GLP-1s Keep Expanding, Alcohol Keeps Retreating, and Prevention Continues to Win

Every week, I look through a pile of studies, press releases, and medical journals, so you don’t have to. Sometimes I am searching for a common thread. Sometimes there isn’t one. This week there was.

We have the new exciting peptides like GLP-1 that are reducing inflammation, decreasing cancer risks, and autoimmune disease, and then we have the other peptides that are scams.

The more we learn about chronic disease, the more everything seems connected.

Obesity affects cancer risk. Inflammation affects arthritis. Alcohol affects cardiovascular disease. Vaccines prevent illnesses that most people never realize they avoided. Wildfire smoke affects lungs, hearts, and long-term health. Pull on one thread and three others start moving.

The biggest story this week continues to be GLP-1 medications. And on the other side are the scammers - the con men selling peptides that are not approved, not tested, and sold to unsuspecting customers.

GLP-1s Continue to Surprise

When semaglutide and tirzepatide first arrived, most of us thought of them as diabetic and then weight-loss medications. That description and what these drugs can help with expands every month.

GLP-1 and Obesity-Related Cancer

Researchers publishing in Annals of Oncology reported that patients receiving GLP-1 receptor agonists had significantly lower rates of obesity-related cancers compared with matched controls.

The largest reductions were seen in several cancers strongly associated with obesity, including colorectal cancer, pancreatic cancer, endometrial cancer, and multiple myeloma. In addition to breast cancer.

It is too early to claim these medications prevent cancer. However, the findings fit a pattern we continue to see repeatedly: when metabolic health improves, many downstream consequences of obesity improve.

For decades, we viewed obesity as cosmetic, then a potential heart issue with increased blood pressure. Evidence increasingly suggests obesity is one of the central drivers of chronic disease.

GLP-1 and Psoriasis

A review published in Frontiers in Immunology examined the growing evidence that GLP-1 receptor agonists may improve psoriasis severity.

This finding makes biological sense. Psoriasis is not simply a skin condition. It is an inflammatory disease. Obesity is also associated with chronic inflammation. Reducing that inflammatory burden may help explain why improvements are being observed.

The evidence remains preliminary, particularly for psoriatic arthritis, but it is another example of these medications affecting systems far beyond appetite regulation.

GLP-1 and Chronic Kidney Disease

Researchers presenting findings at the European Renal Association Congress reported that semaglutide improved quality-of-life measures among patients with type 2 diabetes and chronic kidney disease. Kidney disease is one of the top ten causes of death in the United States.

Physicians often focus on laboratory values and hard outcomes. Patients care about something equally important.

How they feel.

The reported improvements involved mobility, daily activities, discomfort, and overall health status. Those outcomes matter because they are felt by patients, rather than measured solely by statisticians.

GLP-1 and Knee Replacement Surgery

One of the more interesting studies this week appeared in Regional Anesthesia & Pain Medicine, where investigators reported lower rates of total knee replacement among patients with osteoarthritis treated with GLP-1 receptor agonists.

The obvious explanation is weight loss. Less weight means less force across an already damaged joint.

However, the story may be more complicated. Improvements appeared earlier than weight loss alone would fully explain, raising the possibility that the anti-inflammatory effects of GLP-1 medications also contribute.

We increasingly recognize osteoarthritis as more than simple wear and tear. Inflammation appears to play an important role in symptoms and disease progression. If GLP-1 medications reduce that inflammatory burden, they may help knees in more ways than one.

As with many GLP-1 stories, what began as a weight-loss medication increasingly looks like a metabolic medication.

GLP-1 and Pregnancy

Researchers publishing in the Annals of Internal Medicine examined nearly 3,600 pregnancies and compared outcomes among women who continued GLP-1 therapy into the first trimester with those who discontinued treatment.

Reassuringly, investigators did not identify major increases in pregnancy loss, abnormal fetal growth, or major congenital malformations.

This study does not change current recommendations regarding pregnancy and GLP-1 medications. However, it provides useful information for women who discover they were pregnant while taking one of these drugs. If you are taking these drugs and become pregnant, please talk with your OB physician.

The FDA and Unproven Peptides

And speaking of peptides, let’s talk about the shady side of peptides. Just this week, a nurse asked me about peptides.

A coworker had injured himself and was told injecting a peptide would speed healing and recovery. That is how many of these products are marketed. The problem is that marketing is not evidence.

For most of these compounds, we do not know whether they work. We do not know the correct dose if they do work. We do not know the long-term side effects. In many cases, we don’t even know what is actually in the vial.

This week, delegates at the American Medical Association called for stronger FDA oversight of synthetic peptides and similar products marketed without adequate evidence of safety or effectiveness.

To be clear, some peptides are legitimate medicines. Insulin is a peptide. GLP-1 medications, such as semaglutide and tirzepatide, are peptides. Those drugs went through rigorous testing, dose-finding studies, safety evaluations, and large clinical trials.

The peptides being promoted online are different.

Many are sold as “research chemicals,” which is often a legal way to say they have not been approved for human use. They are manufactured overseas, sold through websites, gyms, wellness clinics, and social media influencers, and frequently marketed with claims that far exceed the evidence.

Some of the most common peptides sold without evidence or studies include:

BPC-157 — promoted for tendon healing, ligament repair, gut health, and inflammation. Human evidence is extremely limited. Probably the most common you will hear about. And being “common” does not mean we have good data showing they work - we do not.

TB-500 (Thymosin Beta-4) — marketed as a recovery and regeneration compound for athletes. Despite enthusiastic claims, there is little quality human evidence supporting these uses.

Epitalon — sold as an anti-aging and longevity treatment that supposedly preserves telomeres and extends lifespan. If it actually did what the advertisements claim, I would already be standing in line.

Thymosin Alpha-1 — promoted as an immune booster. While used in some countries for selected conditions, it remains unapproved for most of the claims made by wellness clinics.

Melanotan II — marketed as a tanning peptide. It can darken skin pigmentation but also carries risks including nausea, elevated blood pressure, and other adverse effects.

Dihexa — advertised as a cognitive enhancer. Claims range from improved memory to neuroregeneration.

At present, the evidence remains far behind the marketing. Because these substances have not undergone rigorous, multi-phase clinical trials for consumer use, their long-term effects, optimal dosages, and safety profiles are largely unknown.

If you are exploring peptide therapies, it is highly recommended to speak with a board-certified physician to understand safety profiles and regulatory statuses.

Those peptides above are currently promoted with extraordinary claims and very little data. Some have mouse data, some have small human studies.

A peptide is not a magic spell. It is a drug. And should not be sold by a gym bro trying to increase their revenue stream.

And drugs deserve evidence.

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Alcohol: The News Keeps Getting Worse

A government review published in the Journal of Studies on Alcohol and Drugs concluded that health risks from alcohol begin at levels many people still consider moderate.

The old story that a daily drink improves longevity continues to lose support as larger and more sophisticated studies accumulate. According to the report, the lifetime risk associated with alcohol rises steadily, even at relatively low levels of consumption. One drink a day isn’t improving longevity, it is decreasing longevity while increasing risks of cancer and heart disease.

Market researchers simultaneously project that global alcohol consumption will decline over the next decade.

Several forces appear to be driving the change. Younger adults drink less than previous generations. Health awareness continues to increase. Alcohol has become increasingly expensive. And growing evidence suggests that GLP-1 medications reduce interest in alcohol for many users.

