to restore ancestral health is to consume carefully prepared capsules containing the concentrated essence of organs that our ancestors supposedly prized.

Oh, and his business partner? The Liver King.

You can see how the narrative works. The diet is incomplete. The supplements complete it. And conveniently, the supplements are available for purchase.

It is difficult to know exactly what Saladino earns from this business, but one suspects that selling organ capsules to hundreds of thousands of followers is financially more rewarding than practicing psychiatry in a quiet clinic somewhere. There are many ways to treat anxiety in modern America, but selling supplements to anxious people may be among the most profitable.

Here is the thing - Paul sounds like he is giving nutrition advice.
Don’t eat microplastics, watch out for farm-raised salmon, take in light in the morning. Lots of advice, and by giving advice and making nutrition simple, you are now creating a community for which you will have sales of your supplements for a long time.

Politics Enters the Kitchen

The story becomes more interesting when it leaves the internet and wanders into politics.

Recently Saladino appeared alongside Robert F. Kennedy Jr., now Secretary of Health and Human Services, in a video in which the two men shared raw milk and honey together. It was one of those moments that makes you wonder how the American conversation about nutrition arrived here.

The Mediterranean diet — vegetables, legumes, olive oil, fish, moderate meat — has been studied for decades. Large trials. Cohort studies. Epidemiology. Mountains of evidence.

But olive oil and lentils do not go viral.

Raw milk and steak do.

And so we arrive at the curious moment in which the loudest voices influencing nutrition discussions in Washington may not be epidemiologists or public health researchers, but a collection of internet diet prophets whose primary qualification is that they have microphones and large followings.

The Pattern

Once you see the pattern, it becomes difficult to miss.

First comes the dramatic claim: everything you have been told about food is wrong.

Then comes the simple solution: eat like this.

Then comes the supplement line.

Then comes the podcast tour.

And eventually, if the movement is lucky, the political connections.

None of this means meat is unhealthy. Far from it. Beef is nutritious, and a good steak remains one of life’s small reliable pleasures.

But when a diet becomes a brand, and the brand becomes a business, and the business begins to influence public health conversations, it is worth remembering something very simple.

Nutrition is a science.

Theology is something else.

And the difference between the two is usually evidence.

The Cave Painting Argument

One of the more charming arguments offered by carnivore advocates goes something like this: if humans ate vegetables, why don’t we see vegetables in cave paintings?

Apparently, the absence of broccoli in Paleolithic art is now considered nutritional evidence.

Let’s pause and think about that for a moment.

Cave paintings show dramatic things. Mammoths. Bison. Horses. Deer. They show hunts, danger, and survival. They show the moments that mattered to people living in a world where dinner occasionally tried to kill you first.

No one runs across the tundra chasing a woolly mammoth, and then returns to the cave and says, “Quick — someone grab the charcoal. We must commemorate this turnip.”

Cave art was storytelling. It was not a grocery receipt. If root vegetables had kept you alive all winter, you didn’t paint the turnip. You painted the mammoth.

If cave paintings determined diet, we would also conclude that early humans never ate fish. Except cave paintings show fish, but most of the carnivores are too lazy to look at anthropological sites. In addition, archaeological sites around the world are filled with fishing hooks, nets, and traps dating back tens of thousands of years. Humans clearly ate fish long before the invention of Instagram nutrition.

And then there is the broccoli problem.

Broccoli did not exist during the Paleolithic. It was cultivated from wild brassica plants by Mediterranean farmers — likely the Etruscans — centuries before the Roman Empire.

So the reason you do not see broccoli in cave paintings is the same reason you do not see tomatoes, potatoes, sourdough bread, or espresso machines.

They had not been invented yet.

Using cave paintings to prove humans were carnivores is like using medieval paintings to prove humans never drank coffee.

Humans Were Never Carnivores

Anthropology tells a much less dramatic and far more interesting story.

Humans are omnivores, and always have been. When scientists examine ancient bones, analyze plant residues on tools, or study preserved human feces — an activity politely referred to as coprolite analysis — they find evidence of remarkably varied diets.

Roots and tubers. Seeds and grains. Fruits. Fish. Meat when available.

