Last night, because of several poor decisions, I experienced projectile vomiting, which impressed me.

My job is to keep you from making those same decisions.

I’ve dealt with nausea and vomiting throughout my career as a surgeon, with post operative patients, bowel obstructions, ileus, and when I was in the pediatric wards - well, you can imagine.

Because GLP-1 drugs keep things in the stomach longer than normal (GLP-1 medications “delay gastric emptying”), and that can lead to nausea and vomiting.

What a normal Stomach Does

Normally, your stomach empties liquid quickly. A glass of water leaves the stomach in about 15 minutes. Solid food stays longer. If you eat a steak, the stomach will grind the steak up, attack it with acid and enzymes. After two hours, the steak will have the consistency of a milkshake. The valve at the end of the stomach (the pylorus) will open, and food will go into the first part of the small bowel, called the duodenum. Before that, the pylorus opens only enough to let small amounts of liquids and small particles of food out.

GLP-1 medications Delay That Opening

When you are on a GLP-1, your stomach empties a lot slower. It doesn’t mean you cannot challenge the stomach and add more food, but your stomach will not always appreciate it.

Some see this as one of the reasons we lose weight. We feel full longer. Although I think what happens in the brain is far more important. Still, feeling full with less food is a benefit.

But if your stomach is having an “off” day after you inject (and for some people this could be 1-3 days), it is time to treat it with care. And knowing that high fat foods can cause a problem, it might be time to put pizza, fried foods aside for a bit. Yes, I know the purists out there will say we should never eat such foods, but this isn’t a discussion of perfect nutrition, it’s about what your stomach can handle today.

Foods that Delay the stomach -

Fatty foods delay stomach emptying, fried foods, pizza, cheese, fatty meats. So do high fiber meals. The soluble fibers found in oats and beans form a gel that travels slowly through the stomach. So do large volume meals, high calorie density meals, and smoothies and milkshakes.

If you are feeling a bit full, and the stomach isn’t emptying, the last thing you want is a fried chicken wing and ice cream. Don’t ask me how I know that - OK, I proved that at 2 am.

Comfort Foods

We all want comfort, especially when we don’t feel well. But the comfort foods of our past are often not friendly to a stomach that isn’t emptying well. There is a big difference between how the stomach treats a fried chicken wing, and a bit of chicken breast that is oven roasted. Pizza might be comfort food or even a college diet, but this isn’t the time for that food. Your stomach will rebel. It also isn’t the time for alcohol.

The first priority is hydration.

Not all hydration solutions are created equal. This is not the time to fear a bit of sugar. Pedialyte is found in most grocery stores and pharmacies. It is based on the formula for rehydration solutions that we physicians have used for decades.

Glucose (sugar) helps the intestine absorb the electrolytes more effectively than those products without sugar. I’ve written a post about rehydration solutions on Substack for more information.

I keep Pedialyte popsicles in my freezer. If I get sick, or a member of my family, rehydration can begin sooner. Even diluted apple juice with a bit of salt. There are other high-quality solutions, like Oral Rehydration Salts (ORS), Liquid I.V., or diluted sports drinks.

Instead, think about foods that are easy on the stomach. Toast. Crackers. Applesauce. Rice. Soup. Plain cereal with oat milk. A banana. Plain grilled chicken. They may not sound exciting, but remember, your goal isn’t culinary adventure. Your goal is to let your stomach catch up.

One thing surprised me. Yesterday, my usual protein smoothie didn’t sound good at all. Normally I love it. That’s another lesson. Don’t force food, because it’s on your meal plan. If your stomach says no, listen. There will be another day to get your protein.

Last night taught me something I should have known as a physician. When your stomach talks, listen. Once you have nausea, it is time to pay attention. Most people on a GLP-1 will have a day when their stomach says, "Not today." Knowing how to respond can make the difference between an unpleasant afternoon and a miserable night.

When to Worry, How to take care of yourself

Here is how I took care of myself. Yes, it was a horrible time. But knowing how to recover, what traps to avoid, and when to call for help is important.

Read more

Here is what we know: The outbreak most of you have read about came from a farm in Mexico and involved shredded lettuce sold to Taylor Farms for distribution. That lettuce has been recalled.

Clearly, that is not the only outbreak.

So far, there is another one identified among some 70 people, but there will be more.

When can we eat vegetables again

Food borne illness occurs when a small contamination, like the one farm in Mexico, is mixed with others. But it can happen to any farm where human waste contaminates water used to irrigate crops.

It is the lettuce

Every year, foodborne illness hospitalizes 130,000 people. That is one in six of us who are infected and some sick enough to go to the hospital . About 30,000 of those hospitalizations are from produce. Leafy green vegetables are the most common source, and lettuce is the major culprit.

Probably one of the best articles written was Yang X, Scharff R. Foodborne Illnesses from Leafy Greens in the United States: Attribution, Burden, and Cost. J Food Prot. 2024 Jun;87(6):100275. doi: 10.1016/j.jfp.2024.100275. Epub 2024 Apr 10. PMID: 38609013.

They note that cyclospora is a small minority of foodborne illness from lettuce. The majority come from classics like norovirus, E coli, campylobacter, salmonella and Shigella, producing endotoxin.

To put it another way, lettuce costs over 5 billion dollars in illness every year.

So while we worry about the poopapocalypse, and the sound of this being a “parasite”, make it more headline worthy than it should be.

Epidemiology and Traceback

The work done to identify the parasite, follow up with those infected, and determine the source of the contamination is nothing short of spectacular. It is better than a Sherlock Holmes drama.

I fear most do not understand the time and effort it took to find that source.

The problem is, there are many other sources out there. One for certain, and perhaps others.

Lettuce Entertain You

If lettuce is an important part of your routine, here are the golden rules for lettuce purchase in the summer:

(1) Buy heads of lettuce, not shredded lettuce. The fewer hands touch it, the less chance you have of contamination.

(b) Remove the outer leaves of the head of lettuce. This is where the contamination is likely to be present. Not all of it, but the majority.

(3) Wash the lettuce in cold water. No vinegar, no vegetable washes, no soda, no magic ionizer. Simple water has proven to be the best in multiple studies.

Yes, I know that bacteria are killed in a lab with combinations of bleach or soap, or whatever. But for the practical cook, washing in cold water is the best

And finally, do not get a lettuce salad from a restaurant.

I love a good Cesar salad, but this summer I will go without. Cesar will return later in the year.

And yes, on the rare time when I buy a burger, I ask for it to be free of the lettuce. I noticed that Taco Bell is advertising lettuce free tacos. Good choice.

What About Farmer’s Markets

They are usually fine. I would ask if they grow their own, and I would still wash their vegetables.

Summer has an increased incidence of foodborne illness. No need to shy away from all foods, but being aware of the ones that cause the most and the season they do is good practice.

FORK U, is my food and nutrition podcast that comes out on Thursdays. This week, we’re talking about one of humanity’s greatest foods: cheese.

🍎 Listen on Apple Podcasts

Over the past few episodes, we’ve explored how cooking transformed food, how soup transformed leftovers, and how bread transformed grain. In many ways, bread transformed civilization itself. Once humans could reliably grow, store, and bake grain, we could build cities, support craftsmen, create governments, and eventually invent everything from mathematics to podcasts. Yes, I just used math and podcasts in the same sentence.

If bread helped build civilization, I’d argue cheese made us civilized.

Think about it. You can have a city without cheese. But can you have a dinner party? I mean, don’t dis a brie. OK, my son turned 16 on the 20th. The minute he was born, I became a dad, and the dad joke place of the brain was engaged.

Cheese took a food that spoiled in a day or two, and transformed it into something that could nourish people for months—or even years. It traveled with shepherds, fed armies, filled monastery cellars, and eventually found its way onto charcuterie boards where otherwise reasonable adults argue about Parmesan aging.

Recently, cheese has mystified nutrition. For decades, it was dismissed as little more than saturated fat. But it doesn’t behave like one.

Cheesy Origins

Of course, no one knows exactly when cheese was invented. Like so many important discoveries in human history, it probably wasn’t invented at all. It was discovered.

You’ve probably seen a bota di vino - a container looking like a stomach to carry wine. Stomach’s were some of the first containers used to transport liquids. Imagine putting milk into this container for a long trip. Inside the lining of the young ruminant’s stomach is rennet, enzymes whose job is to help digest milk.

As the horseman rode, the milk mixed with the remnant enzymes, along with naturally occurring bacteria, and began transforming the milk. By the end of the day, instead of milk, he found soft curds floating in watery whey.

Food was a precious commodity, it was scarce, and you didn’t just toss stuff out. You did taste it. And one of our ancestors did this. Took a bite and probably declared, “Now if I could invent a cracker.”

Archaeologists have found evidence of cheese making more than 7,000 years ago, and milk fats preserved in ancient pottery tell us that people separated curds from whey long before written history. Whether it happened in the Fertile Crescent, Central Asia, or somewhere else entirely, we’ll probably never know. I always thought it occurred in Pike’s Market in Seattle.

Someone was curious enough to taste milk transformed into this primitive cheese, that could be carried across mountains, traded between villages, stored through the winter, and eventually aged into hundreds of varieties that still define cuisines around the world.

Sometimes food doesn’t begin with a plan. Sometimes it begins because of a happy accident, and being hungry enough to take a bite.

Many Milk and Hands Make Much Cheese

Once people discovered they could transform milk into cheese, there was no going back.

Different animals produced different milk. Different climates favored different bacteria and molds. Some cheeses were eaten fresh. Others were salted, pressed, smoked, wrapped in leaves, or tucked away in caves to age for months or years. Before long, every region had its own signature cheese, each reflecting its landscape, its animals, and the people who made it.

Goat’s milk gives us tangy chèvre. Sheep’s milk becomes rich Pecorino and Roquefort. Water buffalo milk produces the creamy mozzarella that belongs on a proper Neapolitan pizza. Camel’s milk is made into cheese in parts of Africa and the Middle East. Yak cheese sustains families high in the Himalayas. Reindeer milk has been used in northern Scandinavia, although it is so rich that making cheese from it has always been more curiosity than commerce.

Donkey milk is among the rarest milks in the world for cheesemaking because donkeys produce very little of it. In Serbia, a cheese known as Pule is made from Balkan donkey milk and has become one of the most expensive cheeses on Earth.

One of the funniest scenes in Borat involves cheese. Very nice. If you know, you know.

Roquefort may be the most famous of them all.

One of my favorite examples is blue cheese. The blue veins running through Roquefort, Stilton, and Gorgonzola aren’t accidents. They’re created by Penicillium molds that have been carefully cultivated for centuries. These are relatives of the same family of molds that eventually led Alexander Fleming to discover penicillin, although they are different species and one doesn’t turn into the other. Nature, it turns out, runs more chemistry experiments than a college organic chemistry class.

Legend says a young shepherd was eating his lunch of bread and fresh sheep’s cheese in a cave in southern France when he spotted a beautiful young woman. As young men have done throughout history, he abandoned his lunch to chase after her. By the time he returned—whether days or weeks later—the cheese had become streaked with blue-green mold growing from the cave walls.

He tasted it. The result was Roquefort, one of the world’s first great blue cheeses. He probably didn’t get the girl, we rarely do. But if he discovered the cheese, he did better.

But we do know that the natural caves around Roquefort-sur-Soulzon provide remarkably consistent temperature and humidity, creating an ideal environment for Penicillium roqueforti. Long before microbiologists understood molds, cheese makers understood that those caves produced extraordinary cheese.

Once again, science arrived centuries after observation. People didn’t know why the caves worked. They simply knew they did.

That’s a pattern you’ll see over and over again throughout the history of food. Humans often discovered what worked first. Only later did science explain why.

The Saturated Fat Paradox

But cheese has a lot of saturated fat. Saturated fat is associated with an increased risk of heart disease, atherosclerosis, and stroke. We see this consistently with butter and many fatty cuts of red meat. So for years, because cheese contains a fair amount of saturated fat, we simply put it in the same category. No, I will not bore you with the chemistry of saturated fat.

There is a lesson here. We took that chemical, saturated fat, and made cheese guilty by association. No tests, just guilt by association. And as we learn again and again in nutrition and medicine, that isn’t enough.

We were told to eat less cheese, choose low-fat versions, or avoid it altogether. Yet something didn’t quite fit. And despite the thousands of cheeses in the world, I’ve yet to find a low-fat cheese worth getting excited about. Yes, I’ve tried vegan cheese. It mostly makes me feel sorry for my vegan friends.

The French seemed to enjoy plenty of cheese, butter, and rich food, but for years they had surprisingly low rates of heart disease—a puzzle known as the French Paradox. While we now know that the story is more complicated than the headlines suggested, it forced scientists to ask an important question.

Cheese didn’t seem to behave like butter. It didn’t behave like isolated saturated fat. Again and again, researchers found that cheese told a different story.

That’s where the history ends and the science begins.

Next, we’ll explore the remarkable cheese matrix, why cheese behaves differently from other sources of saturated fat, what the Mediterranean diet teaches us about enjoying cheese, why Parmesan has become the poster child for the MSG debate, and how I personally include cheese in my own diet—even while taking a GLP-1 medication.

Because cheese isn’t just another source of saturated fat. It may be one of the best examples of why studying foods is far more useful than studying nutrients in isolation.

The Problem with Extrapolation

One of the easiest mistakes in science is to find something that is true...and then assume it’s true everywhere.

Read more

The Cyclospora false positive was not found in the lettuce that was recalled. That distinction matters because many people have interpreted the FDA’s announcement to mean we are back to square one—that we no longer know where this outbreak came from. That isn’t what happened.

The laboratory sample that FDA initially reported positive, and later determined was a false positive, came from a different shredded iceberg lettuce product that was not part of the recall. The recalled lettuce had already been identified through an entirely different process. Investigators interviewed hundreds of people sick with Cyclospora, identified shredded iceberg lettuce as the common exposure, and then traced that lettuce backward through restaurants, distributors, processors, and suppliers until the traceback pointed to an independent farm in central Mexico supplying Taylor Farms de Mexico. None of that epidemiology or traceback changed when the laboratory result was withdrawn.

The false positive removed one piece of evidence, but it did not erase the evidence that led investigators to the recalled lettuce in the first place. Today, there is no laboratory-confirmed positive lettuce sample associated with this outbreak, but the epidemiology and traceback remain the foundation of the investigation.

The Independent Farm in Mexico

From there, the story becomes less certain. We know where the traceback led, but we do not know what investigators found once they reached the farm. No public report has described contaminated irrigation water, sanitation deficiencies, worker hygiene problems, or other environmental findings. We also do not know whether the farm was directly inspected by the FDA, Mexican authorities working with the FDA, or whether Taylor Farms identified concerns through its own supplier compliance and food safety audits. Those details have not been made public, and they remain an important missing piece of the story.

Epidemiology and Traceback are the strongest bits of evidence

This illustrates one of the strengths—and frustrations—of outbreak investigations. Epidemiology tells us who became sick and what they had in common. Traceback tells us where that food came from. Environmental investigations try to explain how the contamination occurred. In this outbreak, the first two are strong. The third has not yet been made public.

My suspicion—and I want to emphasize this is inference, not evidence—is that the traceback narrowed the investigation to a small number of growers. Taylor Farms may then have identified concerns sufficient to stop sourcing from one farm while the investigation continued. Large produce companies routinely audit suppliers and can suspend purchases long before every scientific question has been answered. Whether that happened here, and whether specific deficiencies were identified, has not been publicly disclosed.