As someone who enjoys wine, I find this trend fascinating. The issue is not prohibition. The issue is preference. Many patients describe the same thing: they still enjoy alcohol when they choose it, but they think about it less often.

That distinction may prove important, as researchers continue to explore how GLP-1 medications influence reward pathways in the brain.

In the meantime, many restaurants have noticed how much wine sales and alcohol sales continue to decline. That is bad for the restaurants, but good for population health.

Cancer Prevention Is Often Boring

A pooled analysis published in JAMA Network Open followed more than 1.5 million adults and found that sugar-sweetened beverages were associated with increased risks of hepatocellular carcinoma and intrahepatic cholangiocarcinoma.

No, this does not mean a single soda causes cancer. Medicine rarely works that way.

The concern is cumulative exposure. Excess sugar contributes to obesity. Obesity contributes to fatty liver disease. Fatty liver disease contributes to inflammation and fibrosis. Over decades, those processes increase cancer risk.

The lesson is not new, but evidence keeps accumulating. Which means it is time to talk to my 15 year old son about his daily Dr. Pepper.

Another study published in the American Journal of Gastroenterology found significantly lower rates of colorectal cancer among adults aged 40 to 49 who underwent colonoscopy compared with those who did not.

The producer of my social media had a colonoscopy a few months ago. They found a large polyp, the kind that would become cancer if it had been left to grow. Her stool test the year before showed everything was fine, but alas, she listened to me (for once) and got a colonoscopy. The stool test would have been positive much later and it might have meant she had cancer instead of a polyp.

Colorectal cancer remains one of the more concerning cancers rising in younger adults. Studies like this will continue to shape the debate about when screening should begin. I think earlier is better and most surgeons also believe we should begin screening earlier.

Vaccines Continue Delivering Quiet Victories

Researchers publishing in JAMA Network Open reported that maternal RSV vaccination reduced infant hospitalizations by nearly seventy percent.

RSV is respiratory syncytial virus, which is the leading cause of bronchiolitis and hospitalization for infants and young children. We recently approved a vaccine for it and it has reduced hospitalizations among children, as well as prolonged hospitalizations for older adults.

This is exactly what preventive medicine should do.

The baby never knows what illness was avoided. The parents never know what hospital stay never occurred. The vaccine succeeds by making something fail to happen.

Meanwhile, investigators publishing in PLOS One found lower rates of new-onset atrial fibrillation among vaccinated individuals following COVID infection compared with those who were unvaccinated.

The benefit was observed across multiple high-risk groups, including patients with diabetes, obesity, hypertension, coronary disease, and chronic kidney disease.

These studies rarely generate headlines, because prevention lacks drama.

Yet prevention remains one of medicine’s greatest achievements.

Measles Continues Its Comeback

According to the CDC, the United States has now surpassed 2,000 measles cases this year.

More than ninety percent of cases occurred among unvaccinated individuals.

The virus has not changed. Human behavior has.

Measles remains one of the most contagious infectious diseases known. Its resurgence should surprise no one who follows vaccination trends. The issue with measles isn’t death, it’s the two year immunology amnesia, hospitalizations, pneumonias and long-term neurologic consequences. So when someone shows how death rates are low, and we haven’t had a death in 2026, remember we have had many hospitalizations, quarantines, lost days of school and work, and it has cost millions of dollars.

Viruses remain remarkably indifferent to politics, ideology, and internet debates.

Public Health Notes

A New Sunscreen Ingredient Finally Arrives

The FDA approved bemotrizinol, the first new sunscreen ingredient approved in the United States in more than twenty-five years.

The compound has been used in Europe and other countries for years and provides broad-spectrum protection against ultraviolet radiation.

Dermatologists have been waiting for this approval for a long time.

One of the biggest concerns with traditional chemical sunscreens (like avobenzone or oxybenzone) is that they seep through the skin and can be detected in the bloodstream at higher rates. Bemotrizinol is a larger molecule, meaning it sits safely on top of the skin and has very low systemic absorption.

Bemotrizinol holds its ground against UV rays, so if you accidentally stretch your reapplication time slightly past the standard two-hour mark, you will still have significantly more active defense left on your skin compared to traditional chemical sunscreens.Stabilizes Other Filters: In a formulation, bemotrizinol actually acts as a bodyguard for other weaker ingredients, helping prevent the entire sunscreen blend from prematurely degrading.

Why You Still Need to Reapply

Even though the chemical itself does not break down easily, you still must reapply it every two hours when outdoors for a few mechanical reasons:

Physical Friction: Activities like wiping your face, changing clothes, or rubbing against towels physically scrape the product off your skin.

Sweat and Water: Even water-resistant formulas naturally lift off the skin over time when exposed to heavy perspiration or swimming.

Skin Oils: Your skin’s natural sebum production gradually breaks up the even film of sunscreen, causing it to pool or separate over several hours.

Essentially, bemotrizinol solves the problem of the sun destroying your sunscreen, but it cannot solve the problem of daily movement that inadvertently wipes away the sunscreen.

There is a trend these days for some to say we need sunshine, and sunscreen is bad for people, more than sunlight. That is false. To be clear, the basic science has not changed - sunlight can cause DNA damage, leading to mutations. This leads to, at worst, melanomas, other skin cancers, and at best premature aging of the skin. Just find a lifeguard from California over 60 and see their skin.

A bit of sun is great - getting sunburned is not, especially for children.

Wildfire Smoke Is Becoming a Chronic Health Problem

Researchers publishing in Science reported that wildfire smoke is reversing years of progress in air quality and contributing to increased illness and mortality.

For those of us in California, this hardly feels like news. Sadly, I live next to an area that ten years ago led to an evacuation of my neighborhood.

The important point is that the health effects are measurable. Wildfire smoke increases respiratory illness, cardiovascular risk, and overall mortality.

For many Californians, preparation for wildfire season should probably be viewed the same way we view preparing for earthquakes.

Not exciting. Just necessary.

Below is the paid section where we expand about alcohol and air purifiers, but here are the references for those who want to read the studies themselves.

References and Further Reading

GLP-1 Medications and Obesity-Related Cancers

• Annals of Oncology (2026)

Sugar-Sweetened Beverages and Liver Cancer

• JAMA Network Open (2026)

Alcohol and Mortality Risk

• Journal of Studies on Alcohol and Drugs (2026)

GLP-1 Receptor Agonists and Psoriasis

• Frontiers in Immunology (2026)

Semaglutide in Chronic Kidney Disease

• European Renal Association Congress Presentation (2026)

Maternal RSV Vaccination

• JAMA Network Open (2026)

COVID Vaccination and New-Onset Atrial Fibrillation

• PLOS One (2026)

Wildfire Smoke, Ozone, and Mortality

• Science (2026)

Measles Surveillance Data

• CDC Measles Cases and Outbreaks

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Two areas here: Alcohol and Air purifiers this week

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I was going to launch this on Tuesday, so I could call it Tuesday Tirzepatide to Tomatoes, but that level of alliteration is best left to professionals. I'm a surgeon. We remove things; we don't name them.

You Have a Baby Stomach. Now What?

For years, when I performed bariatric surgery, I would tell patients they had a baby stomach.

The surgery was over. The anatomy was different. Now came the learning phase.