The proportions varied enormously depending on geography. Arctic populations relied heavily on animal foods. Equatorial populations consumed far more plant foods.

But nowhere in human history do we find a civilization living entirely on beef — or on any single food.

Flexibility, not purity, was the great evolutionary advantage of our species.

The Forgotten History of Meat-Only Diets

The carnivore diet is often presented as revolutionary.

It is not.

In the nineteenth century, a physician named James Salisbury promoted what became known as the Salisbury diet. His prescription was simple: eat ground beef patties several times a day, drink hot water, and avoid vegetables.

Yes, the original carnivore diet was essentially a hamburger diet.

Like many restrictive diets, some people lost weight. They also developed other problems, including nutrient deficiencies and constipation severe enough that one suspects the hot water was doing heroic work.

The diet eventually faded away.

But like many ideas in nutrition, it seems to have been waiting patiently for the invention of the podcast.

When Diet Becomes Identity

The modern carnivore movement is not about food.

It is about certainty. With certainty, you become a prophet, and with that you can sell people anything.

“Eat a variety of whole foods” is sensible advice, but it does not build a brand.

“Plants are poison” is far easier to market. Or “Kale is b.s.”

Extreme diets attract attention, followers, and eventually revenue streams. Supplements, coaching programs, laboratory panels, and subscription beef boxes all follow naturally once a food ideology has been established.

Nuance rarely sells well on social media.

Absolutes do.

The Scurvy Reminder

History occasionally reminds us why dietary diversity matters.

Recently, the musician James Blunt revealed that he once developed scurvy.

Yes — scurvy, the disease that plagued sailors during the age of wooden ships.

Scurvy occurs when humans fail to consume enough vitamin C, something that tends to happen when fruits and vegetables disappear entirely from the diet.

Centuries ago the British navy solved this problem by issuing sailors citrus fruit. It worked so well that British sailors eventually acquired the nickname “limeys.”

It is slightly astonishing that a lesson learned in the eighteenth century occasionally needs to be rediscovered in the twenty-first.

The carnivores often state that this isn’t an issue, and point to men who were in the Arctic - ignoring that arctic mammals make their own vitamin C and by consuming those, will avoid scurvy. Eating only cows or pork will not do that.

And One More Problem With Carnivore

It is boring.

Human cuisine is one of the great cultural achievements of our species. Every culture has created extraordinary food traditions built on combinations of plants, grains, spices, and animal foods.

Reducing all that to an endless procession of ribeyes is not just nutritionally questionable.

It is culinarily tragic. I grew up on a little island in Alaska, and beef was rare and expensive. So for me, beef is wonderful. But eating only beef every day is not a cuisine. It is a punishment. Ask anyone who has been on the low carbohydrate diet for a time.

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Reports this week suggest that Casey Means may not have the votes needed to become Surgeon General.

If that turns out to be true, it may be one of the more encouraging pieces of public-health news we’ve heard in a while.

The Surgeon General of the United States is not supposed to be a wellness influencer.

Historically, it is one of the most respected medical posts in the country, held by physicians with deep clinical and public-health experience.

Consider a few of the people who have held that office.

C. Everett Koop, a pediatric surgeon, confronted the AIDS epidemic in the 1980s with clarity and courage when many politicians preferred silence. His national HIV education campaign saved lives and helped push the country toward evidence-based policy.

David Satcher served both as Surgeon General and Director of the CDC and used the office to address health disparities and mental health.

Vivek Murthy, a practicing physician and public-health expert, has used the office to confront loneliness, addiction, and the mental-health crisis affecting young people.

These were physicians who had spent years practicing medicine, leading institutions, and grappling with real public-health problems.

The Surgeon General is supposed to be the nation’s doctor.

Instead, we were presented with a candidate who:

• Did not complete a surgical residency

• Has not practiced clinical medicine for years

• Built her public profile largely through wellness media, podcast appearances, and a bestselling book

That alone should raise eyebrows.

But the problem goes deeper.

During a Senate hearing, Senator Tim Kaine asked a simple question:

Do influenza vaccines reduce hospitalization and death?

This is not a trick question.