This is why the story is more nuanced than many headlines suggest. The false-positive laboratory result means we have lost one piece of evidence. It does not erase the epidemiology, and it does not erase the traceback. At the same time, it reminds us not to overstate what has been proven. We have strong epidemiologic evidence and a well-developed supply-chain investigation. What we do not yet have is publicly available environmental evidence explaining exactly how Cyclospora entered the lettuce.

Recalls and Expiration Dates

That may sound surprising, but it is actually typical of fresh produce outbreaks. By the time the FDA issues a recall, the lettuce is often near—or even beyond—its expected shelf life. Fresh produce moves through the food system incredibly quickly, from farm to processor to distributor to restaurant or grocery store, and then into our kitchens. Whether the contamination is Cyclospora, Salmonella, or E. coli, investigators often race against the clock. The recall is still essential, because some products may still be sitting in restaurant coolers, grocery shelves, warehouses, or home refrigerators. But by the time the outbreak has been recognized, patients interviewed, and the traceback completed, much of the original product has already been eaten or discarded. That is one reason laboratory confirmation from the food itself is often difficult—and why epidemiology and traceback play such an important role.

Is there more than one Cyclospora outbreak?

One final point is worth remembering. Cyclospora outbreaks occur every year. Most are much smaller than this one, and several unrelated outbreaks can occur simultaneously. That is one reason epidemiologists work so carefully to separate one cluster from another. Based on the evidence released so far, this particular outbreak has been concentrated in Michigan, Ohio, Illinois, Indiana, and Kentucky, with the traceback pointing investigators toward a common supply chain. There is currently no evidence that this specific outbreak extends beyond those states, although public health officials continue to monitor for additional cases.

The practical advice has not changed. Wash fresh fruits and vegetables under cool running water before eating them, even those you plan to peel. Home-grown produce generally avoids the long, complex supply chains that can amplify a contamination event, but gardens are not immune to contamination from wildlife, irrigation water, manure, or handling. Local farms may have shorter supply chains, making problems easier to identify and contain, but they can also experience food safety issues. No matter where your produce comes from, good washing and proper food handling remain your best defenses.

That uncertainty is not a failure of science—it is part of science. Good epidemiologists know the difference between compelling evidence and conclusive evidence. The FDA deserves credit for correcting a laboratory result that did not withstand review. The next—and perhaps most important—question is whether any environmental findings from the implicated farm will eventually be released. If they exist, they would help complete the story.

For paid subscribers: How outbreak investigations really work

If you’ve ever wondered how public health officials can recall a food before they have a positive laboratory test, or why epidemiologists sometimes sound more confident than the laboratory evidence alone would suggest, this is where the detective story begins.

In the rest of this article, I’ll walk you through how epidemiologists identify patterns, how traceback follows food through one of the most complex supply chains in the world, why companies sometimes voluntarily recall products before every scientific question has been answered, and why conspiracy theories—whether they come from the political left or the political right—are such poor substitutes for evidence.

This is the science behind the headlines, and it may change the way you think about every future foodborne outbreak.

Why epidemiology often matters more than a laboratory test

Read more

It was the shredded lettuce responsible for a major outbreak in five states, Michigan, Ohio, Illinois, Indiana, Kentucky, and West Virginia. It does not explain all the outbreak.

Why “One Source” Doesn’t Mean One Batch of Lettuce

When investigators say they traced the outbreak to a single supplier, they are not saying there was one contaminated pallet or truckload of lettuce that went to one group of restaurants. Modern lettuce processing is far more complex than that. After harvest, lettuce from multiple fields and multiple deliveries is often washed, chopped, and blended together in large, highly automated processing lines capable of handling enormous volumes every hour. By the time shredded lettuce leaves the facility, each bag may contain leaves from many parts of the production stream.

That creates two important problems for epidemiologists.

First, contamination does not remain neatly confined to the original head of lettuce. If a small amount of lettuce carrying Cyclospora enters a processing line, fragments can become mixed with a much larger volume of otherwise clean lettuce. Although the contamination may be diluted, it is also dispersed over many more bags, boxes, restaurants, and ultimately customers.

Second, once the lettuce has been mixed together, reconstructing exactly where the contamination began becomes extraordinarily difficult. Investigators are no longer looking for a single bad head of lettuce. They are trying to unwind a manufacturing process that intentionally combines produce from many sources before distributing it across multiple states.

Cyclospora is like Glitter - it gets everywhere

Think of glitter at a birthday party. Open one small container, and before long it seems everywhere—on your shirt, your hands, the carpet, even places you don’t remember touching. The original source was tiny, but the act of mixing spreads it far beyond where it started. Contaminated shredded lettuce behaves much the same way. The processing line doesn’t create more parasites, but it can distribute a small amount of contamination across an enormous amount of product, making both the outbreak and the investigation far more complicated.

Taco Bell and Partnering with State and Federal Health Investigators

The biggest story this week wasn’t that federal investigators traced a major Cyclospora outbreak to shredded iceberg lettuce. It wasn’t even that the lettuce came from a single supplier in Mexico. The biggest story is that Taco Bell quietly removed lettuce from affected restaurants about a week before the FDA publicly announced its investigation results.

That should make you ask a question.

How did Taco Bell know?

The answer is probably not what many people imagine. There is no evidence of a cover-up, no whistleblower, and no secret laboratory that found parasites on a head of lettuce. Instead, the most likely explanation is also the most reassuring one: public health agencies and responsible companies often begin working together long before the public hears about an outbreak.

That partnership rarely makes headlines.

This week, the FDA announced investigators had traced one major cluster of Cyclospora infections to shredded iceberg lettuce served at Taco Bell restaurants in Indiana, Kentucky, Michigan, Ohio, and West Virginia. By following invoices, shipping records, distributor logs, and grower information backward through the food supply, investigators identified a single supplier in Mexico. Taco Bell had already removed lettuce from restaurants in those states before the public announcement, suggesting the company was acting on developing information, while investigators continued to confirm the source.

That is exactly how a healthy food safety system is supposed to work.

Public health is often portrayed as a battle between regulators and industry. Sometimes it is. We saw that recently during California’s raw milk outbreak, where the producer publicly resisted state and federal investigators instead of working alongside them. When companies refuse to cooperate, investigations become slower, recalls become more difficult, and consumers remain at risk longer than they should.

Most of the time, however, responsible companies behave differently.

Once epidemiologists begin narrowing an investigation, they frequently contact manufacturers, distributors, and restaurant chains before making any public announcement. The companies begin collecting invoices, identifying suppliers, reviewing distribution records, and, when appropriate, voluntarily removing products while the scientific investigation continues. The public usually sees only the press conference. The real work began days or even weeks earlier.

That brings us to the second story hidden inside this outbreak.

We found one outbreak. We probably did not find all of it.

The FDA has been remarkably careful with its language. Officials have described the Taco Bell illnesses as a subset of the national Cyclospora outbreak. That single word tells us something important. A subset is not the whole picture. It is one branch of a much larger investigation that continues today.

If you’ve ever assembled a thousand-piece jigsaw puzzle, you’ll recognize what happened this week. Finding one corner is exciting, because it finally tells you where to begin. It does not mean you’ve finished the puzzle.

Modern epidemiology works the same way.

Most people know the story of John Snow and the Broad Street pump in London. By mapping cholera cases, he showed that contaminated water—not bad air—was responsible for one of history’s most famous epidemics. What is less often remembered is that not every cholera case fit his map. Some patients had never drawn water from the Broad Street pump. Snow had identified one important outbreak, but not every outbreak.

One hundred seventy years later, epidemiologists still ask the same question: Which cases belong together?

However, the tools have changed beyond recognition.

That part of this story is personal for me. Before I became a surgeon, I spent time in a virology laboratory studying herpes simplex virus. We performed restriction endonuclease mapping of viral DNA, cut DNA into fragments, separated those fragments on agarose gels, and compared the resulting patterns. It was painstaking work, but the question was beautifully simple: were two viruses related, or were they different? Long before the public heard the phrase DNA fingerprinting, molecular biology was already helping epidemiologists connect cases that looked alike—and separate those that only appeared connected.

The CDC now asks the same question of Cyclospora. Scientists cannot routinely sequence the parasite’s entire genome because it is difficult to culture, and stool samples often contain very little usable DNA. Instead, they examine multiple genetic markers that together create a molecular fingerprint. Those fingerprints are compared across patients. If many patients share closely related genetic signatures, investigators gain confidence that they belong to the same outbreak. If they do not, investigators may be looking at several outbreaks unfolding simultaneously.

That possibility is what makes this week’s announcement so interesting.

The headlines suggest the mystery has been solved. The science suggests the mystery has only become more precise.

In the paid section, I want to take you inside that investigation. We’ll go from John Snow’s hand-drawn maps of London to glowing DNA bands on agarose gels, and finally to the molecular fingerprinting techniques the CDC uses today. Along the way, you’ll see why epidemiology is still one of medicine’s greatest detective stories—and why the most important word in this week’s announcement may have been subset.

John Snow’s Greatest Discovery Wasn’t the Pump

Read more

You will hear scientists talk about probabilities, you will hear hucksters tell you in confidence - hence the term “con men.”

Below, I am outlining a disagreement about the studies, pointing out that the vaccine against Shingles can decrease the risk of dementia. We don’t have an answer here, but this is an honest debate between two doctors (myself and Dr Prasad) about this data.

Can the Shingles Vaccine Prevent some dementia?

Last week, physician and medical commentator Dr. Vinay Prasad published an article questioning the growing body of research suggesting that shingles vaccination may reduce the risk of dementia.

If you haven’t heard of Dr. Prasad, you’re not alone. He is an oncologist and hematologist who has built a large following by criticizing what he considers weak medical evidence, unnecessary treatments, and the tendency of medicine to adopt interventions before they are adequately proven. On many issues, I’ve found his insistence on rigorous evidence refreshing. Medicine needs thoughtful skeptics.

The issue isn’t whether the shingles vaccine prevents shingles—that question was answered years ago. Shingrix is remarkably effective at preventing shingles and the debilitating nerve pain that can follow.

The question is whether preventing shingles also lowers the long-term risk of dementia.

Dr. Prasad argues the evidence isn’t convincing.

I differ with him - and here is why.

Share

His Title Sets the Tone

His article is titled:

“Shingles Vaccines and Dementia: The Emperor Has No Clothes.”

That’s a provocative title.

It suggests researchers studying this question have collectively fooled themselves—that the apparent benefit is little more than an illusion.

That is a serious claim, and it deserves equally serious scrutiny. So let us go through his reasoning and my counters.

His First Argument: These Are “Just Observational Studies”

This is probably his central point.

He argues that observational studies cannot establish causation, and that people who choose to be vaccinated may simply be healthier than those who decline vaccination. This is called the “healthy user bias.” And it is a real bias. People who are healthier tend to take their medications, get vaccinated, see their dentist, watch their blood pressure, and maintain themselves reasonably well. Meaning, if we look at populations that take care of themselves, there are many reasons they maintain healthier and longer lives.

A broad brush approach claiming that those biases incorporate all observational studies is a mistake in evaluation of studies. Simply put, not all observational studies are equivalent, and not all should be dismissed merely because they were observational studies. And this came from one of those observations that was stunning.

The Observation That Started the Debate

In 2013, Wales introduced a shingles vaccination program. Because vaccine supplies were limited, an arbitrary birth-date cutoff determined eligibility.

If you had already turned 80, you were too old to qualify and would never receive the vaccine through the program.

If you were 79, you were eligible.

Think about what that means. Two people born only days apart lived in the same country, used the same National Health Service, saw the same physicians, had access to the same hospitals, and received the same home and community care. They were virtually identical in every important respect.

One difference separated them. One group became eligible for the shingles vaccine. The other did not. Then you follow the patients, in this case, they were followed for seven years.

Epidemiologists call this a natural experiment. Instead of patients choosing whether to be vaccinated—which always raises the question of whether healthier people are simply more likely to get vaccinated—the government’s eligibility rule effectively assigned people to one group or the other.

Those who became eligible for the shingles vaccine developed dementia about 20% less often than those who were never eligible. That finding didn’t prove the vaccine prevents dementia.

But it was far too large—and the study design far too elegant—to ignore. Naturally, it also attracted critics, like Dr. Vinay Prasad.

Dr. Prasad’s Critique

Dr. Prasad looks at these studies and isn’t convinced.

His first criticism is that these aren’t randomized clinical trials. They’re observational studies. People who get vaccinated may be different from people who don’t in ways we can’t completely measure. Maybe they’re more health-conscious. Maybe they exercise more. Maybe they see their doctor more often.

In a way, they are randomized - but randomized by age.

The Randomized Trial Isn’t the Only Tool We Have

I suspect that part of the difference between Dr. Prasad and me comes from our professional backgrounds.

Dr. Prasad is an oncologist. Oncology lives and dies by randomized clinical trials. If you’re deciding whether a new chemotherapy drug extends survival by three months, a randomized trial is the gold standard. It should be. Patients deserve that level of evidence before we expose them to drugs with significant toxicity.

Randomized trials are a remarkable tool. Not every important question in medicine can be answered with a randomized trial.

As a surgeon, I couldn’t randomize patients to receive an operation. We have choices with operations, but doing a sham operation, a controlled trial, is just something we cannot do. We could randomize who gets which surgery for a condition if we have two operations. But that is also difficult to do. If a patient needs weight loss surgery, the patient wants input into whether they get a gastric bypass or a sleeve, for example. But we can follow those groups, those who had a bypass and those who had a sleeve, and see how well they did over several years after surgery. We could also put them in the same classes for nutritional counseling and exercise, and follow all those variables. And indeed, we do that. But those are not randomized trials, they are not blinded trials, but they are important trials and observational.

In culinary medicine, I can’t lock thousands of people into identical kitchens for twenty years to determine whether olive oil, legumes, or fish reduce dementia. Nutrition researchers are constantly criticized for relying on observational evidence, but much of what we know about healthy dietary patterns comes from the convergence of epidemiology, physiology, metabolic studies, and long-term follow-up—not from perfect randomized trials.

Medicine uses many tools. Randomized trials. Observational studies. Natural experiments. Basic science. Pathology. Mechanistic studies. Genetics.

The art of medicine is knowing when the pieces begin to fit together.

That’s why I don’t dismiss the shingles studies simply because they aren’t randomized trials. Instead, I ask a different question.

Taken together, do the epidemiology, the biology, and the clinical observations point in the same direction?

Increasingly, they do.

Dementia Diagnosis and Time

Prasad’s second point is that dementia isn’t like measuring blood pressure or cholesterol. It develops gradually, the diagnosis can be delayed, and not everyone is evaluated in exactly the same way. If one group has more contact with the healthcare system than another, you could end up diagnosing more dementia simply because you’re looking harder.

In this case, these are older patients at high risk of dementia. One in five people at age 85 develop dementia. If an intervention delays that, and we follow a large group of these patients (age 79 and 80) over seven years, we will have enough data to give us great deal of certainty. This is what we found.

His conclusion is that the excitement over shingles vaccination reducing dementia has gotten ahead of the evidence.

To me, asking these questions is where the scientific discussion begins—not where it ends.

Why I Think the Evidence Is Stronger

If this were just another retrospective review from an insurance database, I’d probably be far more skeptical. But it isn’t.

The Welsh study took advantage of a natural experiment created by the vaccine rollout itself. Another group, the Danish registry study, comes from a healthcare system that follows essentially the entire population. Everyone has access to the same healthcare. Vaccinations are recorded. Hospitalizations are recorded. Dementia diagnoses are recorded. Researchers aren’t piecing together fragments from multiple insurance companies—they’re looking at an entire nation’s experience.

The question isn’t whether a study is perfect. The question is whether it’s good enough to make us pay attention.