A baby's stomach doesn’t know what it likes yet. It doesn’t know which foods settle comfortably and which foods cause trouble. It doesn’t know that one bite too many can mean an hour of regret. Like a parent introducing food to an infant, patients had to pay attention. They had to learn. They had to discover what worked and what didn’t. This is what happened after surgery and what happens with a GLP-1.

Today, I find myself having the same conversation with people taking GLP-1 medications.

No, the medication doesn’t physically shrink the stomach the way surgery does. But many people discover that eating feels different. Portions that once looked normal now seem enormous. Rich foods may sit heavily. Eating too quickly can be uncomfortable. Fullness arrives sooner than expected.

GLP-1 give you a chance to start again - like a baby’s stomach

When we talked about baby stomachs after bariatric surgery, we also talked about protein shakes. Patients often misunderstood their role. They thought the protein shake was the diet. It wasn’t.

Protein shakes were formula. Like infant formula, the kind I would run to Walmart and get at 11 pm because I realized we were out and JJ was crying. Thank goodness they were open late.

Protein shakes were useful. They helped patients meet protein goals while learning how to eat again. But nobody wants a healthy two-year-old living exclusively on formula. Formula is a bridge. It is not the destination.

The same thing is true with GLP-1 medications. A protein shake can be a wonderful tool. It can help preserve muscle while weight is coming off. It can make a busy morning easier. But eventually, the goal is to learn how to eat real food. The goal is not to survive on shakes forever. The goal is to build a way of eating that you can enjoy for years.

That is where many people become stuck.

The weight starts coming off. Food noise becomes quieter. The old cravings lose some of their power. Then comes the inevitable question:

“What should I eat now?”

Unfortunately, diet culture answers that question. Somebody tells you to avoid bread. Another will tell you to count points. And there is always somebody who tells you to count macros.

The low carb evangelist tells you that fruit contains too much sugar. The new carnivore insists that humans should consume roughly half a heifer every week. Then the vegan will tell you that taking honey from bees is immoral.

Then the most common one I hear - “just eat less than before and better.” I don’t even know what that means.

God help them all.

The irony is that many people finally escape the biology that was fighting them, only to become trapped by nutrition rules that have confused them for decades.

The Counters

As a scientist, I understand the appeal of rules. When we conduct nutrition research, we measure everything. We calculate servings. We weigh foods. We count grams. We determine how closely somebody follows a Mediterranean dietary pattern.

That is how research works. But that is not how people live. You will not bring a digital scale to dinner. You will not calculate your Mediterranean Diet adherence score while standing in your kitchen wondering what to make on a Wednesday night.

The Mediterranean Diet score is a research tool. Researchers love counting things. If there are twelve almonds on the plate, they want to know if there were thirteen yesterday. Give a researcher a bowl of beans, and they'll find a way to create a spreadsheet.

It helps scientists compare populations. It was never intended to become a lifestyle religion. When I was seeing how well patients did after bariatric surgery, I used that scale to calculate scores for the patients. But it is a tool to measure adherence, because that is what we have to do. It is not what we want you to do. Yes, someone probably has built some app to do that, but do you want an app telling you that you need two more ounces of legumes today?

I used those scores in research. They are useful. They tell us who is following a Mediterranean pattern and who isn't. But they are measuring tools, not living tools. A thermometer tells you the temperature. It does not tell you what to wear.

What matters is direction. Are you eating more fruit? How many vegetables are you consuming today? Yes, use the Brussels sprouts for the slingshot, that is why God made them round.

But what is your consumption of beans this week? Was fish, be it tuna or shrimp or salmon, in two meals this last week?

Are you cooking with olive oil?

If the answer is yes, you’re probably moving toward better health.

The baby's stomach gives you the opportunity to make those changes. Better yet, having lost that big reward signal for the ultra processed food, whole foods can take on more interest.

Breakfast of champions

One of my favorite examples is breakfast. I’d rather have you learn three breakfasts that you can prepare repeatedly, than hand you a complicated meal plan you’ll abandon in ten days.

My first choice is a smoothie.

I spend a lot of time commuting. A smoothie travels well. I can sip it while driving to Santa Maria before dawn. Most mornings, it contains at least a cup and a half of fruit. Berries, bananas, yogurt, protein, oats—nothing exotic, nothing expensive, nothing that requires a nutrition degree. It is simple, portable, and starts the day with fruit already on board.

Another favorite is overnight oats. The beauty of overnight oats is that tomorrow’s breakfast is prepared tonight. Oats, yogurt, milk, fruit, and a few extras sit in the refrigerator while you sleep. In the morning, breakfast is waiting. There is no decision to make, because the decision was already made yesterday.

The third breakfast is eggs with beans and ranchero sauce. It tastes like real food, because it is real food. Eggs provide protein. Beans provide fiber. Ranchero sauce provides flavor. Nobody has to pretend it is dessert, a supplement, or a miracle food. It is simply breakfast.

The Grapes or Klondike of Wrap

That brings me to grapes.

Every afternoon, my Apple Watch reminds me to eat some. Yes, grapes.

I know that sounds odd, but I think of them the same way I think of medicine. They are washed, prepared, and waiting in the refrigerator. Around 2:30 in the afternoon, I grab a handful.

Now, I should confess something. There is also a Klondike bar in the freezer.

If it is day six before my next Zepbound injection and that freezer drawer opens, I suddenly become much more interested in that Klondike bar than I was a few days earlier. Fortunately, the grapes are ready and waiting. But it sure is easy to unwrap the Klondike bar, and I can have it consumed by the time I make the turn from the refrigerator to where I deposit the foil wrapper in the trash can. If I have not washed the grapes, well, that seems way more effort than unwrapping the Klondike. Human beings are remarkably efficient. We will travel across town to save twenty cents on gasoline and avoid washing grapes, because it seems like too much work.

One of the surprising things I noticed on Zepbound is that fruit became more interesting. Not exciting. Not magical. Just interesting. Before, a bowl of grapes was competing, with a thousand food engineers working overtime to make a snack irresistible. Now the grapes get a fair fight.

Most days, the grapes win. Most days.

I was disappointed to learn that the sprinkles on a doughnut do not count as fruit. Apparently nutrition scientists are strict about these things.

Prepare for the day

The point isn’t that grapes are magical. The point is that healthy habits become easier when they are prepared in advance. If fruit is washed and ready, you’ll eat more fruit. If vegetables are prepared, you’ll eat more vegetables. If healthy food is convenient, healthy eating becomes convenient.

That is how adults learn to feed a baby's stomach. Not through willpower, guilt or perfection. But through preparation.

Eventually, the weight will come off. The clothes fit differently. People start complimenting you. You step on the scale and realize you’ve reached a number you haven’t seen in years.

That is wonderful.

But it is not the end of the story.

For years, I have joked that losing weight makes it easier for your friends to carry your casket. While that may be true, it misses the point entirely.

The goal is not to become a lighter corpse. Yes, that is nice if your pallbearers can say - “sure glad they were on a GLP-1. It makes this easier to carry”. The goal is to avoid becoming a corpse before your time.

You now have the tool to make yourself healthier, stronger and sleek.

Let’s make it easier to travel, play with grandchildren (JJ is 15 years old so hopefully this will be another 20 years away), walk farther, remain independent, and enjoy the life you’ve built.

Weight loss is wonderful. Health is better.

GLP-1 medications have given many people something they haven’t experienced in years: enough quiet to make choices, rather than simply react to cravings. That opportunity is precious.

Use it.