The answer is yes. Decades of epidemiologic data show that influenza vaccination reduces severe disease, hospitalizations, and mortality.

Instead of answering, Means spent three minutes avoiding the question, circling around it even while Kaine had the statistics in front of him.

When someone seeking the nation’s top public-health position cannot clearly state that influenza vaccines reduce hospitalizations and deaths, that is not nuance.

That is evasion.

And evasion on basic public-health questions is disqualifying.

This is not a serious public-health professional.

This is a wellness influencer.

Someone whose business model includes promoting continuous glucose monitors to healthy people alongside her brother, despite the fact that most of those consumers do not medically need them.

That is not clinical medicine.

That is the wellness industry.

And it reflects a larger problem.

Under the orbit of Robert F. Kennedy Jr., qualified scientists have been removed from advisory panels while a loose ecosystem of influencers and contrarians has been elevated.

For those of us who have spent decades practicing medicine, teaching medicine, and working in public health, it is not merely frustrating.

It is insulting.

Public health is not a hobby.

It is the quiet infrastructure that keeps water clean, food safe, and infectious diseases from killing millions of people.

You only notice it when it breaks.

And when it breaks, the reminder tends to arrive in the form of outbreaks.

Which, if you look at the rest of this week’s medical news, may already be happening.

Trust in Medicine Is Falling

A new survey from the Annenberg Public Policy Center found that Americans are losing trust in federal health agencies.

Confidence in the CDC, FDA, and NIH dropped between five and seven percentage points over the past year.

Interestingly, Americans say they trust professional medical organizations more, with 73% saying they trust the American Medical Association.

That finding makes sense.

People trust doctors.

But here is the irony.

Much of the science physicians rely on comes from the very agencies people say they trust less.

The NIH funds the research.
The FDA evaluates the drugs.
The CDC tracks the diseases.

Those institutions are the backbone of American public health.

We need them to function well.

But at the moment they are being hollowed out.

Under the current RFK Jr. orbit, many serious experts have been pushed aside while advisory panels are filled with contrarians and influencers.

Instead of the quiet competence that public health requires, we are increasingly getting performative skepticism.

We are drifting toward a system where some of the loudest voices in health policy make Gary Brecka sound like the adult in the room.

That should concern anyone who cares about science.

Polio Is Showing Up Again

The CDC issued a Level 2 travel advisory after poliovirus was detected in multiple regions over the past year.

Countries where the virus has appeared include:

• Germany

• Israel

• Spain

• The United Kingdom

• Several African nations

Travelers are advised to make sure their polio vaccinations are up to date.

Most Americans received the full childhood series and remain well protected.

Routine boosters are not necessary for most adults, but the CDC recommends one lifetime booster for people traveling to areas where poliovirus is circulating.

For younger generations, polio is something found in history books.

Older physicians remember it very well.

Children in iron lungs.
Hospital wards filled with paralyzed patients.

Vaccination nearly eliminated it here.

But viruses do not respect borders.

Measles Is Back

The United States has already recorded more than 1,100 measles cases this year.

About 96% of those cases occurred in people who were not vaccinated.

More than 80% are in children and teenagers.

Epidemiologists often call measles “the canary in the coal mine.”

It is one of the most contagious diseases known.

When vaccination rates fall even slightly, measles is usually the first disease to return.

And when it does, other vaccine-preventable diseases often follow.

Flu Has Overtaken COVID This Winter

For the second winter in a row, influenza has caused more illness in the United States than COVID-19.

COVID continues to circulate year-round, but widespread immunity from vaccination and prior infection has reduced its severity.

Influenza remains seasonal and unpredictable because the virus evolves each year.

GLP-1 Drugs Continue to Surprise Researchers

GLP-1 medications are quickly becoming one of the most important therapeutic classes in modern medicine.

This week’s research suggests they may:

• Reduce risk of substance-use disorders

• Maintain benefits even with less frequent dosing

• Dramatically lower cardiovascular risk when combined with healthy lifestyle habits

I’ll go through the studies in more detail in the paid section below.

Artificial Intelligence Is Not Ready for the ER

A study published in Nature Medicine tested an AI triage system using 60 real-world clinical scenarios.