When multiple studies, from different countries, using different methods, continue to point in the same direction, scientists should become more interested, not less.

Then there’s the biology.

Varicella-zoster (the chickenpox and Shingles virus) isn’t just a virus that causes a painful rash. It infects nerve tissue, remains dormant for decades, and can reactivate later in life. Shingles does more than cause the most painful rash you ever felt. Shingles virus can cause encephalitis, vasculopathy, stroke, cranial nerve palsies, and long-lasting nerve pain. Basically, it can turn your brain into mush, so you not only have a painful rash whose pain may never go away, but also major brain damage.

So when researchers find that vaccination also reduces the risk of dementia, my first thought is, “That actually makes biological sense. Now let’s see if the evidence continues to support it.”

One comment from Dr. Prasad caught my attention. He jokes that the reported effect works “faster than Tums,” implying that the benefit appears implausibly quickly.

I think that overlooks an important feature of the population being studied. As I mentioned previously, these were adults in their late seventies and early eighties—an age when dementia rises sharply. You don’t need to wait decades to see this effect.

In statistics, one of the biggest challenges is avoiding a Type II error—failing to detect a real difference simply because the study is too small or too few outcomes occur. That’s called being underpowered. These studies weren’t underpowered.

They followed very large populations in an age group where dementia occurs frequently enough that researchers could meaningfully compare vaccinated and unvaccinated groups.

Why I Find This Plausible

Perhaps the reason I see these studies differently is because of the lens through which I’ve spent my career looking at disease.

Chickenpox is a herpes virus, and even that cold sore is more than just a cold sore. I’ve never thought of herpes viruses as “just a rash.” As a physician, I’ve seen what herpes simplex virus can do when it reaches the brain. HSV encephalitis is one of the most devastating infections we treat. Patients can suffer permanent memory loss, personality changes, seizures, and profound cognitive impairment. The virus has an affinity for nervous tissue, and when it causes inflammation there, the consequences can be life-changing.

Varicella-zoster virus belongs to that herpes virus family. It doesn’t simply cause a painful rash. It establishes lifelong latency in nerve tissue. It reactivates years later. It causes post-herpetic neuralgia, vasculopathy, encephalitis, myelitis, cranial nerve palsies, retinal disease, and stroke. Throughout my career, I’ve watched shingles devastate older adults, particularly those in long-term care. It can turn an independent person into someone living with chronic pain for months—or years.

That’s why I received Shingrix (the Shingles vaccine). Not because I thought it might prevent dementia. I got it because I never wanted shingles. If you’ve cared for patients with post-herpetic neuralgia, you don’t need much convincing.

Now we’re seeing evidence that preventing shingles may also delay or reduce the risk of dementia. Do we know that for certain? No. Do I think the evidence is becoming increasingly persuasive? Yes.

And if protecting myself from one devastating neurologic disease also lowers my chances of another, that’s not the reason I rolled up my sleeve—but it’s certainly a welcome bonus.

Where Dr. Prasad and I Really Disagree

I don’t think Dr. Prasad and I actually disagree much about the data. We disagree about how physicians should think about evidence.

Should one observational study change medical practice? We both would agree that it should not. Observational data is what gave us the idea that smoking led to heart disease and cancer. First observed in the 1600’s by physicians, repeated by the AMA in the early 1900’s and then by the surgeon general in 1964. But that was many observations, as well as animal studies, but no randomized trial.

Should several elegant observational studies, performed in different countries, using different methods, all pointing in the same direction, combined with a biologically plausible mechanism, make us pay attention?

Absolutely.

Medicine isn’t practiced with a single tool. Randomized trials are extraordinary, but they aren’t the only way we learn. Surgeons know this. Nutrition scientists know this. Epidemiologists know this. Every specialty has learned that different questions require different tools.

To me, these studies have crossed an important threshold. They haven’t proven that shingles vaccination prevents dementia. They have convinced me that the question deserves to be taken seriously.

And that’s enough for me to be pleased that I received my shingles vaccine.

But this debate raises a much larger question—one that goes far beyond shingles.

How should doctors decide when evidence is “good enough?”

That’s what I’d like to explore next for our paid members. Thank you for reading this- I hoped this helped you see that in medicine we have are less certain than a huckster.

How Physicians Think About Evidence

Read more

For much of the twentieth century, Americans didn’t bake bread. We bought it. Bread became something that arrived in a brightly colored plastic bag from the supermarket. It was convenient, soft, perfectly sliced, and remarkably consistent. There was nothing wrong with that if all you wanted was a sandwich.

But something had been lost.

Bread had once been something families created. Every village had a baker. Every home had its own traditions. Hand mixed Dough, sourdough starters were passed from generation to generation, and the smell of fresh bread drifting from an oven was simply part of everyday life.

When Bread Forgot How to Be Bread

By the middle of the twentieth century, America had become remarkably good at making bread quickly, cheaply and consistently. Unfortunately, we had also become remarkably good at stripping away much of what made bread worth celebrating in the first place.

The neighborhood baker disappeared. Commercial yeast replaced the sourdough starter. Stone-ground flour gave way to highly refined white flour. Bread became softer, sweeter, lasted longer on the shelf, and fit neatly into a plastic bag. It was an engineering triumph.

It just wasn’t much of a culinary one.

So when critics began pointing fingers at bread in the 1970s, they weren’t entirely wrong. Much of what Americans were eating hardly resembled the breads that had nourished civilizations for thousands of years. The mistake wasn’t noticing that modern bread had changed.

The mistake was blaming bread itself.

About the same time, something wonderful was happening on the other side of the cultural conversation. In Northern California, a generation of young cooks, gardeners and seekers began asking a different question. Instead of asking how bread could be made faster, they asked how it had been made before factories.

One of the books that captured that spirit was The Tassajara Bread Book. Published in 1970 by Edward Espe Brown, it became far more than a cookbook. It was a manifesto for rediscovering whole grains, fresh flour, long fermentation, and the quiet satisfaction of making bread with your own hands. For many people, it was their first introduction to bread that tasted like grain instead of packaging.

I was a little too young to be part of the hippie movement, but I’ve always admired what happened in kitchens during those years. Along with questioning politics, music and culture, they questioned food. They pulled flour mills onto kitchen counters. They nurtured sourdough starters. They baked dense whole-grain loaves that would horrify some modern influencers, but those loaves represented something important: a return to food that people recognized.

Whether the revolution succeeded because of idealism or because homemade bread simply tasted better is difficult to say.

I suspect it was both.

The irony is delicious. While one movement was beginning to declare that bread itself was the problem, another was quietly rediscovering that the real problem wasn’t bread at all.

It was forgetting how to make it.

That’s a lesson worth remembering today. When someone tells me bread is unhealthy, my first question isn’t whether they’re right.

It’s, “Which bread are we talking about?”

Then came the Summer of Love.

I was just a little too young to be part of the hippie movement, although being a Californian I’ve always admired some of what they rediscovered. Along with questioning politics, music and culture, they also began questioning food. Instead of buying factory-made white bread, they started grinding whole grains, baking their own loaves, and rediscovering sourdough. They didn’t invent whole-grain bread. Humanity had been making it for thousands of years. They simply reminded America that bread could be more than something wrapped in plastic.

Ironically, what looked like a cultural rebellion was also a return to tradition.

The more I study culinary medicine, the more I realize that progress often looks like rediscovering something our grandparents quietly knew all along. Good olive oil. Beans. Lentils. Soup. Whole grains. Fermented foods. None of them are new. They simply disappeared for a while beneath convenience and clever marketing.

That’s one of the reasons I enjoy freshly made baked bread. I don’t bake bread, as my own efforts produce something better suited for construction than consumption. Every failed loaf reminds me how remarkable those first bakers were. Somewhere, thousands of years ago, someone looked at flour and water and imagined something more. Fortunately for civilization, they were far better bakers than I am.

The Staff of Life

For most of human history, bread wasn’t a side dish.

It was life itself.

That’s where the old expression “the staff of life” comes from. A staff is something you lean on for support. Bread became the food entire civilizations leaned upon. It wasn’t simply nourishment. It was security. A good harvest meant grain in the silo, flour in the mill, bread in the oven, and another year in which children grew up instead of going hungry.

The ancient Egyptians understood this perhaps better than anyone. We often look at the pyramids and marvel at the engineering, mathematics, and sheer determination required to build them. We imagine pharaohs, priests and monuments to the afterlife.

I see bread.

Not because the pyramids were built to celebrate bread, but because they could not have been built without it.

The workers who quarried stone, hauled massive blocks, and shaped one of history’s greatest engineering achievements needed to eat every day. That required farmers growing grain, millers grinding flour, bakers tending ovens, and perhaps most importantly, enough stored grain to feed thousands of people who were no longer spending their days hunting for food.

The real miracle of Egypt wasn’t simply the pyramids.

It was the granary.

Archaeologists have uncovered enormous grain silos throughout ancient Egypt. Some were circular, remarkably sophisticated structures designed to keep grain dry, protected from rodents and insects, and available long after harvest. They were, in many ways, the skyscrapers of food security. Modern grain storage follows many of the same principles because the problem has never changed. If you can preserve grain, you can preserve civilization.

That’s the quiet genius of bread.

Grain can be harvested once and feed people for months. Once enough grain is stored, not everyone has to be a farmer. One person becomes a baker. Another becomes a mason. Another studies the stars and invents a calendar to predict the Nile floods. Someone else learns mathematics to measure fields after the river recedes. Priests, scribes, physicians and architects all become possible because somebody else is growing wheat.

Bread didn’t simply feed civilization.

Bread freed civilization.

It allowed human beings to specialize, and specialization is where remarkable things happen. Medicine appears. Writing appears. Engineering appears. Music becomes something more than rhythm around a campfire. Trade expands because surplus grain can be exchanged for timber, metals, spices and ideas.

The more I think about it, the more convinced I become that bread deserves far more credit than it usually receives. We celebrate kings, generals and inventors. We build museums around pharaohs and monuments around emperors.

Perhaps we should spend a little more time thanking the baker.

Without bread, there may have been no pyramids to admire.

Armies Marched on Bread

Once grain could be stored and bread could be made in quantity, it became the fuel of armies. Soldiers could not march on sentiment, and they could not carry a fresh roast for weeks. Bread was portable, familiar, and reliable. It could be baked into loaves, hardened into biscuits, carried across long distances, and eaten with whatever else the army found. Empires expanded because supply lines held, and those supply lines often began with grain.

Napoleon is usually credited with saying that an army marches on its stomach. Whether he said it exactly that way matters less than the truth behind it. Armies that ran out of bread stopped being armies and became hungry men far from home. Bread was not glamorous, but strategic. Generals may have planned the battles, but bakers helped determine who reached them.

Bread and the Roman Crowd

The Roman emperors understood bread in a different way. They knew that feeding the population was not simply charity; it was political survival. Rome developed an enormous grain distribution system to supply the city, and free or subsidized grain became part of the relationship between the state and its people. Later, bread joined the circuses as shorthand for keeping the public fed and entertained.

It sounds cynical, and it was, but it also recognized a basic truth. Speeches rarely impress hungry people. When bread became scarce or expensive, unrest followed. The emperors could tolerate criticism, satire, and even the occasional bad chariot race. What they could not tolerate was an empty grain supply.

The Sourdoughs Head North

Thousands of years later, that same tradition traveled with prospectors into Alaska and the Yukon. My grandfather was one of them. He was born in 1870 and headed north in search of gold, carrying the same basic technology that had fed Egyptians, Romans, and soldiers across history: grain transformed by microbes into bread.

Those prospectors became known as Sourdoughs because they carefully guarded their starter. They fed it, carried it from camp to camp, and kept it warm through brutal winters. Some even slept with it so it would not freeze. In a place where supply lines were uncertain and winter could isolate a settlement for months, a living sourdough starter was more than a culinary curiosity. It was insurance.

My grandfather was not marching with a Roman legion or building a pyramid, but continuing the same human story. Bread traveled with people because bread made travel, settlement, and survival possible. From the Nile to Rome to the Alaskan frontier, civilization often moved forward with a loaf in hand.

So...Should We Eat Bread?

That brings us back to the question that started this article.

Is bread good for us?

Like so many questions in nutrition, the answer isn’t simply yes or no.

It’s, “Which bread?”

One of the great mistakes we make in nutrition is treating all bread as though it were the same food. It isn’t. A naturally fermented whole-grain sourdough loaf and a highly refined white sandwich bread may share the same name, but nutritionally they’re distant cousins.

Whole grains are remarkable little packages. The bran provides fiber that feeds our microbiome. The germ contains healthy fats, vitamin E, minerals and thousands of plant compounds that we’re still learning about. The starchy endosperm provides energy. Strip away the bran and germ and you’ve removed much of what made the grain interesting in the first place.

The science here has become remarkably consistent. People who eat more whole grains tend to have lower rates of heart disease, type 2 diabetes, obesity, colorectal cancer and premature death. That’s one of the reasons whole grains remain a cornerstone of the Mediterranean diet. The recommendation isn’t based on nostalgia or tradition. It’s based on decades of research that keeps arriving at the same conclusion.

One of the ironies of modern nutrition is that many whole-grain breads now technically qualify as “ultra-processed foods” under classification systems such as NOVA. That label often surprises people. A loaf made from whole-grain flour, water, yeast, salt and perhaps a few ingredients to improve consistency may still fall into that category. Yet when we look at the actual health outcomes, whole-grain breads consistently perform very differently from sugary snacks, soft drinks and many other highly processed foods that share the same label.

That’s a good reminder that food isn’t judged by a classification system alone.

It’s judged by what happens when people eat it.

One of my favorite lunches remains wonderfully uncomplicated. A slice of toasted whole-grain sourdough, a little peanut butter—remember, peanuts are legumes—and perhaps a piece of fruit. Or tear off a warm piece of bread, dip it into good extra-virgin olive oil, and you’ve recreated one of the oldest and healthiest meals in the Mediterranean.

Simple food.

Good science.

A little history in every bite.

The story of bread, however, doesn’t end with whole grains. Social media has placed bread on trial for everything from inflammation to dementia, from gluten to “brain fog,” and the verdict often arrives long before the evidence.

Let’s look at what the research actually says.

The Trial of Bread

If social media had been a courtroom, bread would have been convicted years ago.

The charges are extensive. Bread causes obesity. Bread causes diabetes. Bread causes heart disease. Bread causes dementia. Bread causes inflammation. Bread causes autoimmune disease. Bread causes “leaky gut.” Bread spikes insulin, destroys your microbiome, and according to a few influencers, probably knocked the dinosaurs off the planet.

It’s quite a rap sheet.

The problem is that the jury reached a verdict before anyone bothered to examine the evidence. Here is that evidence:

Read more

The Cyclospora outbreak continues to grow, with more than 3,300 reported cases in Michigan alone and cases now identified across more than 30 states.

Michigan health officials now say that lettuce and packaged salad greens are the leading suspects based on patient interviews. Importantly, no specific brand, grower, distributor, or supplier has yet been identified, so this remains an active investigation.

A few important points:

• Cyclospora is NOT a worm. It is a microscopic, single-celled parasite.

• Those online “parasite cleanses“ are not an effective treatment.

• The usual symptoms are profuse watery diarrhea, bloating, cramping, fatigue, loss of appetite, and weight loss. Unlike a typical stomach bug, symptoms can come and go for weeks if untreated.

• The standard treatment is trimethoprim-sulfamethoxazole (Bactrim). If you’ve had persistent watery diarrhea, ask your healthcare provider whether you should be tested specifically for Cyclospora, as it may not be included in every routine stool test.

Should you stop eating salads?