So I want to make this simple, and the answer is that we humans are very simple. Consider breakfast. Most of us eat the same thing, or at most we have three types that we like. In my case, two for the week when I am busy and then my weekend eats. There are more. But start by learning three breakfasts.

Next is lunch and the afternoon snacks. It is not hard to learn three lunches. I used to eat out for lunch, and most days the choice I made before GLP-1 was between a fried chicken sandwich and a burger.

But for dinner, we expand it a little. So I say, Learn five dinners. And in the paid section, I will go through mine and show you how I cook them.

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The greatest gift of a GLP-1 isn’t the weight you lose.

It’s the opportunity to decide what kind of life you’re building after the weight is gone.

In the paid section: three lunches, five dinners I use to keep healthy eating simple—even on the weeks when life gets busy.

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A few years ago, researchers at the National Institutes of Health performed one of the most expensive nutrition studies imaginable. Rather than asking people what they ate—which is a remarkably unreliable way to learn what people eat—they brought volunteers into a metabolic ward where every meal was prepared, every serving was weighed, and every leftover morsel was measured. There would be no guessing, no food diaries, and no wishful thinking. If someone ate a cookie, the researchers knew it. If they left half a sandwich on the plate, the researchers knew that too.

The study itself was deceptively simple. Participants were given two diets. One consisted largely of ultra-processed foods, while the other was built around minimally processed foods. The volunteers could eat as much as they wanted, and nobody instructed them to count calories or lose weight. Nevertheless, something fascinating happened. When eating the ultra-processed diet, participants consumed roughly 500 more calories each day than when they ate the minimally processed diet.

Five hundred calories.

Not because they were forced to eat more. Not because they lacked discipline. Not because they suddenly forgot everything they knew about nutrition. Instead, the food itself appeared to change their behavior.

Most people hear that finding and immediately ask why obesity occurs. However, the question that has always interested me is slightly different. If foods can influence calorie intake that dramatically, why doesn’t everyone become obese?

For those who listen to my podcast FORK U, we covered this partially in that podcast. Here are the details. If not, FORK U can be found where you subscribe to most podcasts. It typically comes out on Thursdays.

The Grocery Store Didn’t Happen by Accident

To understand how we arrived here, it helps to step back a few decades and visit a place that rarely appears in discussions about nutrition. While most of us imagine food evolving in kitchens, restaurants, farms, and family traditions, another form of evolution was taking place inside corporate research laboratories.

One of the most influential figures in that story was Howard Moskowitz, a statistician hired to help food companies create products that consumers would love. At the time, the prevailing assumption was that there must be a perfect spaghetti sauce, a perfect soda, or a perfect level of sweetness waiting to be discovered. Moskowitz, however, found something far more valuable. There was no perfect spaghetti sauce. There were many perfect spaghetti sauces.

Some consumers preferred smooth sauce. Others wanted chunks of tomato. Some liked sweeter flavors, while others preferred something more savory. Consequently, the goal shifted from creating one product for everyone to creating multiple products for different groups of consumers. Once food companies learned that lesson, grocery stores began to change. Suddenly there wasn’t one barbecue sauce, there were twelve. There wasn’t one yogurt, there were thirty. Entire aisles became exercises in consumer segmentation.

Today, when you stand in front of a shelf and wonder why there are twenty versions of the same product, you are looking at Howard Moskowitz’s legacy.

Then Came the Food Scientists

Knowing what people like is only half the battle. Once a company understands your preferences, the next question becomes how to maximize the pleasure associated with those preferences. This is where food scientists such as Steven Witherly enter the story.

The sensory experience fascinated Witherly. Flavor mattered, of course, but so did crunch, aroma, texture, temperature, and even the sound food makes when it breaks between your teeth. Long before social media influencers recorded themselves eating for millions of viewers, food scientists studied why certain foods seemed so rewarding.

One of Witherly’s most memorable observations involved what he called vanishing caloric density. Certain foods, particularly puffed and extruded snacks, dissolve so quickly in the mouth that they create the sensation of disappearing. The crunch arrives, the flavor explodes, and then the food is gone. Unfortunately, the calories remain very much present, but the sensory experience is so brief that the brain receives surprisingly little resistance during the process.

A carrot, by contrast, insists on being chewed. An apple demands attention. A piece of fish requires time and effort. A cheese puff, on the other hand, performs a magic trick. It appears substantial when it enters the mouth and then vanishes almost immediately afterward.

That difference may sound trivial until you remember Kevin Hall’s study. Suddenly, the extra 500 calories begin to make a little more sense.

Extrusion, Engineering, and Eating Faster

In previous articles, I discussed extrusion, the manufacturing process responsible for many breakfast cereals, puffed snacks, chips, and countless other packaged foods. At first glance, extrusion appears to be a discussion about machinery. Ingredients are ground, heated, pressurized, and forced through specially designed openings to create a desired shape.

Yet the more I think about Hall’s study, the more I suspect that extrusion is not merely a manufacturing technique. It is also a behavioral technique.

Structure influences texture. Texture influences chewing. Chewing influences eating speed. Eating speed influences satiety. Consequently, when we alter the structure of food, we may also alter how much of it people consume before fullness has the opportunity to catch up.

That idea does not mean ultra-processed foods are poison, nor does it mean every packaged food is part of a conspiracy. It simply means that modern food manufacturers employ scientists, engineers, statisticians, and sensory researchers, whose job is to understand how people interact with food. When enough bright people spend enough years studying the same problem, they tend to become good at solving it.

The Question I Can’t Stop Asking

I am the youngest in my family. My brothers grew up only a few years before I did, and although those years were not enough to alter our genetics, they were enough to place us in somewhat different food environments. They experienced more meals prepared at home, fewer convenience foods, and less of the fast-food culture rapidly expanding across America.

I became the one who struggled with weight.

Now, before anyone rushes to draw conclusions, let me save you the trouble. This proves absolutely nothing. Anecdotes make poor evidence, and medicine is littered with bad ideas that began with a convincing story. Nevertheless, anecdotes often generate useful questions, and this one has remained with me for years.

If much of our DNA is shared, why did our experiences diverge? Why do some people seem naturally protected from a food environment that others find extraordinarily difficult to navigate?

Every family has its version of this puzzle. One sibling struggles. Another does not. One parent gains weight. Another remains lean. A single factor rarely explains the differences, because biology seldom provides simple answers.

What GLP-1 Medications Revealed

One of the most fascinating developments of the past few years has been listening to patients describe their experiences with GLP-1 medications. Interestingly, many do not talk about hunger first. Instead, they talk about silence.

Foods that once demanded attention become easier to ignore. Cravings become less urgent. The constant background conversation about food begins to quiet down. As a result, many patients ask a question that obesity researchers have been circling for decades.

“Is this how other people think about food?”

That question may be more important than it appears. Before taking tirzepatide, I assumed hunger was the primary story. After taking tirzepatide, I became increasingly convinced that food noise often deserves equal billing. The food itself remains unchanged. The grocery store remains unchanged. The restaurant remains unchanged. What changes is the conversation occurring inside the brain.

Perhaps that is the most important lesson hidden inside Kevin Hall’s experiment. The difference between two people is not always knowledge. It is not always discipline. It is not always character. More often than we care to admit, biology interacts with an environment that has become extraordinarily sophisticated at capturing our attention.

Howard Moskowitz helped companies discover what we like. Steven Witherly helped explain why we like it. Kevin Hall showed what happens when real people are exposed to those foods under controlled conditions. Yet despite everything we have learned, the most fascinating question remains unanswered.