The AI under-triaged emergency cases more than half the time, recommending routine care when patients should have gone to the emergency room.

Artificial intelligence will absolutely play a role in medicine.

But for now it occasionally behaves like a first-year medical student who stayed up all night reading WebMD.

The Microbiome Testing Industry Is Still the Wild West

Researchers sent identical stool samples to 21 direct-to-consumer microbiome tests.

The results varied wildly between companies.

In some cases even tests from the same company disagreed.

The microbiome is a fascinating field of science.

But the commercial testing industry has gotten far ahead of the evidence.

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Drumsticks never tasted so good and the sauce

Normally, I’m skeptical of another way to do chicken.

We have grills.
We have cast iron.
We have sous vide.
We have ovens that work perfectly well.

While YouTube has never been my medium, turkey and chicken sous vide have been staples.

And my friend Zach got a tajine.

He told me it was transformative.

Years ago, a friend who spent time in Morocco loved chicken this way.
Then it was mentioned on a podcast (Skeptics Guide to the Universe).
Then Instagram.

At some point — around the 1,000th person telling me how good this clay cone was — I did what any rational adult does.

I bought one. Okay, I am not rational when it comes to things for the kitchen. If someone says a tool is great, I will get it. Many of these end up at good will and well - here we go.

I would love to do a live cooking show with it.

But this is slow cooking at its finest — not “set it and forget it” slow cooker food. This is controlled, deliberate, collagen-converting, moisture-recycling cooking. Which means we could do the prep - then come back in a few hours to taste the food.

So instead of a live, I’ll give you the recipe I used, some photos, and a bit of history.

Because this tool deserves context.

The Tagine: Clay, Empire, and Slow Fire

The word tagine — Arabic ṭajīn (طاجين) — likely descends from the Ancient Greek tágēnon, meaning “frying pan.” Before hashtags, before food influencers, there were trade routes. Language traveled with cumin and coriander. The Mediterranean has always been one long argument conducted over dinner.

By the 9th century, tagine-style cooking appeared in One Thousand and One Nights, and during the Abbasid era, under Harun al-Rashid, slow-braised, spice-laden stews were already cultural currency. In the 13th century, Ibn al-Adim described simmering meat with coriander, onion, garlic, fennel hearts, and sheep’s tail fat until the broth reduced and clung to the flesh. Read it slowly. That’s not rustic improvisation. That’s technique.

The distinctive conical clay vessel most associated with Morocco likely arose in the Anti-Atlas Mountains — elegant engineering disguised as peasant cookware. The lid traps steam, condenses it, and returns it to the stew below. In arid climates where fuel mattered, waste was not an option. Perfected over years, this method provides a great way to cook meats that are high in collagen, inexpensive cuts.

Nineteenth-century European travelers found them everywhere in Algeria and Tunisia — red clay, varnished with pine resin and olive oil, shaped by women who understood thermodynamics long before the word existed.

The tagine endures because it works. Low heat. Patience. Spice. Time.

And like most things worth eating — or believing — it was perfected slowly.

What a Tagine Actually Does

The tagine isn’t magic.

It’s physics.

The tagine is both the vessel and the dish cooked in it.

Wide base.
Conical lid.

That cone is the engineering.

As food simmers:

• Steam rises

• Condenses along the interior

• Drips back down

Moisture is recycled.

Flavor concentrates without drowning the food in liquid.

This matters in arid climates. Water is precious. Cooking methods that preserve moisture are practical, not decorative.

The tagine allows you to use less liquid than a Dutch oven, while still preventing drying.

It’s elegant thermodynamics — developed long before stainless steel and temperature probes.

The tajine (I know, I’m spelling it both ways) has to warm in the oven. You don’t want to put hot liquids in a cold ceramic. Some use the tagine on a stove top - but I have an induction stove top, so ceramic won’t heat. But think about it - in North Africa, this is buried with coals around it. The best way to imitate that is with a nice warm oven.

The First Cook: Drumsticks

I kept it simple. I wanted skin on, bone in chicken - the best way. Thighs were not available that day, so drumsticks it was.

Twelve air-chilled drumsticks (Costco).
Carrots.
Onion.
Preserved lemons.