No. But this is a good reminder to wash fresh produce, keep it refrigerated, and pay attention to public health advisories as investigators continue tracing the source.

I’ll continue to update you as more information becomes available.

The autopsy has now confirmed that Senator Lindsey Graham died from an acute aortic dissection associated with atherosclerotic cardiovascular disease. It is a devastating diagnosis, one that remains among the deadliest emergencies in medicine.

Listening to Senator Graham’s recent public appearances, I noticed that his voice had become raspy. We will never know whether that change was caused by the dissection, nor do we know whether he experienced chest pain before his collapse. But as a surgeon, it immediately caught my attention.

Why?

Because one of the classic—but uncommon—clinical clues to an ascending aortic aneurysm or dissection is new-onset hoarseness. As the enlarged or dissecting aorta expands, it can stretch or compress the left recurrent laryngeal nerve, producing a raspy voice. Most physicians will never encounter it. Surgeons are taught never to forget it.

During my surgical residency at Virginia Mason, we learned about another Washington senator, Henry “Scoop” Jackson, who died from an aortic dissection in 1983. One of the lessons passed down through generations of surgeons was to pay attention to a new raspy voice. Whether every detail of that story has been preserved over the decades is less important than the clinical lesson it taught us: sometimes the diagnosis is hiding in something as subtle as a change in the way a patient speaks.

These are the observations that don’t always make it into textbooks but become part of surgical training. They are drilled into residents because the consequence of missing an ascending aortic dissection is enormous.

Time matters.

For an untreated Stanford type A aortic dissection, mortality increases by approximately 1–2% for every hour that passes without treatment during the first day or two. Early recognition, rapid CT angiography, and emergency surgery save lives.

So why does a dissection happen?

The aorta is not simply a pipe that suddenly tears. Over years, atherosclerosis and aging change the structure of the aortic wall. Cholesterol-rich plaques, inflammation, and even relatively small areas of calcification are signs that the wall has been injured over decades. The elastic fibers that normally allow the aorta to expand and recoil gradually weaken. Hypertension adds constant mechanical stress. Eventually, a tear can develop in the inner lining, allowing blood to split the layers of the artery apart.

Not everyone with aortic calcification develops a dissection, and many dissections occur in people whose primary problem is longstanding hypertension or an inherited connective tissue disorder. But atherosclerosis is another marker that the artery has undergone years of damage.

This is one more reason prevention matters.

Lowering LDL cholesterol, controlling blood pressure, avoiding smoking, exercising regularly, and treating diabetes are not simply about preventing heart attacks. They are about preserving the health of the entire arterial tree—including the aorta itself.

The lesson from Senator Graham’s death is not simply that aortic dissections are deadly.

It’s that medicine often depends on recognizing subtle clues before catastrophe strikes. A change in a patient’s voice. Chest pain that doesn’t quite fit the usual story. A blood pressure difference between the arms. A patient who simply says, “This feels different.”

Sometimes those small observations make all the difference.

And they’re why, even in an era of extraordinary technology, careful clinical observation remains one of the most powerful tools in medicine.

Medicine This Week: Good News, Bad News, and What Actually Matters

Medicine is rarely all good news or all bad news. This week is a perfect example.

We have encouraging news: more Americans than ever are receiving treatment for obesity. The U.S. death rate has reached its lowest point on record, and influenza vaccination continues to save children’s lives.

We also have concerning news: Cyclospora continues to spread across multiple states, measles is approaching yet another record year, and we’re reminded again how quickly speculation can outpace facts when a public figure suddenly dies.

Let’s separate what we know from what we don’t.

Lindsey Graham: What We Know—And What We Don’t

The death of Senator Lindsey Graham has led to the inevitable speculation online. As of this writing, no official cause of death has been released.

We know he reportedly experienced chest pain before collapsing into cardiac arrest.

It’s important to understand that cardiac arrest is not a diagnosis. It simply means the heart has stopped beating effectively. The real question is: what caused it?

While we don’t know the answer in Senator Graham’s case, we know the most common life-threatening causes of sudden chest pain followed by cardiac arrest.

Many conditions can cause chest pain—acid reflux, muscle strain, gallbladder disease, pneumonia, and even anxiety. But when someone develops sudden chest pain and then collapses into cardiac arrest, the most common cause is an acute problem with the heart’s blood supply.

The leading possibility is an acute heart attack, or myocardial infarction. This occurs when a cholesterol plaque inside one of the coronary arteries becomes unstable and ruptures. Many people imagine a heart attack happens because an artery slowly narrows until it is almost completely blocked. Surprisingly, that’s often not the case. A relatively small plaque can suddenly tear. The body sees that tear as an injury and quickly forms a blood clot over it. Within minutes, that clot can completely block the artery.

The heart muscle beyond the blockage is suddenly deprived of oxygen and begins to die. If the blocked artery supplies a large enough portion of the heart, the muscle becomes electrically unstable, causing a fatal rhythm, such as ventricular fibrillation, and sudden cardiac arrest. Smaller heart attacks often damage less muscle and can often be treated successfully if blood flow is restored quickly.

You may have heard the term “widow maker.” This usually refers to a blockage high in the left anterior descending (LAD) coronary artery. That vessel supplies blood to a large portion of the heart muscle, so when it suddenly becomes blocked, a tremendous amount of muscle is at risk. Without immediate treatment, these heart attacks can be rapidly fatal.

Another important possibility is pulmonary embolism. After prolonged sitting—such as during long-distance air travel—a blood clot can form in the deep veins of the legs or pelvis. If that clot breaks loose, it travels through the bloodstream and lodges in the arteries of the lungs. A large pulmonary embolism can cause sudden chest pain, severe shortness of breath, collapse, and cardiac arrest within minutes. Since he just returned from a long flight, this is always a possibility. This is why we want you to walk a lot on planes and keep up your hydration.

A third life-threatening cause is an aortic dissection. In this condition, the inner lining of the aorta, the body’s largest artery, tears. Blood enters the wall of the vessel and creates a false channel between its layers. If that tear extends to the coronary arteries that supply the heart, it can suddenly cut off blood flow to the heart muscle, causing severe chest pain, heart attack, and death. It is one of the true emergencies in cardiovascular medicine.

There are other causes of sudden cardiac arrest, including serious heart rhythm disorders, myocarditis, and inherited heart conditions. These three represent some of the most common life-threatening causes of chest pain followed by collapse.

The same lesson applies to Senator Mitch McConnell. We still do not know exactly what caused his medical emergency. The encouraging news is that he survived the initial event, received CPR, and remains hospitalized. Surviving long enough to reach the hospital generally carries a much better prognosis than dying before medical care can be provided. However, until physicians identify the underlying cause, it would be irresponsible to speculate.

That’s really the lesson here.

Medicine isn’t about making the fastest diagnosis on social media. It’s about making the right diagnosis. Sometimes the most accurate answer is also the least satisfying:

We don’t know yet.

If there is one takeaway from these events, it is this: never ignore sudden chest pain, especially if it is accompanied by shortness of breath, sweating, nausea, fainting, or collapse. Call 911 immediately. Minutes matter, and early CPR and rapid defibrillation remain the best chance of surviving sudden cardiac arrest. Don’t assume it is heartburn, because it could be your heart burning.

Share

Cyclospora Continues to Spread

Last week I wrote about the growing Cyclospora outbreak. Unfortunately, it has continued to grow.

By the time you’re reading this, the number of reported cases will likely be approaching 3,000 across more than 30 states, with Michigan remaining the epicenter. Investigators continue to search for the source, but no specific food has been identified despite an extensive investigation.

I’ve seen rumors online—and even a report briefly appeared before disappearing—suggesting investigators had narrowed the search to certain vegetables. Until the FDA or CDC officially identifies the source, I’d be cautious about repeating those claims. Early leads in food-borne outbreak investigations often turn out to be dead ends.

So what am I doing?

I’m not avoiding fruits and vegetables. Evidence supporting diets rich in produce hasn’t changed because of one outbreak.

I am making a few temporary changes to my own routine.

For now, I’m avoiding bagged salads and pre-cut leafy greens. I’m choosing vegetables that I can peel or cook, and this week I’ve been cooking most of my vegetables rather than eating them raw. Even if I order a burger, I’m skipping the lettuce and tomato until we know more.

The silver lining? It’s a great week to make vegetable soups, roast vegetables, or throw together a ratatouille. Cooking vegetables won’t erase all risk from every food-borne illness, but it does reduce the risk of many pathogens. It is an easy way to keep eating the foods we know are good for us.

Now, about washing produce.

You’ll hear all kinds of advice online about soaking vegetables in vinegar, baking soda, special produce washes, or other concoctions. None of those has been shown to reliably eliminate Cyclospora from contaminated produce. Plain, cold running water is still the recommendation. Washing may not remove every Cyclospora oocyst, but it helps remove dirt, bacteria, pesticide residues, and many other unwanted contaminants. So keep washing your fruits and vegetables—just don’t expect vinegar to perform miracles.

If you own a home plutonium-powered irradiation unit, that would probably solve the problem. I don’t know anyone who has one. Irradiation of produce can be done, and would solve this problem, but hey…

And yes, if you’ve been looking for an excuse to launch Brussels sprouts across the yard with a slingshot...well...I’m not officially recommending that either.

One final reminder: this is not a worm. Parasite cleanses won’t prevent or treat it. Ivermectin will not treat it either. If you’ve had several days of persistent watery diarrhea—especially after eating fresh produce—ask your physician whether Cyclospora testing should be included with your stool studies. Standard ova-and-parasite examinations may not detect it unless the laboratory specifically looks for it. Fortunately, when diagnosed, the infection usually responds well to the antibiotic trimethoprim-sulfamethoxazole (TMP-SMX, Bactrim or Septra), which significantly shortens the illness.

GLP-1 Medications Reach Mainstream America

One of the most remarkable stories this week came from Gallup.

Fifteen percent of American adults report having used a GLP-1 medication for weight loss at some point.

Eleven percent say they are currently taking one. I am one of those people.

Pause for a moment and think about that.

Just a few years ago, many people had never heard the words semaglutide or tirzepatide. Today, more than one in ten American adults reports using one of these medications.

Even more interesting, Gallup found that the nation’s obesity rate has fallen from a peak of 39.9% in 2022 to 36.4% this year.

The survey cannot prove that GLP-1 medications caused that decline. Many factors influence obesity rates. But this is the first bump in the curve we have seen, despite the popularity of low carb diets and carnivorism.

But for years obesity specialists argued that when effective treatments became available, we should expect to see changes at the population level.

For the first time in decades, we’re beginning to see those numbers move in the right direction.

The conversation has also changed.

A few years ago, people asked whether these medications worked.

Today, the better question is: How do we use them well? Or how can we afford them.

That means preserving muscle through resistance exercise, eating adequate protein, getting enough fiber, staying physically active, and recognizing that these medications are tools—not magic.

Your Smartwatch Knows More Than Your Doctor

Nearly every physician surveyed by the American Medical Association would gladly review information collected by wearable devices.

Fewer than six percent have actually integrated that information into routine practice. Why?

Because our healthcare system wasn’t built for continuous streams of data. Most physicians use an electronic medical record system, and some are not equipped to integrate the data. Some are, check with your primary care physician.

Your watch may collect heart rhythm information every few minutes, monitor sleep, detect falls, measure activity, estimate oxygen saturation, and increasingly use artificial intelligence to identify trends.

Meanwhile, your physician often has fifteen minutes to review medications, examine you, answer questions, document the visit, complete insurance requirements, and formulate a treatment plan.

The technology is ready. The healthcare system isn’t.

I remain a fan of wearable technology. Detecting atrial fibrillation, identifying abnormal heart rhythms, recognizing falls, and allowing someone to call for help from almost anywhere are meaningful advances in preventive medicine.

One big one - I am a fan of home blood pressure monitoring. Learn to do this at home, and bring your unit to your doctor to calibrate it against yours. Bringing your information to the doctor is helpful.

Now we simply need healthcare to catch up.

Measles Continues Its Comeback

Unfortunately, measles continues to spread across the United States.

The country is rapidly approaching last year’s record number of reported cases, and we’re only halfway through the year.

Measles was declared eliminated in the United States in 2000.

That didn’t mean it disappeared worldwide. It meant imported cases rarely produced sustained transmission.

That protection depends on maintaining high vaccination rates.

When communities become under-vaccinated, measles finds opportunities.

This isn’t a theoretical discussion anymore.

It’s happening.

Some Good News for a Change

Medicine isn’t only about problems.

Sometimes we should celebrate progress.

The U.S. Death Rate Reached Its Lowest Level Ever Recorded

That headline deserved far more attention than it received.

Despite an aging population, despite chronic disease, despite the challenges facing healthcare, Americans experienced the lowest recorded death rate in our nation’s history.

Medicine often gets criticized—and sometimes deservedly so—but it’s worth recognizing when decades of better prevention, better treatments, and better emergency care produce measurable improvements.

Influenza Vaccination Continues to Save Lives

A new study found that influenza vaccination reduced children’s risk of dying from influenza by approximately 80%.

Think about that. Not preventing sniffles. Preventing death.

Vaccines don’t have to be perfect to make an extraordinary difference.

One Outbreak Ends

The World Health Organization officially declared the recent hantavirus outbreak aboard a cruise ship over.

After months of investigation, contact tracing, and quarantine, the outbreak has ended.

It’s a reminder that public health successes rarely become headlines.

Food Matters—Especially Early in Life

Researchers continue to examine the relationship between diet and brain development.

A new study found that higher consumption of ultra-processed foods during early childhood was associated with measurable differences in brain regions involved in reward and emotion by age six.

Association is not causation. The study cannot prove that ultra-processed foods caused those differences.

But it adds to a growing body of evidence suggesting that the foods children eat during the earliest years of life influence far more than weight.

Another international study reached a different but equally important conclusion: children simply aren’t eating enough fruits and vegetables.

Ironically, American toddlers perform relatively well.

Teenagers? Not so much.

Healthy eating isn’t built in high school. It’s built long before then. This week, roast the vegetables and use an immersion blender to put them into the marinara sauce with the whole wheat pasta. They won’t know it is good for them.

Quick Notes

Alcohol after bariatric surgery

Researchers continue to confirm what bariatric surgeons have observed for years: alcohol is absorbed more rapidly after gastric bypass and sleeve gastrectomy. One drink after surgery may have a much greater effect than patients expect. If you’ve had bariatric surgery, drink cautiously—and never assume your previous tolerance still applies.

This Week’s Note to Paid Subscribers

Normally this is where I close the door and invite paid subscribers into the library.

We’d spend another 2,000 words dissecting one paper, looking at the statistics, discussing the limitations, and separating what the research actually showed from what the headlines claimed.

This week feels different.

Every one of these stories affects patients, families, and the conversations we have every day.

So this week’s newsletter is free for everyone.

To those who support this work with a paid subscription, thank you.

Your support lets me spend hours reading original studies instead of repeating press releases. It gives me the freedom to write without chasing clicks, and allows me to make weeks like this available to everyone.

Next week, we’ll return to our usual format with a members-only deep dive into one topic that deserves more than a headline.

Until then, wash your vegetables, don’t ignore chest pain, wear your smartwatch if you have one, get vaccinated when appropriate, and remember:

The goal isn’t to win arguments. The goal is to get the science right.

Senator Mitch McConnell reportedly needed CPR.

Since then, everyone seems to have become a neurologist, a cardiologist, or both.

Is he alive, brain dead, on a ventilator, being kept alive by machines? Is he going to recover? Why won’t anyone tell us what’s going on?

Fair questions. They’re questions I’ve been asked all week. They’re questions Katie Couric has asked. They’re questions millions of people are asking online.