Why are some people protected?

Because if we can understand that, we may finally learn more about obesity than ever, by blaming the people who develop it.

The Food Supply Miracle—and the Problem That Came With It

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As I write this, I am drinking a cup of Nespresso Stormio. For years, my morning coffee was Peet’s Major Dickason’s Blend. It still shows up regularly in the rotation, but this morning the Nespresso machine won the argument.

The coffee is black, of course.

Partly because I like it that way, and partly because after spending thirty years helping people lose weight, I learned that if you put enough cream and sugar into coffee, eventually it becomes a milkshake with a caffeine problem.

This week brought one of the stranger collections of medical stories I have seen in a while.

A flesh-eating fly has returned to Texas for the first time since Lyndon Johnson was in the White House. GLP-1 medications continue to rack up benefits that nobody predicted when they were developed for diabetes. Researchers are questioning whether BMI is missing millions of people with obesity. Ebola remains in the headlines. A new COVID prevention drug has arrived. And pancreatic cancer patients may finally have reason for optimism.

Let’s get into it.

This Week in Obesity Medicine

When GLP-1 medications first appeared, many people dismissed them as weight-loss drugs.

That description becomes less accurate every month.

A new study found that patients taking GLP-1 medications were less likely to require knee replacement surgery. The simple explanation is weight loss. Less weight means less force crossing the knee joint every time you walk.

However, obesity is not simply extra weight.

Fat tissue is biologically active. It releases inflammatory molecules that affect blood vessels, joints, the liver, and nearly every organ system. Reducing that inflammation may help protect the knee as much as reducing body weight.

Do you know what else is anti-inflammatory and helps people with “bone on bone” osteoarthritis? Walking. We used to think that people with osteoarthritis of the knee should not walk, use non-weight bearing exercise. We were wrong. That is the beauty of science and medicine - we learn new things and move forward. Turns out people with bone-on-bone arthritis who walk keep their own knees a few years longer than those who don’t.

Another study followed more than 111,000 women and found that GLP-1 users had a significantly lower risk of breast cancer. By one third!

Before anyone starts claiming GLP-1 medications cure cancer, take a breath.

This was an observational study, not a randomized trial. Yet the finding makes biological sense. Obesity increases inflammation, insulin resistance, and estrogen production. All three are associated with increased breast cancer risk. When you improve those factors, risk may fall.

The larger story is becoming difficult to ignore.

Every month, we discover another disease influenced by excess adipose tissue.

Obesity may not be the final domino.

It increasingly looks like the first one.

Maybe BMI Isn’t Telling the Whole Story

One of the most interesting studies this week received far less attention than it deserved.

Researchers applied the new Lancet Commission definition of clinical obesity to Americans across multiple BMI categories.

The surprise?

More than one-quarter of adults with a “normal” BMI met criteria for clinical obesity. Read that sentence again.

According to BMI, these individuals were not obese. They were obese according to body fat distribution, metabolic dysfunction, organ impairment, and health consequences.

As surgeons, we have seen this for years. Two patients can be the same height and weight. One has a healthy liver, normal blood pressure, excellent glucose control, and good muscle mass.

The other has fatty liver disease, sleep apnea, insulin resistance, and visceral fat packed around the abdominal organs.

BMI sees twins. Biology sees strangers.

I suspect we will spend the next decade redefining obesity based less on weight and more on function. And if you have a scale that measures fat and muscle mass, that helps even more.

Viral Update

The disease making the biggest headlines is Ebola.

The disease that worries me most is measles.

The Bundibugyo strain of Ebola continues to spread in Central Africa. Public health officials are responding aggressively, and the risk to Americans remains extremely low. What is interesting is now we are getting solid numbers, meaning we have laboratory confirmation. So to some, it might appear Ebola has fewer cases than originally reported. While we have confirmed 86 deaths from Ebola, the number is likely double that. Remember, many were buried without a laboratory diagnosis, but a clinical diagnosis, and those are not being counted. Just like now, we have fewer cases of “confirmed” Ebola, but we have many cases that were not confirmed. In the Congo, it takes four days to get blood to a lab for testing, and many clinics don’t have the ability to get a test and send it off.

Meanwhile, the hantavirus continues to make occasional appearances in the United States and remains under surveillance following the cruise-related cases that received attention last month. In the US it is not person-to-person transmission but comes from mouse droppings. This is seen in New Mexico, Arizona, and California. If you live in these areas and see mouse droppings please don’t clean them up with a dust buster. To clean mouse droppings safely in a potential hantavirus area, your main goal is to avoid stirring up dust. NEVER sweep or vacuum dry droppings. Instead, soak the area thoroughly with a bleach solution (1.5 cups of bleach per gallon of water) and wipe everything up while wearing protective gloves. In the paid section, I go into detail about how to clean mouse droppings in a Hanta virus infected area (Arizona, New Mexico, and California)

However, when I look toward the coming months, I keep coming back to three familiar viruses.

Measles.

Influenza.

COVID.

The upcoming World Cup will bring millions of international travelers together. Southern Hemisphere flu season is already underway. Measles outbreaks continue to appear anywhere vaccination rates fall. COVID remains with us, even if most people would rather stop talking about it.

Sometimes the biggest infectious disease threat is not the exotic virus making headlines.

It is the familiar virus we stopped worrying about.

The Flesh-Eating Fly Returns

There are few creatures whose name sounds like the nightmare they are.

Screwworm is one of them.

Texas recently reported its first cases since 1966. Screwworm is not actually a worm. It is a fly. Unfortunately, it is a fly with terrible parenting skills.

A female lays hundreds of eggs into an open wound. When the larvae hatch, they do something unusual.

Most maggots feed on dead tissue. Screwworm larvae feed on living tissue.

Cattle are the most obvious victims, which is why ranchers pay close attention. However, the fly does not care whether the victim has hooves, paws, or opposable thumbs.

Dogs can be infected. Cats can be infected. Wildlife can be infected. And if you haven’t figured this out, humans can be infected. Yes, photos in the paid section.

The United States eradicated screwworm in 1966 using one of the most successful biological control programs in history.

Now it is back.

And if you think that sounds like the opening scene of a horror movie, you’re not wrong.

Drug Watch

The FDA approved ensitrelvir, marketed as Xocova, for prevention of COVID following exposure.

Think of it as the next step beyond treatment. Instead of waiting until someone becomes sick, the goal is to prevent illness after a household exposure.

The medication reduced the risk of developing COVID by more than half in clinical trials. This may prove especially useful in nursing homes, assisted living facilities, and households caring for vulnerable family members.

Another encouraging COVID story involved MIS-C, the inflammatory syndrome that frightened parents during the pandemic. Cases continue to decline.

The most striking finding was that nearly eighty percent of cases occurred in vaccine-eligible children who had not been vaccinated. All four deaths reported during the study period occurred among unvaccinated children.

The lesson is not political. It is biological. Immunity works and that is how the vaccine works.

Pancreatic Cancer Finally Gets Good News

For decades, pancreatic cancer has been one of the most frustrating diseases in medicine. I operated on my fair share of pancreatic cancer cases and often we would see no evidence of spread when we looked at a CAT scan or MRI, and then we would open the patient and find it was spread throughout the abdomen.

Patients often present late. Treatments frequently disappoint. Outcomes remain poor.