Preserved lemons are whole lemons cured in salt — sometimes with their own juice — and left to soften and ferment gently over weeks. In Moroccan cooking, they’re less about sharp acidity and more about transformation. The flesh becomes mellow and almost jammy, but it’s the peel that matters: intensely aromatic, floral, saline, and deeply citrusy without the bite of fresh lemon.

They don’t shout “sour.” They murmur complexity.

In a tagine, preserved lemon dissolves into the sauce, lifting spices, brightening olives, and cutting through slow-cooked richness. It’s citrus that has learned patience — which may be the most Mediterranean quality of all.

I bought mine from Amazon.

Dried apricots.
Cumin. Coriander. Turmeric. Classic spice
A touch of cinnamon.

Dark meat only.

Because dark meat contains collagen.

And collagen, or that grisle or fascia is the entire point.

After browning the chicken hard — real color, not polite tan — I built the base in the same pan, scraping up the fond (the stuff that sticks to the pan) with onions and stock.

That liquid becomes the foundation.

Carrots went into the warmed tagine.
Chicken nestled on top.
Liquid poured around, not over.

Lid on.
325°F.
Two hours.

The result:

• Fall-off-the-bone tender meat

• Carrots soft but intact and they soaked up all those spices and are delicious.

• Sauce glossy, not soupy

• Preserved lemon bright but integrated

Finished with sumac, za’atar, fresh herbs, and olive oil.

It wasn’t “diet chicken.”

It was layered, structured, and deeply satisfying.

The Recipe

Preserved Lemon & Apricot Chicken Tagine

Serves 4 generously

Ingredients

• 12 chicken drumsticks

• 4 large carrots, thick diagonal chunks

• 1 large onion, diced

• 1½ tsp kosher salt (I don’t measure it, I just sprinkle)

• 1 tsp black pepper (just grind it baby)

• 1½ tsp cumin

• 1½ tsp coriander

• ¾ tsp turmeric

• ½ tsp cinnamon (optional)

• 2 tbsp olive oil

• ¾–1 cup chicken stock

• 1½ tbsp finely chopped preserved lemon rind

• 8–10 dried apricots

• 3 cloves of garlic sliced

• 1 inch of ginger root, dice it

Finish

• 1–2 tsp sumac

• 1–2 tsp za’atar

• Fresh herbs

• Olive oil drizzle

Method

1. Warm tagine in cold oven set to 325°F. Meaning - set the tagine in the oven, then turn the oven to 325 degrees.

2. Season (just salt and pepper) and brown drumsticks in batches. You do not want to cook them through but you do want them to be browned to get that nice fond.

3. Sauté onion in same pan, scraping up fond. The onions release water and then you can scrape up the fond and incorporate it.

4. Add garlic and ginger, stir for a few seconds then. Just enough to smell it then

5. Add the spices to the onion. This forms a nice sticky bit of onion and wonderful smells. Once you have that then add the stock- here is a trick, if you don’t have stock, just add water - its ok. But you want to add it before the spices burn.

6. Add stock, preserved lemon, and apricots. For the lemon, I use a spoon to remove the fruit. What you want is the lemon peel -where the essential oils are.

7. Layer carrots in tagine, place chicken on top, pour liquid around.

8. Lid on, 325°F for 2–2½ hours.

9. Rest 15 minutes. Finish with sumac, za’atar, herbs, olive oil.

No rushing.
No stirring every five minutes.
Let physics work.

🔒 Collagen Physics & Why the Tagine Is Special

Now let’s talk about what’s actually happening inside that cone.

This isn’t nostalgia.

It’s protein chemistry. Ok, I am a nerd in the kitchen, and everywhere else.

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One of my paid subscribers brought this topic to my attention — so thank you. I am always looking for topics for you.

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Here is the real issue.

If you are 65 or older and sustain a hip fracture, your risk of death in the following year rises dramatically — approaching 30–40% in many cohorts.

This is not about a DEXA scan.

This is about survival.

I had a delightful man who came into one of the nursing homes I visit. He was well known locally as a world-class bowler. Outgoing. Sharp. Social. Independent.