Let's talk about them. I'm a physician, and while I don't know exactly what happened to Senator McConnell, I know how physicians think about these situations.

Every episode of my podcast, Fork U, ends the same way. After I’ve finished talking, there’s a brief pause. Then comes the little “Hey Evo” exchange that regular listeners have come to expect.

Then you hear three heartbeats.

Three steady beats.

Then they stop.

A second later comes the long, unmistakable tone...

Beeeeeeeeeeep.

Until this week, it was simply the way we ended the show.

This week it sounded different.

Twenty-five years ago, my brother Jimmy developed crushing chest pain and did exactly what we hope every patient will do. He called 911.

During the ambulance ride to the hospital, his heart went into a lethal rhythm three different times. Three different times, the paramedics shocked him back into a rhythm capable of sustaining life.

I wasn’t in that ambulance.

Years later, I stood beside his hospital bed when I watched the monitor trace his final three heartbeats before the line became perfectly still.

That sound at the end of Fork U isn’t there because it sounds dramatic.

It’s there because I’ve heard it before.

Can Someone Be Brain Dead and Still Be in the Hospital Weeks Later?

One of the first questions I was asked was whether Senator McConnell could be “alive but brain dead.”

The short answer is no.

Brain death is one of the most misunderstood terms in medicine. It isn’t a coma. It isn’t a vegetative state. It isn’t someone who is “mostly gone.” Brain death is the complete and irreversible loss of function of the entire brain, including the brainstem. Under the law and in medicine, brain death is death.

People often become confused because they see a ventilator moving the chest, a heart monitor showing a heartbeat, or warm skin, and assume the person is still alive. Those are understandable observations, but they don’t change the diagnosis. Machines temporarily move air into the lungs or support circulation, but they cannot restore a brain that has permanently ceased functioning.

If Senator McConnell had been declared brain dead shortly after his hospitalization, we would not be discussing his recovery several weeks later. Brain death is not a prolonged medical condition. It is a legal declaration of death.

That means we can move that possibility off the table.

The next question is much more realistic—and much more difficult to answer.

Could he be in a coma? Could he be in a vegetative state? Could he be awake but recovering from brain injury?

Those are very different conditions with very different prognoses, and they deserve their own discussion.

Share

The First Thing We Can Tell You

There is one thing we can tell you, even without knowing exactly what happened to Senator McConnell. If he required CPR, the odds were against him from the moment his heart stopped.

In the United States, only about 10% of people who suffer an out-of-hospital cardiac arrest survive to leave the hospital. If the arrest occurs inside the hospital, where physicians, nurses, monitors, medications, and defibrillators are only seconds away, survival improves to about 24%—better, but still sobering. Among those who survive, roughly one in five is left with a significant neurologic disability, ranging from problems with memory and executive function to weakness, impaired speech, vision loss, or other permanent deficits. Cardiac arrest remains one of the most lethal emergencies in medicine.

But those numbers tell only the beginning of the story. Survival after cardiac arrest isn’t a single event—it is a series of milestones. Someone begins CPR. The heart starts beating again. The patient survives the trip to the hospital, then the first day, then the intensive care unit, then wakes up, and eventually goes home. Each milestone changes the prognosis. Those statistics describe patients at the moment their heart stops—not patients who have already survived the next several hours, days, or weeks. That’s why physicians become more optimistic with each passing day, even though we may still not know the final outcome.

My brother taught me that lesson. During the ambulance ride to the hospital, his heart went into a lethal rhythm three separate times. Three separate times, the paramedics shocked him back. He underwent emergency heart surgery, recovered completely, and never suffered any permanent neurologic injury.

Five years later, metastatic lung cancer took his life. That seems sad, but it isn’t. Those five years mattered. I would not have had them with my brother had he been riding in the front seat of a family car instead of the back of an ambulance.

Cardiac arrest doesn’t just happen to senators. It happens every day, roughly once every few seconds in the United States, to people at home, at work, at church, on golf courses, and in grocery stores. Understanding why some survive—and, more importantly, what you can do to improve those odds—is far more valuable than trying to guess the medical details of Senator McConnell.

If Not Brain Dead, Then What?

That brings us to the next question I see over and over online.

If he isn’t brain dead, then what is he?

The honest answer is that we don’t know. I see people confidently claiming they’ve spoken with Senator McConnell. Others confidently say those reports aren’t true. Some insist he’s recovering. Others insist he’s in a coma. None of us outside his family and medical team knows enough to say.

Could he be in a coma? Yes.

Could he be in a vegetative state or another disorder of consciousness? Yes.

Could he be awake, talking with family, beginning rehabilitation, and simply choosing to keep the details private? That’s also possible.

Those possibilities have different prognoses, but without knowing what happened in those first minutes after CPR, how long his brain was deprived of oxygen, and how he has progressed since then, they’re simply possibilities.

There is also a legitimate tension between a public official’s right to medical privacy and the public’s interest in knowing whether that official can carry out the duties of office. Reasonable people can disagree about where that line should be drawn. Since Senator McConnell has already announced his retirement, and there are no immediate constitutional questions before the Senate, I’ll resist the temptation to join the political speculation.

A few journalists have called to ask what I think is happening. I’ve told them that eventually, one of a few things will become clear. We may learn more because his condition changes or his office decides to release details. We may learn that he recovered, but only after enough time has passed that the political question has largely resolved itself. Or we may hear of his death when that day comes, whether it is related to this hospitalization or not. None of those possibilities allows me to diagnose him today.

That may not produce a satisfying headline, but it is the honest answer. In the meantime, I have something more useful to offer: what cardiac arrest means, why the odds change every day a patient survives, and what you can do to improve those odds for yourself and your family.

What interests me far more is the question that applies to every one of us. Not whether one senior senator will recover. But whether you or someone you love will survive if a heart suddenly stops tomorrow.

Because unlike Senator McConnell, this is about you.

This Is About You

The numbers are staggering. I’d be willing to wager that you know someone who died from sudden cardiac arrest. A family member. A friend. A coworker. Maybe the parent of one of your children’s friends.

Some had no warning at all. Others ignored symptoms they hoped would go away. Some tried to drive themselves to the hospital. And there are people who would have died even if they had collapsed in front of a board-certified cardiologist outside a cardiac operating room. Medicine doesn’t save everyone. But it can dramatically improve the odds.

My brother’s decision to dial 911 saved his life and gave him five more years. It put him in the back of an ambulance, instead of the front seat of a car. When his heart went into a lethal rhythm three separate times, the paramedics were there with a monitor, a defibrillator, medications, and the training to use them. Those first few minutes changed the rest of his life—and mine.

There is a reason you find automated external defibrillators in airports, sports arenas, schools, casinos, shopping malls, and many office buildings. Every minute without CPR and defibrillation reduces the chance of survival. Those devices aren’t decorations. They’re there because someone else’s worst day may become yours.

A few months ago, during a TikTok Live, someone commented she had chest pain. I told her to get off TikTok, call 911, and let me know how she was later. Six weeks afterward, she came back to tell me what happened. She’d been having a heart attack. The ambulance took her directly to the hospital, where she went straight to the cardiac catheterization laboratory and received a stent. She thanked me for saving her life. I didn’t save her life. She did. She listened, picked up the phone, and gave herself a chance instead of becoming another statistic.

So what can you do? Learn CPR. Know where the nearest AED is at work, at your gym, and where you worship. If you’re older or have heart disease, talk with your physician about whether a wearable device, such as an Apple Watch or a Withings watch, might be appropriate. They aren’t a substitute for common sense or emergency medical care, but they may detect certain rhythm abnormalities, recognize a serious fall, or prompt you to seek care sooner. Most importantly, if you think you’re having a heart attack, don’t drive yourself to the hospital. Call 911. Give yourself the same chance my brother gave himself.

But More Important - All Roads Lead to JJ

My brother’s decision to dial 911 saved his life and gave him five more years. Five years may not sound like much until you begin to fill them.

Those were five more birthdays. Five more Christmases. Five more phone calls. Five more chances to laugh at bad jokes and argue about things brothers argue about.

Four years after Jimmy died, I met someone. A little later, despite being at an age when many of my friends became grandparents, we decided to have a child. Long before we knew whether we were having a boy or a girl, the baby already had a name. We didn't know if it was a boy or a girl, but the fetus already had a name: JJ. It stood for Jimmy Junior.

His birth certificate says James George Terry Simpson. We still call him JJ. Except for a brief period in grade school when he wanted to be called James, everyone knows him as JJ—and I mean everyone. (He's a ham, unlike his father.)

Without those paramedics in the back of that ambulance...without CPR...without three shocks...without my brother making one smart decision and dialing 911...

...my son would never have been JJ.

Medicine doesn’t always give us forever. Sometimes it gives us enough time to change generations. And when I look at JJ’s smile, sometimes I see my brother—and I wipe my eyes.

Read more

Life, love, and libido. Spend enough time on social media, and you’ll find people claiming that GLP-1 medications ruin all three. According to some critics, these drugs don’t simply quiet food noise—they flatten emotions, destroy romance, eliminate sex drive, and even make people fall out of love. It is a remarkable claim, and fortunately, one we can actually investigate.

As someone taking tirzepatide myself, I can only speak for one patient—me. I haven’t noticed any loss of libido, any decline in romantic interest, or any diminished interest in romance. If anything, feeling healthier, moving more easily, and becoming more comfortable in my own body has probably nudged things in the opposite direction. Before my inbox suddenly becomes much more active, let me add one disclaimer: this is not an invitation to slide into my direct messages.

Still, I couldn’t completely dismiss the question.

One thing became obvious as I began looking into this question. Nearly every confident assertion that GLP-1 medications destroy romance, libido, or the joy of living came from the same corner of the internet—the people who oppose these medications almost on principle. They repeat the claim so often that it begins to sound like an established fact. It isn’t. The published scientific evidence simply does not support the notion that GLP-1 medications routinely rob people of their sex drive, their capacity for love, or their enjoyment of life. Quite the opposite. Many patients describe feeling healthier, more energetic, more confident, and more engaged with the world around them. So before we accept the mythology, let’s examine the biology. The real story is far more interesting than the rumor.

Share

A Dose Dependent Loss of Interest in Food

One of my friends is a board-certified obesity medicine physician who cares for hundreds of patients using GLP-1 medications every year. During one of our conversations, he mentioned that a handful of patients taking the highest doses of Zepbound had described something that sounded like anhedonia—a reduction in the pleasure they experienced from food. He had even seen patients improve after reducing the dose.

That caught my attention, because another friend had recently told me a remarkably similar story.

He and his wife are the kind of people who make me just a little jealous. They travel the world, stay in beautiful hotels and castles, and plan trips around memorable restaurants. If I didn’t enjoy my work so much, I’d probably want their life. Food has always been part of their adventures together.

Then he told me something unexpected.

At a higher dose of Zepbound, he simply wasn’t interested in food anymore. He wasn’t nauseated. He wasn’t avoiding meals. He just didn’t care much whether he ate. Wine still interested him. Traveling still interested him. His wife certainly still interested him. The joy of discovering the next great restaurant, however, had largely disappeared.

When he reduced his dose, his interest in food returned. The food noise remained quiet, but the pleasure of eating came back.

His interest in his wife never changed.

In fact, if you ask him, she’d probably tell you she’s smiling even more these days.

That conversation sent me to the medical literature. If GLP-1 medications can reduce the reward we experience from food—and in some people perhaps reduce it a little too much—could they also affect romance, intimacy, or emotional attachment? Or are we confusing a specific change in food reward with something much broader?

Can GLP-1 Medications Cause Anhedonia?

The first thing we should do is define the word, because anhedonia isn’t simply “not enjoying dessert.”

Psychiatrists use the term to describe a diminished ability to experience pleasure. People with true anhedonia often lose interest in food, but also in hobbies, music, relationships, work, exercise, and the activities that once brought them joy. It is one of the hallmark symptoms of major depression.

That distinction matters because my friend’s experience was much narrower. He still loved traveling. He still enjoyed a good glass of wine. His marriage hadn’t changed. His curiosity about the world remained intact. What disappeared was something very specific: the excitement of finding the next great meal. Oh, and his sex life was better than before.

That observation fits well with what we know about GLP-1 medications.

These drugs were designed to reduce the rewarding properties of food. They quiet food noise, reduce cravings, slow gastric emptying, and alter activity in brain regions involved in reward and motivation. In many ways, that is precisely why they work so well.

The scientific question is whether those effects spill over into other parts of life. If they dampen the pleasure of eating, could they also dampen the pleasure of romance, sex, music, travel, or simply being alive?

Researchers have asked exactly that question.

One reason scientists took it seriously is history. Older readers may remember rimonabant, a weight-loss medication introduced in Europe nearly twenty years ago. It also acted on brain reward pathways and was initially greeted with tremendous enthusiasm. Unfortunately, it produced depression, anxiety, and suicidal thoughts in enough patients that it was withdrawn from the market. Nobody wanted history to repeat itself.

Fortunately, that isn’t what has happened with GLP-1 medications.

A 2026 review in JAMA Psychiatry acknowledged the theoretical concern and concluded it deserved careful study. Then came something even better than theory: a randomized clinical trial that directly measured motivation. Instead of finding evidence that semaglutide reduced people’s willingness to pursue rewarding experiences, investigators found exactly the opposite. Participants became more willing to work for worthwhile rewards, suggesting that the medication reduced the perceived cost of effort, rather than flattening pleasure itself.

That is a very different picture from true anhedonia.

Food Reward Is Not the Same as Falling in Love

The concern isn’t as far-fetched as it first sounds.

GLP-1 medications absolutely change activity in some of the brain’s reward circuits. They reduce cravings for food, and researchers are now studying them for alcohol use disorder, nicotine addiction, and other compulsive behaviors. These drugs clearly influence motivation and reward.

The question is whether all rewards are created equal.

The answer appears to be no.

The same brain that decides whether a slice of chocolate cake is worth eating is not using exactly the same circuitry that allows you to fall in love with your spouse, delight in your grandchildren, or spend an evening laughing with old friends. Those experiences overlap in the brain, but they are not identical.

Romantic attachment depends heavily on oxytocin, vasopressin, memory, shared experiences, and complex social networks that have evolved over millions of years. Food reward relies much more heavily on metabolic signaling and dopamine pathways that help us seek calories when they are needed. The systems communicate with one another, but they are not interchangeable.

If they were, dinner and marriage would be the same thing.

Fortunately for all of us, they are not. Oh do I have some stories about that. Moving on…

That distinction is important, because the strongest clinical evidence we have doesn’t show widespread emotional blunting. In fact, the only randomized trial designed to measure motivation found that people taking semaglutide became more willing to work for worthwhile rewards, not less. Large meta-analyses have also found no evidence that higher doses increase the risk of depression or other psychiatric disorders compared with lower doses.

None of that means individual patients cannot experience something different. Medicine is filled with uncommon side effects that never become common enough to appear in large trials. It does mean that, based on everything we know today, the evidence does not support the claim that GLP-1 medications routinely make people stop loving their partners or lose interest in intimacy.

The science points in a different direction.

Read more

Everyone seems worried about Cyclospora. Or E. coli. And a month ago I had norovirus - oh what a great week to be stuck in a hotel room. Then again, maybe what people are worried about is the explosive diarrhea that comes with them.

I’ve spent the past few weeks reading comments from people who suddenly don’t trust vegetables anymore. They’re wondering whether it’s still safe to shop at the farmers market. The answer is usually yes—with one important caveat. Many farmers market vendors are exactly that: farmers. Others, however, are simply reselling produce from the same distributors that supply large grocery chains. So “farmers market” isn’t automatically a guarantee of where the produce came from.