That is why a study presented this week generated so much excitement.

An experimental medication called daraxonrasib doubled survival among patients with previously treated metastatic pancreatic cancer.

Researchers have spent decades trying to target KRAS mutations. Many scientists referred to KRAS as “undruggable.”

Medicine has a habit of making fools of anyone who uses the word “never.”

This may be one of the most important cancer stories of the year.

Paid Subscriber Section

Today in the paid section:

• Photos of screwworm infections and what pet owners should know

• Why veterinarians are taking the Texas cases seriously

• The astonishing story of the sterile-fly program that eradicated screwworm in America

• Why the new obesity definition may change medicine more than most people realize

• What the pancreatic cancer breakthrough tells us about the future of cancer treatment

• Why I believe GLP-1 medications follow the same path statins did thirty years ago

Paid subscribers make this work possible. Thank you for supporting independent medical journalism and helping me make sense of the madness, bust a few myths, and teach a little medicine along the way.

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How a discussion about calculus readiness became a culture-war argument about merit, DEI, and the future of public education

A note to my usual readers.

This isn’t about GLP-1 drugs, Mediterranean diets, or medical myths. It is about something I care deeply about: education.

Over the past several weeks, I have watched a remarkable transformation take place online. A report written primarily by mathematics faculty at UC San Diego has been turned into proof of everything from the collapse of higher education to the triumph of DEI over merit.

The claims are familiar. Depending on who tells the story, UC students can no longer do middle-school math, admissions standards have collapsed, grade inflation has rendered transcripts meaningless, and DEI has replaced merit. If you spend enough time on social media, it is possible to conclude that the University of California admits students who cannot add fractions while rejecting future Nobel Prize winners.

After reading the report itself, I came away with a different conclusion.

The mathematics faculty have identified a real problem. The internet has made up another story.

Before going further, let me make something clear that may disappoint people on both sides of this argument. I am not opposed to bringing back SAT or ACT scores.

Standardized tests provide useful information. The UCSD mathematics faculty make a reasonable case that SAT Math scores were useful in predicting placement into their mathematics sequence. If the University of California decides to reconsider standardized testing, I would not oppose that discussion.

What the SAT scores actually do is help kids who come from poor high schools often overlooked. One irony in this debate is that standardized tests often help students assume they hurt. A gifted student from a small rural town, an underfunded school district, or a school nobody on an admissions committee has ever heard of can suddenly be seen. ZIP code does not distribute talent.

What I oppose is pretending the report says things it does not say.

And that is exactly what has happened.

Curiously, the report contains detailed information about mathematics preparation, but not the information most commonly cited in online arguments: where the students were educated, their socioeconomic backgrounds, or their racial composition.

What The Report Actually Found

The report documents a substantial increase in students requiring remedial mathematics before entering UC San Diego’s standard precalculus sequence. The authors note that between 2020 and 2025, the number of students whose mathematics skills fell below high-school expectations increased dramatically. They are clearly concerned. They should be.

If I were responsible for teaching calculus, I would be concerned too.

But there is an important distinction between the report’s conclusions and the conclusions people have projected onto it. The report identifies a mathematics preparedness problem.

It does not demonstrate an admissions failure.

Those are not the same thing.

That distinction matters, because most of the online discussion immediately skips the first question and assumes the second has already been proven.

Are California Schools the Problem

The longer I sat with the report, the more one question bothered me.

Not whether the mathematics faculty had identified a problem. They clearly had.

Not whether some students were arriving less prepared for calculus than their professors would like. The evidence for that was right there in the report.

The question I kept returning to was much simpler: Where did these students come from?

The report spends considerable time describing the students who need additional mathematical preparation. It discusses placement. It discusses preparedness. It discusses the possible causes. Yet I found myself searching for something that seemed obvious.

Were these graduates of California public schools?

California private schools?

Out-of-state schools?

International schools?

I may have missed it, but I never found that breakdown.

That omission matters, because much of the online reaction has transformed this report into an indictment of California education. Perhaps the data ultimately supports that conclusion. Perhaps they do not. The point is that we cannot know from the evidence presented.

Before I declare California schools the culprit, I would like to know whether the students in question were educated in California.

Is this another failure of DEI

One thing surprised me while reading both the report and the commentary surrounding it. The report is frequently cited as evidence of a DEI problem, but I could not find a breakdown showing the racial or ethnic composition of the students in remedial mathematics.

That does not mean such a pattern does not exist.

It means the report itself does not appear to establish it.

Before concluding that a preparedness problem is the result of any particular admissions policy, I would like to see the evidence.

The Table Everyone Keeps Posting

If you spend enough time on X, eventually someone posts a screenshot showing students struggling with fractions, decimals, or basic arithmetic.

The implication is always the same:

“These are the students UC is admitting now.”

The reality is more complicated.

The students in that table had already been placed into Math 2, a preparatory mathematics course. The assessment was not administered to all UC students. It was not administered to all STEM students. It was not administered to every student admitted to UC San Diego.

The students represented in that table matter. Their struggles are real. They deserve support.

What the table does not tell us is that all UC students are unable to perform those tasks. Some even made errors when they tested for basic fractions. The internet looked at two students missing a fractions question and declared that UC students cannot do fractions. I looked at the same table and saw two students who either did not know the answer or clicked too quickly. Out of thousands of students, that is not evidence of civilizational collapse. It is a rounding error.

The Number That Should Concern Us

The figure that deserves more attention is not the famous screenshot.

It is the finding that approximately 8.5 percent of students entering majors requiring mathematics were placed into Math 2, while additional students required Math 3B before entering precalculus pathways.

That is a real concern. Unlike the social media screenshots, this finding reflects a broader pattern observed by the mathematics faculty.

But even here, context matters.

The report discusses students entering majors that require mathematics. It is discussing placement into a mathematics curriculum. It is discussing preparedness for calculus pathways. This could be students studying biology, economics, psychology.

It is also not saying what happens to these students over time. It is not discussing whether they will graduate. It is not discussing whether they will become physicians, lawyers, researchers, teachers, or scientists.

It is discussing whether they arrive prepared for the mathematics sequence expected by their intended major. That is an important question.

It is not the only question a university must answer.

The Part Nobody Wants To Talk About

One of the reasons this debate frustrates me is that many who criticise the UC system based on this report want a villain.

For some people, the villain is DEI. For others, it is grade inflation. For others still, it is the SAT. Many of my conversations in social media were with people outside of California telling me, again, how terrible this state is. I love California, my only regret is not moving here sooner.

The report itself points in a different direction. It points to something far more complicated: an entire generation of students whose education was disrupted during some of the most important years of their academic development.

When COVID arrived, schools closed almost overnight. Teachers who had spent careers teaching in classrooms suddenly found themselves teaching through screens. Parents who had never imagined becoming part-time teachers found themselves supervising lessons, troubleshooting technology, and trying to keep children focused while also doing their own jobs.

Some families hired tutors. Many could not.

Some schools adapted quickly. Others were inventing solutions day by day, because there was no playbook for educating millions of children from their bedrooms and kitchen tables.

For younger children, some of that lost time could be recovered. A fourth grader who falls behind in multiplication still has years to catch up. A motivated student can accelerate, take summer courses, and regain lost ground.

My son moved to California when he was in the middle of 4th grade. He had a great school in Phoenix, a charter school. Then he came here, and six weeks after school started, we had to shelter in place. His school had to develop curriculum on the fly, lesson plans translated to Zoom. His mom stayed home and became his teacher. He easily lost half a year.