He lived alone.

One day he slipped at home. A simple fall. He was later found by a friend. He was taken promptly to the hospital. The hip was repaired. Technically, the surgery went well.

But he never saw his home again.

He stayed in bed more than he should have. He rarely got up. The spark was gone. Eventually, he developed COVID — the same infection that has taken too many people — and died. Less than a year after his fall.

When I spoke with his family, they described a different man. Active. Laughing. Surrounded by friends. Bowling several nights a week.

One slip. One fracture.

And that was the beginning of the end. This is why we care.

The Phone Call You Don’t Want

My dad lived alone in Oregon.

And three times in the last few years of his life, I got the phone call.

Sometimes it was the neighbor. Sometimes it was the paramedics.

“Your dad fell.”

Thankfully, he didn’t break anything. But each time, it could have gone differently.

Once he decided the tree needed trimming. He was 95. Apparently ladders still looked reasonable to him. Another time he didn’t bring his walker from one room to the next. He tripped over a rug.

Small things. Ordinary things. The kind of things that happen in real houses to real people.

My dad lived to nearly 99. We were lucky.

But any one of those falls could have put him in the hospital. Any one of them could have been the fracture that started the cascade.

That’s the part people miss.

Osteoporosis is quiet — until it isn’t.

And when gravity wins, biology takes over.

The difference between a fall and a fracture is often bone strength. And the difference between a fracture and independence is often preparation.

Prevention doesn’t feel dramatic.

But it is the difference between going home and never seeing it again.

I swear, we need to wrap all of you in bubble wrap.

Why Hip Fractures Kill

The fracture rarely kills.

The cascade does.

• Immobility

• Sarcopenia (inability to get in protein)

• Delirium

• Pneumonia

• Thromboembolism

• Pressure injury

• Institutionalization

Hip fractures are physiologic catastrophes in older adults. Many who survive never regain independence.

This is why osteoporosis therapy is not cosmetic medicine.

It is fracture prevention.

What Actually Prevents Fractures

Professional guidance from the American College of Physicians and the Endocrine Society is remarkably consistent:

Treat high-risk patients with therapies proven to reduce fractures.

First-Line: Bisphosphonates - Names you may have heard

• Alendronate

• Risedronate

• Zoledronic acid

• Ibandronate

Fracture Reduction:

• Vertebral: 31–56%

• Hip: 26–42%

• Nonvertebral: 17–20%

They are inexpensive, durable, and well studied. They remain first-line because they offer the best balance of benefit, harm, and cost.

Rare risks exist:

• Osteonecrosis of the jaw

• Atypical femur fractures

But these are uncommon relative to the fractures prevented.

Denosumab

A RANK ligand inhibitor given every 6 months.

Fracture Reduction:

• Vertebral: 68%

• Hip: 40%

• Nonvertebral: 20%

Powerful. Convenient.

However, stopping it without follow-up therapy can cause rebound bone loss and vertebral fractures. Transition to a bisphosphonate is mandatory.

Anabolic Therapy

For very high-risk patients:

• Teriparatide

• Abaloparatide

Fracture Reduction:

• Vertebral: 74–87%

• Nonvertebral: 39–46%

Given daily for up to 2 years (18 months for abaloparatide), then followed by antiresorptive therapy.

Romosozumab

Dual action: increases formation and decreases resorption.

Fracture Reduction:

• Vertebral: 73%

• Hip: 38%

• Nonvertebral: 19%

Monthly for one year, then transition.

Avoid in patients with recent stroke or myocardial infarction.

The bowler did not die from a rare medication side effect.

He died from a fracture cascade.

And that is why treatment matters.

PAID SECTION

Risk Stratification and Sequencing: Where Mistakes Happen

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The pandemic did not end when the ventilators quieted. It simply moved online.

What began as a novel virus became a second contagion — denial. From “it’s just the flu” to “the hospitals were empty” to “the vaccines did nothing,” the arguments evolved even as the evidence accumulated. A biological event became a rhetorical war. And long after the oxygen lines were dismantled and the surge wards closed, the fight continued — not over policy, but over memory itself.