Then there are the home gardeners. Relax. Your tomatoes are still your tomatoes. Your basil is still your basil. Most of you use city water, which is safe to water your garden.

But all this anxiety reminded me that our ancestors figured out an answer to this problem thousands of years ago. They made soup.

Imagine it. A little fire. A pot of water. Whatever vegetables they could gather. Some tubers. Wild onions. Maybe a little garlic mustard. A few herbs. Perhaps the leftover deer the lions graciously decided not to finish. Into the pot it all went. Ah garlic-mustard - something to saute with the onions to build great flavor with a potato soup, or fish chowder. Ah, garlic mustard. Today, we think of it as an invasive weed. Put it in a potato soup or a fish chowder, and suddenly you've forgiven it for invading the neighborhood.

Why did they make soup? Why throw everything together into a pot, add water and heat it? What magic is this? At first, they probably did it because it stretched the meal. For most of human history, Homo sapiens lived one bad season away from hunger. Stretching food wasn’t clever—it was survival.

I suspect they also discovered something by accident. The old deer that was too tough to chew suddenly wasn't. Those roots that tasted like chewing on a stick became soft. Yesterday's leftovers became tomorrow's dinner. Soup didn't just stretch food—it rescued food.

That wasn’t magic. It wasn’t a witch standing over a cauldron. It was transformation. Heat changed proteins. Vegetables softened. Flavors blended together. Just as importantly, many of the bacteria, parasites, and viruses that wanted to eat us more than we wanted to eat them were left behind.

Soup wasn’t just comfort food. It was one of humanity’s first public health interventions.

It may also have been one of humanity's first community meals. It's hard to eat soup by yourself around a campfire. A pot naturally gathers people.

Which brings me back to that refrigerator drawer. You’ve got parsley that’s looking a little tired. Cilantro that’s lost its enthusiasm for life. Celery that’s flopped over like it just watched one too many Viagra commercials. The spinach has wilted. The carrots are beginning to wonder whether anyone still loves them.

Don’t throw them away.

Pour a little olive oil into a pot. Dice an onion. Let it soften. Add garlic, herbs and spices. Pour in some water or broth. Chop up those vegetables and let them join the party. Then bring it all to a boil.

The heat does something remarkable. It destroys organisms like Cyclospora, kills disease-causing bacteria, softens vegetables, releases flavors, and transforms ingredients that looked destined for the compost into tomorrow’s lunch.

That’s the thing about soup. It doesn’t ask for perfect vegetables. It rewards imperfect ones.

Maybe that’s why every civilization eventually invented it. Long before anyone understood microbiology, proteins, antioxidants, or fiber, people noticed something simple. Food that spent time in a pot over a fire tasted better, made people sick less often, and somehow turned a handful of leftovers into a meal worth sharing.

Thousands of years later, we’ve given those ideas impressive scientific names. Our grandparents just called it soup. It nourished generations before Pasteur, Koch, or anyone else had ever seen a bacterium through a microscope.

Soup provided hydration and electrolytes long before they were sold by the shirtless salesmen of supplements and scams.

Oh, and those people who say bone broth is good - well, make soup, much better than bone broth, less expensive. Ever notice most bone broth tastes like someone overcooked the meat and is selling us bad broth? Don't misunderstand me. A properly made stock is one of the foundations of good cooking. In fact, one of the greatest soups in the world is consommé, where French chefs use egg whites to clarify a stock until it's crystal clear. That's culinary science at its best. My problem isn't with stock. My problem is paying twelve dollars for a cup of something that tastes like someone forgot to season the soup.

And here’s one more thing about soup. It ages well. The next day it will taste better. One of the best examples came after dinner at the Ritz in London. I couldn’t finish the soup, so I took it back to my room at the Shard. The next afternoon, I heated it up for lunch.

It was better.

Not different.

Better.

That’s one of the remarkable things about soup. It spends the night improving itself.

Dr. Terry Simpson's Substack is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.

Why Soup and GLP-1 Medications Are Such a Good Match (For Paid Subscribers) - and for people needing calories in - like post chemotherapy

Read more

Weekly I sit down with a cup of coffee, look over the week’s medical news, and ask myself the same question: What would I tell my patients if they were sitting across from me? This week the answer came quickly. We’d spend a few minutes talking about a microscopic parasite called Cyclospora cayetanensis, then we’d probably wander into coffee, dementia prevention, obesity, and somehow Norwegian soccer. Medicine has a way of doing that.

Speaking of Norway, I have something to confess. After watching Norway knock Brazil out of the World Cup, I ordered a Norwegian soccer jersey. They haven’t paid me. They haven’t promised me salmon. They certainly haven’t offered me lutefisk. I simply decided that if Erling Haaland is going to keep scoring goals like that, I should probably support the homeland. Don’t worry if you’re not cheering for Norway. I’ve accepted that not everyone gets to be Norwegian.

Now, back to the parasite.

When I wrote about Cyclospora a few days ago, the CDC was reporting just over one hundred confirmed cases across the country. Since then, Michigan has reported more than 700 cases (30 hospitalizations) in what officials are calling a large and growing outbreak, New York continues to identify additional cases, and investigators are still trying to determine which food links them together. That’s how outbreak investigations work. We usually know what is making people sick before we know which food is responsible.

One of the reasons this outbreak is so difficult to solve is that Cyclospora is in no hurry. Most food poisoning announces itself within hours. Cyclospora waits. Symptoms usually begin seven to ten days after you eat contaminated food. By the time you’re making repeated trips to the bathroom, the salad that caused the problem is the one you don’t even remember eating. It may have been the lettuce on a hamburger, a little cilantro sprinkled over tacos, or the side salad that came with dinner because you were trying to make one healthy decision that day. Epidemiologists are asking people to remember meals from last week, and most of us can barely remember breakfast.

A parasite isn’t a parasite, unless it is

Another misconception that filled my inbox this week is the word parasite. People immediately picture worms. Cyclospora isn’t a worm. A parasite isn’t defined by what it looks like; it’s defined by how it lives. A parasite survives at the expense of another organism. Think of it as biology’s version of the cousin who still lives in the basement, eats somebody else’s food, never pays rent, and somehow always has time to comment on my Substack. Cyclospora is actually a microscopic protozoan, much more like the paramecium you looked at under a microscope in high school biology than a tapeworm.

It’s tiny—only about eight to ten microns across. Remember the old philosophical question about how many angels could dance on the head of a pin? I have a different question: how many Cyclospora could fit there? Quite a few. You won’t see them on your lettuce, you won’t smell them, and no amount of staring at your Caesar salad is going to reveal them.

How to Wash your Produce - and why

That naturally led to another flood of questions: vinegar? Baking soda? Vegetable washes? Ultrasonic cleaners? Ozone machines? Running water is still the recommendation. I wash every fruit and vegetable under running water. I use a vegetable brush on carrots, potatoes, parsnips, cucumbers, and melons, then I throw the brush into the dishwasher. If I’m peeling vegetables, I wash them first, wash the peeler afterward, and then give the peeled vegetable one more rinse. Will that remove every Cyclospora organism? Probably not. Trying to get every one of these tiny protozoa off a head of lettuce is like trying to get glitter out of shag carpet—or cleaning up after somebody throws a glitter bomb while you’re wearing Velcro. It isn’t going to happen perfectly. That’s not why we wash produce. We wash it because we’re removing dirt, bacteria, pesticide residues, and a whole collection of other things we’d rather not eat. Reducing risk has always been the goal.

I also continue to recommend salad spinners. I seem to buy one every time I move because they disappear somewhere between kitchens, but they’re worth replacing. Dry lettuce tastes better, and if we’re trying to encourage people to eat more vegetables, making salads more enjoyable isn’t exactly a bad strategy.

A Parasite Cleanse

One final myth deserves to die. Please don’t buy a “parasite cleanse.” It won’t treat Cyclospora. It won’t reliably treat intestinal worms. It will, however, improve the financial health of the person selling it. If you truly have Cyclospora, the treatment is trimethoprim-sulfamethoxazole—Bactrim. If you’re allergic to sulfa antibiotics, your physician has other options, but first you need the diagnosis. Remember, not every case of explosive diarrhea is Cyclospora. Norovirus, Salmonella, Campylobacter, certain strains of E. coli, inflammatory bowel disease, and even medications can all produce similar symptoms. Not every stool test automatically looks for Cyclospora, so if you’ve had persistent watery diarrhea during this outbreak, it’s worth mentioning that possibility to your physician.

Heia Norge!

Now that I’ve thoroughly ruined your appetite, let’s improve your morning. Another study this week found that coffee drinkers continue to enjoy lower risks of serious liver disease and liver-related death. Since Norwegians are among the world’s greatest coffee drinkers and have now reached the World Cup quarterfinals, I’m choosing to believe these facts are somehow connected. They probably aren’t, but it’s a pleasant thought while wearing my new Norwegian jersey.

Coffee Is Still Winning

After spending the better part of this newsletter talking about explosive diarrhea, I think we’ve earned a cup of coffee.

Fortunately, science agrees.

Another study this week found that people who drink coffee have lower risks of cirrhosis, liver cancer, and dying from liver disease. We keep looking for reasons to tell people to stop drinking coffee, and instead coffee keeps quietly accumulating evidence in its favor. No, that doesn’t mean six caramel frappuccinos count as preventive medicine, but your morning cup? I’m not worried about it.

Of course, I was delighted to read that paper because my Norwegian side immediately claimed victory. Norway is consistently one of the world’s biggest coffee-drinking countries, and after watching them advance in the World Cup I celebrated by ordering a Norwegian soccer jersey. They didn’t send it to me. They didn’t pay me. They certainly didn’t promise me free salmon. I simply decided that if I’m going to cheer for Norway, I ought to look the part. Don’t worry if you’re rooting for another team. I’ve accepted that not everyone gets to be Norwegian.

Our family farm is still there, in Otnes. The farm and the family have carried that name since the 1300s. There are sheep everywhere, and my grandfather left there in 1919, settled in Portland, and met my grandmother through the Norwegian community. They had a soccer club, just like so many immigrant communities did in those days. Italians played Italians, Swedes played Swedes, Norwegians played everybody, and somewhere along the line my grandparents met. Without soccer, I might not be writing this newsletter.

People assume that means I grew up on lutefisk.

Absolutely not.

Lutefisk was banned from our house.

It was banned from my grandparents’ house.

Lefse, however, was another story. My grandmother would spread butter over that warm lefse, sprinkle it generously with cinnamon and sugar, roll it up, hand it to me, and for a few minutes the world was a pretty wonderful place. That is Norwegian cuisine worth preserving. Lutefisk? That belongs in the history books under the chapter titled, “People Will Eat Almost Anything If Winter Lasts Long Enough.”

The Mediterranean Diet Refuses To Become Unfashionable

If you’ve been reading this newsletter for any length of time, you probably knew what the next study was going to show before I even opened the journal.

Researchers followed older adults for years and found that those eating a less inflammatory diet were significantly less likely to develop dementia, even among people who already had blood markers suggesting Alzheimer’s disease was quietly beginning its work. Every few months another study arrives with a different group of patients, a different country, or a different way of measuring diet, and somehow the conclusion keeps sounding familiar.

It isn’t exotic berries harvested during a full moon. It isn’t a supplement whose label promises to “unlock your brain.” It isn’t a powder sold by someone standing shirtless next to a rented Lamborghini. Once again, the winning diet looks remarkably like the Mediterranean diet: vegetables, beans, fruit, whole grains, olive oil, fish, nuts, and meals shared with people you enjoy. The longer I practice medicine, the more convinced I become that the healthiest diets are also the least interested in becoming social media influencers.

Here’s Some Quietly Good News About Obesity

One paper this week caught my attention because I could already imagine how it would be misinterpreted on social media.

Researchers found that older adults living with obesity today often have blood pressure and cholesterol levels much closer to those of people with normal body weight than they did thirty years ago. I have no doubt someone will turn that into, “See? Obesity was never the problem.”

That’s like saying seatbelts don’t prevent injuries because trauma surgeons have gotten better at repairing broken bones.

The real story is actually encouraging. Physicians are treating blood pressure earlier. We’re using statins more appropriately. Diabetes care has improved dramatically. GLP-1 medications are helping many people lose weight while improving blood sugar, blood pressure, fatty liver disease, and sleep apnea. In other words, we haven’t made obesity harmless—we’ve become much better at reducing the damage it causes. That is exactly what good medicine is supposed to do.

Vaccines Continue To Surprise Me

One of the pleasures of medicine is watching a treatment prove useful for something nobody expected.

The shingles vaccine was developed to prevent shingles, one of the more miserable infections we see in older adults. Yet study after study now suggests that people receiving the vaccine appears to have a lower risk of developing dementia later in life. We don’t completely understand why, and that’s perfectly acceptable. Science often discovers that something works before it fully understands every mechanism behind it.

The important point is that prevention has a funny way of paying dividends we never anticipated. Sometimes preventing one disease gives another disease fewer opportunities to do its damage.

A Word About Peptides

The FDA also spent part of the week asking a question I’ve been asking for some time.

Where is the evidence?

There are peptides with solid science behind them, just as there are medications that have transformed entire fields of medicine. There are also peptides whose greatest accomplishment has been separating hopeful people from their money. Social media has done a remarkable job convincing the public that if something ends with the word “peptide,” it must represent the next breakthrough in longevity. Biology is rarely that generous.

Whenever I read claims that a peptide builds muscle, melts fat, improves memory, restores youth, and makes your dog love you more, I reach for the original paper rather than my credit card. If the evidence isn’t there, no amount of enthusiastic marketing can manufacture it.

Share

One Last Story Before We Go

Reading medical journals every week has taught me something I wish were more exciting.

The things that make the biggest difference are usually the things nobody wants to hear because they aren’t glamorous.

Wash your vegetables.

Drink your coffee if you enjoy it.

Eat more beans than protein bars.

Take a walk.

Lift something heavy once in a while.

Get vaccinated.

Take your blood pressure medication if you need it.

Most of medicine’s greatest successes don’t come wrapped in revolutionary packaging. They arrive quietly, accumulate evidence over decades, and eventually become so ordinary that we forget how remarkable they are.

That may not make for the most exciting TikTok video, but it has a wonderful habit of helping people live long enough to annoy their grandchildren, cheer for questionable soccer teams, and argue with me about lutefisk.

Finally, thank you to everyone who supports this newsletter. Your subscriptions give me the time to read the journals, chase down the original studies, and translate them into English, before the headlines can translate them into nonsense. I appreciate your trust, your questions, and your willingness to spend part of your day with me. Until next week, stay curious, stay skeptical, and if Norway somehow wins the World Cup, please don’t tell JJ I bought the jersey before they reached the final.

Anthony Fauci has become that figure for our generation.

You probably only know Anthony Fauci as the quiet man standing behind the podium during the COVID pandemic. The bespectacled physician, who calmly explained why we were asking people to stay home, why hospitals were filling, why we needed to flatten the curve, and why scientists were racing to develop a vaccine. He was rarely the loudest voice in the room, but for months he became the public face of American medicine, trying to explain a frightening new virus while the world seemed to be coming apart.

If that’s all you know about Anthony Fauci, you know only the final chapter of a remarkable career. This is a bit more about him, and to discuss why some make him a villain in the story.

AIDS and the virus

When I began graduate work in virology, we didn’t even know what caused AIDS. Healthy young men died from infections we had previously seen only in profoundly immunocompromised patients. The idea that a retrovirus caused AIDS was still controversial, because there were no known human retroviruses. We weren’t arguing about treatments. We were still trying to identify the enemy.