The challenge is different for students whose disruption occurred during the years when mathematics becomes increasingly cumulative, in high school. Meaning, those students at the UC system today were the ones in high school during COVID. And if you want to be painfully reminded about math in high school: Algebra builds on arithmetic. Trigonometry builds on algebra. Calculus builds on all of them.

Miss a concept in fourth grade, and you may struggle for a while. Miss a concept in Algebra, or just have rudimentary algebra in high school and your chance of making that up is not great. We can see the consequences.

The students entering college today are the students who experienced those disruptions during that critical time in high school. Many learned algebra, geometry, trigonometry, and precalculus through a laptop screen, while the world around them was shutting down.

Some students adapted well. Others struggled. Most probably fell somewhere in between.

The good news is that technology can also be part of the solution. Many mathematics programs now provide immediate feedback, alternative explanations, and individualized examples that simply did not exist when I was a student. Students often receive more practice and guidance than a traditional worksheet ever provided.

But technology does not erase disruption.

When educators talk about the “lost year,” they are not describing a single missed semester. They describe the ripple effects that occur when foundational skills are interrupted during critical stages of learning.

That reality does not fit neatly into a political argument. It does not provide an easy villain. It does not generate viral social media posts.

It does, however, provide a plausible explanation for at least some of what the UCSD mathematics faculty observe.

The Missing Outcome Data

It is not bad to have remedial programs in math for students. It is a proper way to handle the situation. The question becomes, were they so slowed down that it affected them throughout their college years?

Meaning, just because the kids need some remedial math does that mean they are behind in everything else? Are these students graduating? Are they completing their majors? Are they succeeding in graduate and professional schools? Are they becoming successful professionals?

Here is one fact: the University of California schools graduate more of their students than most public schools in the nation. Over 90% of the people who enter the UC system graduate. If the purpose of admissions is to identify students who can succeed at the University of California, graduation remains one of the most important outcomes we can measure. Those are the questions that ultimately matter.

The University of California remains one of the most selective public university systems in the world. It draws from the highest-performing students in the largest state in the nation. Every year, tens of thousands of qualified applicants are denied admission because there are simply not enough seats.

The system is not struggling to find talented students.

The challenge is to decide among many talented students.

That is a very different problem than the one being described online.

What We Should Actually Be Worried About

If there is a lesson in the UCSD report, it is not that higher education has collapsed. It is that educational preparation remains uneven.

Some schools recovered quickly after COVID. Others did not. Some students arrived with strong foundations. Others arrived with significant gaps.

The mathematics faculty at UC San Diego have identified a problem worth taking seriously. They have not proven the collapse of admissions, nor are they sounding that alarm.

The math teachers are not stating that the University of California has abandoned merit.

But they have identified a mathematics preparedness problem. That alone is important enough to deserve our attention. The other question is, will this still be an issue once the crop of students in high school during COVID goes through?

Conclusion:

I still think the mathematics faculty have identified something worth paying attention to. They may even be right that SAT Math would help identify students who need additional preparation before entering the mathematics sequence.

But after reading the report, I came away with a different concern than the one dominating social media.

I am less worried about DEI. I am less worried about California. I am less worried about merit.

I am more worried that we are still seeing the educational aftershocks of COVID, and that we are trying to explain them with political narratives instead of data.

The report raises important questions.

The answers are still being written.

Also this week: an experimental gene-editing treatment that may permanently lower LDL cholesterol after a single infusion, new evidence suggesting long COVID may be far more common than official estimates, the FDA’s review of reports of child deaths following COVID vaccination, and research showing that better cardiovascular health is associated with lower risk of severe COVID infection.

From outbreak preparedness to cutting-edge genetic medicine, Dr. Simpson separates evidence from headlines and explains what these stories mean for patients, physicians, and the future of public health.

Data beats dogma.

The question is what caused all this in the first place. What made those little insulin factories work so hard that they eventually became overwhelmed? If you spend enough time on social media, you already know the list of suspects. Sugar. Fat. Seed oils. Carbohydrates. Your grandmother’s dinner rolls. You’ve seen the social media wrestling matches, as people swear they stopped sugar and their diabetes disappeared. Somewhere there is an influencer explaining that the answer involves sunlight, grounding, beef tallow, and possibly the position of Jupiter.

The stories all follow a familiar pattern. Someone gives up sugar. Someone else gives up carbohydrates. Another person starts eating nothing but steak. Someone discovers oat groats and declares civilization saved. Their blood sugars improve. Their weight comes down. They claim victory and then assume they have discovered the universal answer for everyone else.

The trouble is that every one of these suspects has at least a little evidence against them. Sugar certainly looks guilty. Excess calories are clearly involved. Genetics matter. Activity matters. Stress matters. The problem is that none of them completely explain the mystery that bothered me when I was taking care of bariatric (weight loss surgery) patients.

Those patients improved before they lost enough weight to explain it.

The pancreas was behaving differently. Blood sugars improved. Insulin requirements dropped. Yet the scale had barely moved. If the pancreas was the struggling factory, somebody was sending it all those work orders. Somebody was demanding more and more insulin. Somebody was creating the environment that eventually overwhelmed those cells.

To understand modern type 2 diabetes, we need to leave Toronto, leave the pancreas for a moment, and follow the clues to another organ. As it turns out, the pancreas wasn’t acting alone. It had an accomplice, and, like many accomplices in detective stories, it had been standing in plain sight the entire time.

The liver.

Now before every hepatologist writes me an angry email, let me be clear. The liver is one of the most remarkable organs in the human body. It stores energy, detoxifies chemicals, manufactures proteins, regulates hormones, and generally works harder than most of us. But like many hardworking employees, when it becomes overwhelmed, it starts making mistakes.

The Pâté Is Not a Party

The liver is one of the great storage organs of the body. Earlier, I described glycogen as the snack drawer in the kitchen. If glycogen is the snack drawer, then the liver is the person responsible for stocking it.

When blood sugar rises after a meal, insulin tells the liver to take some of that glucose and store it as glycogen. Glycogen is simply glucose linked together into long chains, a form of energy that can be quickly broken apart when you need it. If you suddenly decide to run, climb a flight of stairs, chase your dog, or flee a bad lecture on nutrition, glycogen can be mobilized quickly.

That is what the liver is supposed to do.

But like the muscle cells and fat cells we discussed earlier, the liver can also become resistant to insulin. At first, this doesn’t seem like a major problem. The pancreas simply produces more insulin. Then more. Then more still. The blood sugars often remain normal, which is one reason type 2 diabetes can hide in plain sight for years.

Eventually, however, the liver begins changing its behavior.

Instead of efficiently storing glucose as glycogen, the liver increasingly converts excess energy into fat. At first, the fat accumulates inside the liver itself. This condition, called fatty liver disease, has become extraordinarily common. For some people, it remains relatively silent. For others, it progresses to inflammation, scarring, cirrhosis, liver failure, and eventually transplantation.

If you’re a goose in southwestern France, all that liver fat may eventually become pâté. If you’re a human, it becomes a referral to a hepatologist. One is served with toast points. The other usually comes with bad news.

But for our diabetes story, another problem emerges.

The liver does not simply store fat.

It exports it.