There is something uniquely cruel about telling the people who stood in those wards that the fire never burned.

It is not skepticism.

It is erasure.

In the last few days on X (formerly Twitter) I have been seeing the people who were once COVID deniers (some still are) and are now moving to Anti-vax types arguing with me about what happened during COVID.

And Some of Us Are Still Smelling the Smoke

There is a particular cruelty in being told that what you lived through did not happen.

During the worst waves of COVID, I worked in two hospitals. In one, we reopened an older, previously closed facility to accommodate the surge. Beds were added. Oxygen lines were extended. Staffing was stretched beyond anything I had seen in my career.

That was not theater. It was capacity management during a respiratory disaster.

Years later, people circulate videos of someone wandering through a shuttered hospital in Chicago — a building long decommissioned — and declare it proof that hospitals were “empty.”

An abandoned structure proves only one thing: the building was abandoned.

It does not negate:

• ICU occupancy data

• State-reported bed utilization

• Oxygen consumption spikes

• Excess mortality curves

• Surge expansion protocols

Major Chicago institutions such as my alma mater, The University of Chicago or Rush University Medical Center and Northwestern Memorial Hospital publicly reported surge strain during peak waves, consistent with statewide reporting from the Illinois Department of Public Health.

Hospitals are ecosystems. When elective surgeries were canceled, OR schedules collapsed. PACUs emptied. Outpatient clinics paused. Some nurses took PTO. Some were furloughed. Revenue plummeted.

At the same time, ICUs in hotspot regions were running continuously.

Both realities can exist simultaneously.

The mistake — or the manipulation — is presenting a quiet surgical floor as evidence that no surge occurred.

The Workforce That Did Not Come Back

After the acute waves passed, something else happened.

Healthcare workers left.

Nurses moved to outpatient clinics.
Respiratory therapists transitioned to non-hospital roles.
Some left medicine entirely.

Hospitals across the country later offered substantial sign-on bonuses to bring experienced bedside nurses back.

Many declined.

Burnout does not come from boredom.

It comes from sustained exposure to suffering.

During 2021–2023, workforce surveys documented elevated rates of anxiety, depression, and intent-to-leave among frontline clinicians. The moral injury of prolonged crisis care does not evaporate when case counts fall.

If hospitals had truly been “empty,” there would not have been a nationwide staffing crisis in acute care that followed.

The labor market tells the story.

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“Dancing Nurses”

The dancing nurse videos are frequently used as rhetorical ammunition.

They prove nothing.

During surges, visitor restrictions made hospitals visually quiet in hallways. Staff recorded brief morale clips during breaks. A 30-second video does not erase weeks of ventilator management.

When you have spent hours watching oxygen saturations fall despite maximal support — when you have held phones for final goodbyes — a moment of levity is not denial.

It is coping.

Humans require oxygen. So do souls.

The Trauma Reopened

Every time someone claims:

• “Hospitals were empty.”

• “It was just flu.”

• “Doctors lied for money.”

Those who worked those wards relive it.

Excess mortality data reported by the Centers for Disease Control and Prevention and independently analyzed by academic institutions, including Johns Hopkins University documented historic death surges during pandemic waves.

Excess deaths do not arise from choreography.
They do not appear because a nurse made a TikTok.
They do not manifest because someone filmed an empty lobby in a closed hospital.

They arise because people died in numbers beyond seasonal norms.

The Part That Needs Saying

There is something uniquely indecent about telling a firefighter there was no fire.

About telling a combat medic there was no battlefield.

About telling ICU nurses that the wards were “empty” because someone filmed a quiet lobby in a decommissioned building.

Excess deaths were real.
Ventilators were real.
Reopened wards were real.
The attrition of the workforce was real.

What is unreal is the fantasy that millions of clinicians across political parties, hospital systems, states, and countries simultaneously hallucinated the same catastrophe.

The people who say “it wasn’t that bad” were not there at 3 a.m. adjusting oxygen for the fourth crashing patient of the shift.

And every time the denial resurfaces, so does the memory.

You are free to dislike public health policy.

You are not free to rewrite the lived experience of those who bore the cost.

History will not remember the TikTok clips.

It will remember the mortality curve.

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