By the time I entered medical school, the mystery had become heartbreak. I remember the married man with children whose diagnosis revealed a life he had hidden for years. While drawing his blood, I accidentally stuck myself with the needle.

Medicine and HIV

The HIV antibody test itself was new. We had no effective treatment. We didn't know the true risk of transmission after a needlestick. As best we understood it, I was only the ninth documented healthcare worker to sustain an occupational HIV needlestick exposure. Every few months, I returned for another blood test, wondering whether my own future had changed forever. Years later, a letter finally arrived telling me I no longer needed testing. I still remember the relief.

Fauci Rises

For most Americans, COVID is their first pandemic. Wall to wall coverage, from a little outbreak in China, carried to Italy, and then to the world. But back in the late 1970’s-80’s we had another one. And Fauci was there.

There was no cable news, no social media. My personal computer was a Radio Shack TRS-80, and my internet connection—when I eventually had one—was through CompuServe.

A new disease. Frightened patients. Frightened physicians. A medical community trying to understand a virus before it claimed even more lives. Young men wasted away from Pneumocystis pneumonia and Kaposi sarcoma. Families struggled to reconcile love with fear. Every week seemed to bring another discovery, another setback, another funeral.

A Deadly Disease without A Cure

Those of us who trained during that era remember what uncertainty feels like. We remember making decisions without complete answers, because waiting for certainty meant watching more patients die. Medicine wasn’t practiced from the comfort of hindsight. It was practiced one patient at a time, using the best evidence available that day.

Even as a surgical intern, one of my fellow interns came down with HIV. Later he almost died, but for an experimental treatment of AZT. He is alive today, some 30 plus years later, but he almost became a casualty of a disease that we didn’t know well.

A Service in Public Health

I also know something else.

Early in my career, I served as a physician in the Indian Health Service. I know what federal service looks like. It isn’t glamorous. Bureaucracy is real. Recognition is rare. When things go well, nobody notices. When something goes wrong, everyone suddenly knows your name.

I eventually chose a different path.

Anthony Fauci stayed.

For more than forty years he devoted his career to infectious diseases. HIV. Anthrax. SARS. Influenza. Ebola. COVID. Long before the public ever heard his name, physicians already knew it.

Every medical student did.

His name appeared on Harrison’s Principles of Internal Medicine. Harrison’s wasn’t simply another textbook. It was the textbook.

Long before America met Anthony Fauci at a White House podium, physicians had already spent decades learning from him—page by page.

Then COVID ARRIVED

Anthony Fauci didn’t suddenly become a different man.

America simply discovered the man physicians had known for decades. To most Americans, Anthony Fauci was born in 2020. To those of us in medicine, he'd already spent a lifetime preparing for that moment.

He spoke the same way he always had—carefully, probabilistically, acknowledging uncertainty, changing recommendations when better evidence emerged. That’s how scientists speak. It’s how physicians think.

It was a frightening time. The very breath of a person could kill you. Businesses were shut down, the world was told to shelter in place, masks were scarce, and distance was a proper Norwegian six feet.

As the pandemic wore on, another epidemic of misinformation spread alongside the virus. Social media rewarded certainty over evidence. Every revised recommendation became proof of deception. Every email became a smoking gun. Every government grant became a conspiracy. Every scientific debate became evidence of a cover-up. After spending hours caring for ICU patients with COVID, I would come home to find on social media that people said the hospitals were empty, and it was all a conspiracy.

Probably because Fauci was the face of science, information, and medicine, he became a villan. It didn't take long before social media accounts, podcasters, and political activists began accusing Fauci of creating COVID, funding Wuhan, and lying to Congress. Soon, the accusations took on a life of their own. Today many insist he belongs in prison.

During the pandemic, Dr. Anthony Fauci appeared before Senate committees time and again. Senator Rand Paul repeatedly accused him of lying to Congress, funding dangerous research in Wuhan, and covering up the origins of COVID-19. Those exchanges became political theater, replayed endlessly on cable news and social media.

Senator Paul is not an uninformed commentator wandering into a field he doesn’t understand. He is a physician. He knows how scientific evidence is weighed. He knows the difference between a hypothesis and a conclusion, between association and causation, between a regulatory definition and a scientific one.

That should concern every physician, scientist, and citizen. Because we can tell you for certain, there will be another pandemic. But there is good news, because somewhere today, a young student decides whether to become a microbiologist, virologist, or infectious disease physician. They’ll spend decades studying diseases most of us hope never to encounter. They’ll work in government laboratories, universities, and public health agencies. They’ll prepare for disasters that may never come.

If our message to them is this—“Dedicate forty years of your life to public service, and if politics changes, we’ll rewrite your career as a conspiracy”—we shouldn’t be surprised when fewer choose that path.

Anthony Fauci doesn’t need my defense. But our future will need physician-scientists like him.

The paid section will go through the case against Fauci - answering those accusations.

Read more

There comes a point on almost every GLP-1 journey when the question changes. At first it's all about the scale. The food noise is quieter. The weight begins to come off. Clothes fit differently. Friends start noticing. Then, almost without realizing it, the question changes from "How much weight have I lost?" to "Now what do I do with this second chance?"

Then one day you wake up and think:

“I have more energy.”

“Maybe it’s time to exercise a little more.”

Or perhaps you’ve been doom-scrolling through social media and have been told that GLP-1 medications cause muscle loss. Suddenly, you’re wondering whether all the weight you’re losing is muscle rather than fat.

Let’s take a step back.

One of my favorite sayings is, “You can’t manage what you don’t measure.”

That’s why I use a Withings scale. In fact they just came out with version 2 and I love that scale. If you use the same device under the same conditions, it becomes a useful way to follow body trends, rather than obsess over single measurements.

The Withings scale estimates body weight, body fat percentage, lean body mass, muscle mass, and visceral fat. I don’t pay much attention to any one day’s number. I pay attention to where the trend is going.

Before I show you my own data, let me make something clear. This isn't evidence. It's an anecdote. I'm an N of 1. The studies come first. My experience simply illustrates them.

But after nearly two years on tirzepatide, I have watched my muscle mass increase. My fat mass has steadily declined, while my estimated muscle mass has been maintained—and even increased slightly. I don’t obsess about protein, and I don’t go to the gym.

Over the past year, I gradually increased my yoga classes until I attended three classes each week. Two of those classes are vigorous. They challenge my balance, strength, and keep my heart rate comfortably in Zone 2 for much of the session. Saturdays are different. That class is restorative—a chance to stretch, recover, and prepare for another week.

Yoga may not look like traditional weight training, but anyone who has held a long plank, balanced in Warrior III, or moved through repeated standing sequences knows that body weight can be a remarkably effective resistance tool.

Has yoga been the only reason? I can't say. But it has certainly become an important part of the story.

More importantly, it made me realize that the conversation around GLP-1 medications and muscle is often far too simplistic.

So let’s look at what the studies actually show.

What Is “Lean Muscle Mass,” Anyway?

Before we start worrying about losing muscle, let’s make sure we’re talking about the same thing.

One of the most common misunderstandings I see is that people think every pound of “lean mass” lost on a body composition scale represents muscle disappearing. It doesn’t.

When your scale reports “lean mass,” it isn’t measuring muscle fibers alone. Lean mass includes muscle, but also glycogen and water, both of which make up a large portion of what is inside healthy muscle.

Think of glycogen as your muscles’ rechargeable battery. It is the storage form of glucose, ready to provide quick energy when you exercise. Your muscles don’t store glycogen by itself. Every gram of glycogen is stored along with water. Depending on the study, each gram of glycogen is associated with roughly three grams of water, although the exact number varies.

The important point is simple. Lose glycogen and you lose water. Lose water, and the scale says your lean mass has fallen. That does not mean your body has started consuming muscle fibers.

This is one reason people often lose several pounds quickly when they begin a low-carbohydrate diet. They haven’t suddenly burned several pounds of fat in a few days. Much of that early weight loss comes from using stored glycogen and the water that accompanies it. It’s real weight loss, but it isn’t the same as losing body fat.

The opposite happens too. Enjoy a carbohydrate-rich weekend, refill your glycogen stores, and your muscles pull water back in. The scale goes up, but you haven’t suddenly gained several pounds of fat overnight.

Body builders use this trick. When they want their muscles to pop, and which body builder doesn’t, they eat a high carbohydrate diet and add creatine to increase the glycogen and water in the muscle. Great body builders, before stepping on stage often manipulate carbohydrate intake, glycogen, water, and even creatine to make their muscles look fuller. It isn't new muscle. It's physiology.

Every effective weight-loss intervention behaves this way. Lifestyle programs do it. Bariatric surgery does it. GLP-1 medications do it. Low-carbohydrate diets do it. Any time the body begins using stored glycogen, some accompanying water leaves.

Over thirty years of performing bariatric surgery, I heard countless patients worry they were “eating their muscles.” In reality, what we usually observed early after surgery was exactly what physiology predicts: glycogen depletion, water loss, and then gradual fat loss. True muscle tissue is far more valuable to the body than social media would have you believe. Your body does not casually dismantle muscle fibers the moment you start losing weight.

That is also why I prefer to look at trends rather than individual weigh-ins. If I eat a particularly salty dinner, I’ll often weigh a pound more the next morning. I didn’t gain a pound of fat overnight. I retained water. If I enjoy a glass of wine with dinner, I often notice I retain water for a few days afterward. That’s just my physiology.

Oddly enough, between that and the fact that GLP-1 therapy has made alcohol far less interesting to me, my alcohol consumption has dropped dramatically. But that’s a story for another article.

The lesson is this: don’t let one number on a scale define your progress. Understanding what that number represents—and what it doesn’t—is one of the best ways to make this journey less frustrating.

Muscle Is Your Retirement Account

A few days ago I wrote that muscle is your retirement account. In fact, I think it’s a better investment than your 401(k). Money can hire someone to push your wheelchair. It can't buy back the muscle that would have kept you out of it.

So if you’re fortunate enough to live into your nineties, the question won’t be how much money you accumulated. It will be whether you can get out of a chair without someone pulling you up. It will be whether you can carry your groceries, climb a flight of stairs, travel with your family, or simply maintain your independence.

My father lived to almost 99 years old. One of the things I admired most about him was that he kept moving. He walked every day for years, and although age eventually catches all of us, that lifetime of movement paid dividends that no financial investment ever could.

Resistance training is part of that investment. Whether it’s lifting weights, yoga, Pilates, resistance bands, body-weight exercises, or simply finding ways to challenge your muscles, you are making deposits into a bank account that your future self will draw from.

So what does that have to do with GLP-1 medications?

Everything.

One of the myths surrounding these medications is that they somehow “eat your muscles.” That’s simply not what the evidence shows. Like every successful weight-loss intervention, GLP-1 therapy results in some loss of lean mass, particularly early in treatment, as glycogen and the water stored with it are depleted. But the more important question isn’t whether lean mass changes.

The real question is this:

What can we do to preserve—and even build—muscle while losing fat?

Should you exercise? Absolutely. Should you lift heavy things? If you enjoy it, why wouldn’t you? Resistance training is one of the best investments you can make in your future. It builds strength, improves balance, preserves independence, and pays dividends long after you’ve forgotten what you lifted on a Tuesday afternoon. If you are fortunate enough to live into your nineties, your future self will thank you every time you stand up from a chair without needing someone else’s hand.

My advice, however, is not simply to find a gym. It is to find the right gym culture. There is a tremendous difference between someone who teaches people how to become stronger and someone who teaches people to feel ashamed because they needed help getting there. Those are two very different philosophies, and they produce very different results.

When I came out publicly and said I was taking a GLP-1 medication, two people in the fitness world immediately reached out to encourage me. Jeremy the Hulk, who lives here in Southern California, even said, “Come by and let’s work out.” Ziegler Monster, whose wife is a veterinarian and every bit as science-minded as he is, was equally supportive. Neither one viewed medication as a shortcut. Neither one questioned my commitment. They simply saw another person trying to become healthier and wanted to help. They understood something many people still don't: medication doesn't replace discipline. It makes discipline possible for people whose biology has been fighting them for years.

Those are exactly the kinds of trainers I recommend to people. They know how to build muscle. They understand resistance training. They appreciate a Mediterranean approach to eating instead of pretending there is only one way to be healthy. Most importantly, they understand that biology and behavior are teammates, not competitors.

That, to me, is what the future of fitness should look like. If someone comes to you after losing fifty pounds on a GLP-1 and says, “I want to get stronger,” the correct response is not, “You should have done it my way.” The correct response is, “Fantastic. Let’s build some muscle.”

GLP-1 medications don’t replace exercise any more than eyeglasses replace reading. They remove one barrier. What comes next is still up to us. We still have to move. We still have to challenge our muscles. We still have to nourish ourselves well. The difference is that many of us are finally doing those things without constantly fighting a brain that is telling us to eat.

That is why I believe the best fitness professionals are not the ones who spend their time arguing about medication. They are the ones who understand how to help people take advantage of the opportunity that medication provides. They welcome people into the gym instead of testing whether they deserve to be there. In my experience, those are the coaches who help change lives.

Share

Let me leave you with one final thought.

You don’t have to become a weightlifter. If you enjoy lifting weights, wonderful. If your passion is Pilates, yoga, Lagree, calisthenics, dancing, swimming, pickleball, cycling, or running, that’s wonderful too. The best exercise has always been the one you’ll still be doing ten years from now.

If there is one prescription I would write for almost everyone, regardless of what else you do, it would be this: spend at least twenty minutes outside every day and go for a walk.

Walk around your neighborhood. Walk through a park. Walk with your spouse, a friend, or your dog. Walk without your phone once in a while and pay attention to the world around you. You’ll improve your cardiovascular fitness, strengthen your muscles and bones, help maintain your weight, improve your mood, and probably make your dog the happiest member of the family.

We spend far too much of our lives indoors. My friend Dr. John La Puma wrote an excellent book called Indoor Epidemic, and I recommend it highly. His message is simple and important: our health suffers when we disconnect from the outdoors.

GLP-1 medications can quiet the food noise and help you lose weight. Exercise can make you stronger. Good food can nourish you. But don’t forget one of the simplest medicines we have ever known: put on a comfortable pair of shoes, step outside, and take a walk. Leave your phone in your pocket once in a while. Listen to the birds. Let your dog decide where to sniff. There is something restorative about walking that has nothing to do with burning calories.

Sometimes the best prescription doesn’t come in a bottle.

Sometimes it comes with a leash.

Paid Subscribers: What I’ve Learned Living on Tirzepatide

Read more

Over the past several days, my TikTok comments have become a master class in human curiosity. People wanted to know whether vinegar kills parasites. They wondered if frozen blueberries are safe. Someone insisted salt water would solve the problem. Another asked whether the government should simply wash vegetables better. One pregnant woman worried about her baby. Several people with sulfa allergies wondered if they were doomed.

Welcome to the world of Cyclospora, a microscopic parasite that suddenly became one of the hottest topics in food safety. It has also reminded me of something I learned years ago as a surgeon: when people have diarrhea for three weeks, they stop asking whether they should eat organic and start asking much better questions.

Share

“Doctor, how do I wash my vegetables?”

That was probably the most common question I received this week after posting a short video about a parasite called Cyclospora. Close behind were questions about vinegar, baking soda, salt water, frozen fruit, sulfa allergies, pregnancy, and one particularly optimistic viewer who was convinced a salad spinner was the missing link in infectious disease prevention.

There are only a few things in medicine guaranteed to unite Republicans, Democrats, vegans, carnivores, gastroenterologists, and surgeons. Explosive diarrhea is one of them.

As I write this over a cup of coffee—thankfully brewed with boiling water—state health departments continue to report new cases. The CDC’s national surveillance has documented more than one hundred confirmed infections across multiple states, but those numbers always trail reality because diagnosis, laboratory confirmation, and reporting take time. Michigan alone is experiencing one of its largest outbreaks in years, with more than two hundred reported cases across more than twenty counties in little more than a week, compared with the roughly fifty cases the state typically sees in an entire year.

That’s why I wanted to write this article. The questions you’ve been asking are exactly the right ones. They also reveal how little many ever learn about parasites unless we happen to get one.

First, this is not a worm.

When most people hear the word parasite, they picture something long, squiggly, and horrifying enough to become the subject of a late-night cable television documentary.

Cyclospora is nothing like that.

It is a microscopic, single-celled protozoan. You could fit thousands of them across the tip of a pin (it isn’t angles dancing on them either - maybe in your colon). You don’t see worms in your stool. Your doctor isn’t looking for eggs. Instead, this tiny organism infects the cells lining your small intestine and quietly begins interfering with one of your body’s most important jobs—absorbing water and nutrients.

That disruption explains almost every symptom people experience.

Watery diarrhea.Cramping. Bloating. Fatigue. Nausea. Loss of appetite. And not the way you want it, but Weight loss.

The remarkable thing is not that people become ill. It’s how long they stay ill. Unlike the twenty-four-hour stomach bugs that circulate through schools and cruise ships, Cyclospora often waits about a week before symptoms begin. Then it may continue for weeks, sometimes improving just enough to fool you into thinking you’ve recovered before returning for another round.

If you’ve ever wondered why physicians ask whether your diarrhea has lasted “more than a few days,” this is one reason. Time matters. The longer symptoms continue, the broader the list of possible causes becomes.

So where does it come from?

Most outbreaks are linked to fresh produce.

Not hamburgers.

Not chicken.

Not sushi.

Fresh herbs, leafy greens, berries, and vegetables are the usual suspects because they are eaten raw. Once food is cooked thoroughly, Cyclospora is no longer a concern. The challenge is that salads rarely spend fifteen minutes in a frying pan.

The contamination usually occurs before the produce reaches your kitchen. That may happen through contaminated irrigation water, contaminated wash water during processing, or other environmental exposure on the farm. By the time the lettuce or cilantro arrives at your grocery store, the opportunity to prevent contamination has largely passed.

That brings us to the question that flooded my comments.

“Should I wash my vegetables?”

Yes.

Absolutely.

I wash mine.

I hope you wash yours.

Just understand what washing can—and cannot—do.

Rinsing fruits and vegetables under cool running water removes dirt, reduces many bacteria, and lowers your exposure to contaminants. It is one of the simplest and most effective food safety habits you can develop.

Unfortunately, Cyclospora doesn’t read household cleaning blogs.

The parasite is enclosed within a tough microscopic structure called an oocyst. Think of it as a tiny survival capsule. Those oocysts can lodge within the folds of lettuce, cling to herbs, or remain attached to berries despite vigorous rinsing. Think of being glitter bombed - you can’t get that glitter out easily.

That is why studies have not shown that soaking produce in vinegar, baking soda, salt water, or commercial produce washes reliably removes or kills Cyclospora. Those methods may make us feel industrious, but they have not demonstrated a meaningful advantage over plain running water for this parasite.

Wash your produce anyway.

Wash it because it removes dirt.

Wash it because it reduces many other contaminants.

Wash it because good food safety is built from many small habits.

Just don’t expect your kitchen sink to undo something that happened hundreds of miles away on a farm.

So how do I wash produce?

Keep it simple. Wash your hands first, first you don’t want to add anything to the mix and secondly, always wash your hands when going into the kitchen and handling food. It is a good idea.

Rinse fruits and vegetables under cool running water while gently rubbing the surface.

Use a clean vegetable brush for firm produce like carrots, potatoes, cucumbers, melons, and apples. Do you put your brush in the dishwasher after each use? Why not - do it.

Remove the outer leaves from lettuce or cabbage. They are usually the most exposed to contaminants and the most wilted.

Wash produce immediately before using it rather than when you unload groceries because excess moisture encourages spoilage.

Notice what isn’t on that list.

Soap.

Bleach.

Vinegar.

Baking soda.

Salt water.

The evidence simply doesn’t show they outperform running water for routine home use. Yes, I know, everyone has their own cocktail for washing produce. But the data isn’t there to show that these help. Besides, while I love getting a chemistry set out and doing experiments, I prefer to use tap water and scrubbing for the produce. Keep it Simple Simpson (KISS).

How do doctors know it’s Cyclospora?

Here’s something that surprises many people.

Your doctor doesn’t usually know just by hearing your symptoms.

The diagnosis is made with a stool sample. Modern laboratories often detect the parasite using PCR, looking for its genetic material. Other laboratories identify the microscopic oocysts using specialized staining techniques.

One important point is worth remembering: Cyclospora isn’t included in every routine stool test. If the story fits—a week after eating fresh produce followed by prolonged watery diarrhea—your clinician may need to specifically consider Cyclospora when ordering laboratory studies.

That is one reason these infections are occasionally missed.

What about treatment?

The preferred antibiotic is trimethoprim-sulfamethoxazole, better known by the brand name Bactrim.

Most people improve rapidly once treatment begins.

The question I was asked most often, however, wasn’t about Bactrim.

It was about allergies.

“I’m allergic to sulfa. Am I out of luck?”

Fortunately, no.

First, the healthiest people eventually recover even without antibiotics, although the illness can linger for weeks and sometimes relapse.

Second, not everyone who carries the label “sulfa allergy” has a true allergy.

Medicine has become remarkably good at placing allergy labels into charts, and surprisingly poor at taking them back out.

Some people experienced nausea twenty years ago and have been “allergic” ever since.

Others developed a rash that may or may not have represented a genuine allergic reaction. And some of those rashes were not to the antibiotic, but to the fillers they used to put into the pills that also had the antibiotic.

Still others truly cannot receive sulfonamide antibiotics safely.

Those are different situations.

If you’ve been told you’re allergic to sulfa antibiotics, don’t assume you’re out of options, but don’t experiment with herbal remedies or leftover antibiotics either. Your healthcare provider can determine whether the allergy history suggests a true contraindication, and recommend the safest approach based on the severity of your illness.

When should you call your doctor?

Most cases of ordinary viral diarrhea improve within a few days.

Cyclospora is different.

If your diarrhea persists beyond several days, you’re becoming dehydrated, you’re unable to drink enough fluids, you’ve lost significant weight, you’re pregnant, or your immune system is weakened, it’s time to seek medical care.

Diarrhea is inconvenient.

Dehydration can be dangerous.

There’s a difference.

And this is one of the few times I say - get electrolytes. No, not the paleo sugar free stuff. Get some real electrolytes like Pedialyte (see my previous post about these).

The bottom line

Cyclospora reminds us that food safety begins long before we walk into the grocery store. Farmers, processors, distributors, public health investigators, and clinicians all play a role in preventing outbreaks and identifying them when they occur.

You still should wash your fruits and vegetables.

You still should enjoy salads.

You should not become afraid of fresh produce.

But you should also understand that no home washing technique can completely sterile food. Sometimes, the most important part of medicine is recognizing the limits of what we can do at home.

Although if you happen to have a food radiation device at home, this would be the time to use it on your spices (Ok, I haven’t seen one of these, but I would get one if they had it).

For paid subscribers below, let’s take a fascinating journey through the life cycle of this remarkable little parasite. Ironically, the organism leaving your body today probably isn’t capable of infecting anyone else—yet. That’s one of the reasons Cyclospora behaves differently from the stomach viruses we’re used to seeing.

Paid Subscriber Section

The Secret Life of a Parasite

Read more

The lamb was extraordinary.

I’ve been fortunate to eat lamb prepared many ways. I’ve enjoyed it slowly roasting on a spit in Turkey, tucked into delicate meatballs in Stockholm. One of my favorite recipes is the rack of lamb I make at home—if you’re interested, you’ll find it on my website. I love lamb.

But there’s one way I’ve never really eaten it.

Raw.

Yes, out of curiosity, I’ve taken a tiny nibble before it reached the grill. It wasn’t terrible. It just wasn’t memorable. Then a few minutes later, that same piece of meat came off the fire transformed. The aroma filled the air. The texture softened. The flavors became deeper, richer, and somehow more complete.

That simple experience made me wonder whether cooking was doing far more than simply making dinner taste better.

Share

What if cooking changed us?

One of the strongest advocates for that idea is Harvard anthropologist Richard Wrangham, who has argued that learning to cook may have been one of the defining moments in human evolution. Not agriculture. Not writing. Not even the wheel. Cooking. I think he’s right about the importance of cooking, although, like every good scientific idea, the details continue to be debated and refined.

Unfortunately, that’s not what happened on social media.

Instead, the idea became flattened into a slogan.

“Humans evolved eating meat.”

“Therefore humans should only eat meat.”

That’s a shame, because the real story is so much more interesting.

The story isn’t steak.

The story is transformation.

Cooking Chemistry

When we cook meat, proteins unfold and connective tissue softens. Suddenly, our digestive enzymes don’t have to work nearly as hard because we’ve already started digestion before the first bite ever reaches the stomach. The same thing happens with carbohydrates. Heat gelatinizes starches, softens plant cell walls, and unlocks calories that were difficult—or in some cases nearly impossible—for our ancestors to obtain from raw foods. A raw potato is hard, chalky and uninspiring. Bake it and you’ve completely changed both its texture and the way your body can use the energy inside it.

Fire didn’t simply improve meat.

Fire improved almost everything.

That may be the real evolutionary story. Humans didn't discover the perfect food. We discovered how to make almost every food better. Meat became more tender. Tubers yielded more calories. Grains softened. Beans became digestible. Fire wasn't choosing sides in a dietary debate. Fire was expanding the menu.That adaptability, I suspect, is one of the reasons humans spread into almost every environment on Earth. We didn’t evolve because we found one perfect food. We evolved because we became extraordinarily good at transforming many different foods.

Then there is another benefit that, as a surgeon, I think may be even more important.

Cooking made food safer.

Our ancestors didn’t know bacteria existed. They had never heard of parasites, Salmonella, or E. coli. They didn’t need microscopes to understand the practical lesson. They simply observed that people eating cooked food often became sick less frequently. Heat kills many bacteria. Heat destroys many parasites. It reduces the chance that dinner becomes tomorrow’s dehydration and diarrhea.

Imagine two groups living side by side thousands of years ago. One regularly cooks. The other doesn’t. Which group raises more healthy children? Which group spends less time weakened by foodborne illness? Which group passes more knowledge to the next generation?

Natural selection doesn’t require understanding microbiology.

It simply favors survival.

Fire and Flavor

And then something happened that probably reinforced the whole process.

Cooking made food irresistible.

The smell of bread baking. Coffee roasting. Onions caramelizing. A steak developing a beautifully browned crust. None of those flavors exist without transformation. We often say we eat to live, but evolution has always known something we sometimes forget—we’re much more likely to eat foods we enjoy.

That’s why I always smile when someone points to steak tartare as proof that raw meat tastes just as good as cooked meat.

I enjoy a good steak tartare.

But let’s be honest.

Steak tartare isn’t simply raw beef. It’s raw beef elevated with egg yolk, mustard, capers, shallots, herbs and the skill of someone who understands flavor. Take away everything except the beef and compare it to a beautifully grilled steak.

Fire wins.

Every time.

The Science of Transformation (For Paid Subscribers)

Several years ago I was talking with my good friend Simon Majumdar about sous vide cooking, ceviche and why I find cooking endlessly fascinating. Simon listened for a while, smiled, and finally said, “You’re a protein denaturer.”

By the way - you can find Simon’s substack and he is worth following. If you don't know Simon, you probably recognize him as one of the toughest judges on the Food Network, when he first debuted on Iron Chef America, but I've been lucky enough to cook and teach with him around the country. Simon tells the history of food. I explain the science. Between us, dinner usually gets cold before the conversation does.

I laughed because he had accidentally summarized both my career and my hobby in three words.

He’s right.

Whether I was standing in an operating room repairing tissue or standing in my kitchen making dinner, I’ve spent most of my life watching proteins change.

That’s really what cooking is.

Protein denaturation.

Now don’t let the term scare you. It sounds like something reserved for graduate biochemistry, but you’ve watched it happen thousands of times. Crack an egg into a pan. The clear egg white turns white because the proteins unfold and reorganize themselves. Put a steak on a grill and the muscle proteins change. Cook fish and it becomes opaque. Hold salmon at precisely the right temperature in a sous vide bath and those same proteins change more gently, giving you a texture that’s almost impossible to achieve any other way.

Heat is only one way to accomplish this.

Acid works too.

One of my favorite summer meals is ceviche. When I lived in Phoenix, turning on the stove in July felt like declaring war on my air conditioner. Instead, I’d make fish ceviche and pile it into tacos. Lime juice transforms the fish. The proteins denature, the flesh firms, the texture changes and the bright acidity creates one of my favorite meals.

I sometimes joke that ceviche is culinary cold fusion. We figured out how to transform proteins without fire centuries before physicists figured out cold fusion in the laboratory.

Score one for the biology majors.

But this is also where food science gives us an important teaching moment.

People often say the lime juice “cooks” the fish.

That’s true if we’re talking about texture.

It is not true if we’re talking about food safety.

Acid changes proteins beautifully, but it is not a reliable way to kill parasites or dangerous bacteria. If you’re making ceviche at home, the fish should either be commercially frozen for raw consumption or frozen according to FDA recommendations before you ever squeeze the first lime. That means temperatures of -4°F (-20°C) for seven days, or -31°F (-35°C) for fifteen hours. Most home freezers simply don’t get cold enough to do that reliably, which is why buying fish specifically intended for raw preparations matters.

People ask me whether I eat ceviche in Cabo.

The answer is yes.

But only in restaurants I know and trust.

I’ve spent too many years as a surgeon to confuse confidence with food safety. I want to know the fish has been handled properly before anyone starts marinating it.

The more I study culinary medicine, the more I realize my kitchen has quietly become my laboratory. If you walked into it, you’d notice something unusual. My measuring cups have largely been replaced by laboratory beakers. My favorite cookware sits on induction burners. I don’t even cook with fire very often anymore.

I cook with magnets (induction burners).

Take that, physics majors.

What’s funny, of course, is that the joke is only half a joke. Whether it’s a charcoal fire in Xi’an, a sous vide water bath in my kitchen, a squeeze of lime over fresh fish, or the invisible magnetic field beneath an induction cooktop, I’m doing exactly what cooks have been doing for tens of thousands of years.

I’m transforming food.

Our ancestors didn’t know words like denaturation, enzymes, collagen, or starch gelatinization. They simply noticed that transformed food tasted better, nourished them more effectively, and made them sick less often.

Science eventually explained why.

Cooking taught us how long before we understood the chemistry.

That’s one of the reasons I love culinary medicine. Every meal is really an experiment, every recipe is a hypothesis, and every kitchen is a laboratory where biology, chemistry and history come together three times a day.

Perhaps that’s why cooking fascinates me as much now as surgery once did.

In the operating room I spent thirty years helping the human body heal.

In the kitchen I spend my time understanding why it works in the first place.

A special thanks to my paid subscribers for making essays like this possible. I know many of you joined me because of discussions about medicine, vaccines, and the science behind the headlines. I hope you'll indulge me when I wander into the kitchen, because I've come to believe that some of the most interesting science in the world isn't happening only in research laboratories. It's happening every evening around a stove, a grill, or even an induction cooktop. As always, thanks for reading, thanks for your support, and I'll see you next week.