Warehouses do not like being overfilled, and neither do livers. Once the shelves are full, inventory starts leaving the building, whether you intended it to or not. The liver begins packaging fat into triglyceride-rich particles called VLDL, and sending them out into circulation. Some of that fat ends up in muscle. Some ends up in fat tissue. Some eventually reach the pancreas itself.

At the same time, the increasingly fatty liver becomes less responsive to insulin. Insulin is supposed to tell the liver to stop releasing glucose when enough is already present in the bloodstream. The liver begins ignoring that message. Fasting blood sugars rise slightly. Not enough for a diagnosis. Not enough for a patient to notice. Just enough for the pancreas to notice.

And the pancreas responds exactly the way it always has.

It produces more insulin.

For years, that strategy works. Blood sugars remain normal. Physicians are reassured. Patients are reassured. Meanwhile, inside the pancreas, the factory is running longer hours, adding extra shifts, and asking the cleanup crews to work overtime.

The VLDL particles create another problem, one that takes us from diabetes into cardiovascular disease. These particles are not simply little fat delivery trucks. Each VLDL (cholesterol carrying particle) carries an ApoB molecule. As the liver exports more VLDL, the number of ApoB-containing particles circulating through the bloodstream increases. Many of those VLDL particles will eventually be remodeled into LDL particles, but from the standpoint of the artery wall, that distinction is less important than people think. The artery sees ApoB-containing particles, and ApoB-containing particles drive atherosclerosis.

This is one reason type 2 diabetes and cardiovascular disease travel so often together. The liver is not merely creating a problem for the pancreas. It simultaneously increases the number of particles capable of entering the artery wall. The pancreas notices the increased demand. The arteries pay the price.

Now the pancreas has two problems instead of one.

The first is that the rest of the body is becoming more resistant to insulin, which means every tissue demands more of it. The second is that the pancreas is increasingly exposed to the very fatty acids exported from the liver. Those fatty acids, particularly one called palmitate, produced by the liver during de novo lipogenesis, do more than simply sit there. They impair insulin secretion, increase cellular stress, and make it harder for the beta cells to do their jobs.

In other words, the liver is not simply sending pollution downstream.

It is increasing demand, while simultaneously making production harder.

If you were running a factory, it would be like receiving larger and larger orders every week, while somebody slowly filled the machinery with dust. The workers are asked to produce more product with equipment that works a little worse every month. For a while, they compensate. Then they begin making mistakes. Then the cleanup crews fall behind. Then production begins to suffer.

This was the observation Roy Taylor helped put together. The liver and the pancreas were not separate stories. They were feeding each other. More liver fat led to more insulin resistance, more fat export, and more stress on the pancreas. A more stressed pancreas produced more insulin. Higher insulin levels stimulated the liver to create and store even more fat. Around and around the cycle went.

Taylor called it the Twin Cycle Hypothesis.

I still think of it as two factories making each other’s problems worse.

The reason this mattered is that Taylor made a prediction. If the cycle was real, then interrupting it should reverse the process. Reduce liver fat, reduce pancreatic fat, reduce insulin demand, and some exhausted beta cells should begin functioning again.

That prediction turned out to be correct.

And suddenly, the mystery of bariatric surgery begins to look very different. Maybe those beta cells weren’t magically recovering. Maybe, for the first time in years, somebody had stopped piling new work orders on the manager’s desk.

Continuous Glucose Monitors and Weight Loss Surgery

About this time, the continuous glucose monitor companies began making the rounds.

If you’ve never met a medical device representative, they are among the most optimistic people on Earth. They can look at a surgeon who has been awake since four in the morning, is covered in coffee stains, has dictated thirty notes, and somehow conclude that what he needs in his life is another device.

In this case, they were probably right.

The pitch was straightforward. Put this little sensor on the patient, and instead of getting a handful of blood sugar measurements each day, you can see everything. Every rise. Every fall. Every spike after a meal. Every low blood sugar at two in the morning. No guessing. No relying on patient memory. Just data.

Now I love data.

I became interested in cell biology because of data. I spent years studying viruses because of data. One of my favorite phrases is that science is delighted to be wrong, because when we are wrong, nature usually has a more elegant explanation than the one we invented.

So I thought the glucose monitors were a terrific idea. More importantly, I thought they were finally going to explain what I was missing.

By this point, I had patients who were no longer taking diabetes medications. I had stopped routinely restarting those medications after surgery because of the occasional emergency room visit from patients whose blood sugar had dropped too low. The nurses rarely called for insulin coverage. The glucose logs looked good.

Frankly, they looked too good.

I had spent enough years caring for diabetic patients to be suspicious of anything that looked too good. The nurses rarely called for insulin coverage. Patients returned to clinic reporting normal blood sugars. They weren’t refilling medications. The emergency room visits from low blood sugars had already convinced me to stop automatically restarting diabetes medications after surgery.

Yet I remained convinced there was something I wasn’t seeing.

The CGM would reveal the truth.

Then we started putting them on patients.

These were not “free” because I liked data. Patients paid for them out of pocket. They paid for them, because I told them we didn’t want to miss worsening diabetes or medication adjustments. They trusted me. Looking back, some early monitors cost more than my monthly car payment.

Which only increased my determination to find what I thought I was missing

The CGM would reveal the truth. Then we started putting them on patients. Now these were not “free” because I like data. Patients paid for these, out of pocket. They paid for them, because I told them we didn’t want to miss them needing medication. They believed me, and the price of the early monitors was more than my car payment.

Before surgery, the graphs looked exactly the way you would expect. Blood sugar climbed after meals. Medications pushed it back down. Sometimes it went too low. The patient felt shaky and miserable, drank orange juice, ate crackers, or grabbed whatever carbohydrate was within reach, and then the blood sugar shot back up again.

The graph looked less like a smooth metabolic process and more like a seismograph during a California earthquake. You could practically hear the pancreas screaming.

Then the patient had surgery. I expected improvement. Everyone expected improvement. What I didn’t expect was boredom. The curves flattened. The dramatic swings disappeared. The graphs became boring. And in medicine, boring is beautiful.

The blood sugars weren’t perfect every minute of every day, because human beings are involved and human beings have a remarkable ability to surprise physicians. But the pattern was unmistakable. The chaos was gone. The highs were lower. The lows were less common. The wild oscillations that had characterized diabetes seemed to settle down with surprising speed.

The device I thought would prove my patients wrong instead proved them right.

That is not always a comfortable moment in medicine.

Physicians like to think we are objective observers, but we carry our own assumptions around just like everyone else. I assumed there were blood sugar excursions hiding between measurements. I assumed the diabetes was not improving as quickly as it appeared. I assumed the scale would eventually explain everything.

The CGM quietly disagreed.

Day after day, patient after patient, it showed the same thing. Blood sugars were normalizing long before the weight loss story should have reached that chapter.

The pancreas had gotten the message.

The scale had not.

Now, when something doesn’t fit the model, you have two choices. You can ignore it and defend the model, which is popular on social media. Or you can assume the observation is trying to teach you something.

Fortunately, medicine eventually found people willing to ask the next question. If the pancreas was improving before the weight loss arrived, what exactly was changing first?

What elegant story was mother nature trying to tell me?

The Lives of a Cell, a Beta Cell

The answer, it turned out, was both simpler and more complicated than I expected.

One thing I noticed over the years was that not every patient responded the same way. That should not be surprising, but it turned out to be important.

Most of my patients were relatively young. Many had been diagnosed only a few years earlier. They were developing diabetes, not carrying it around like an old suitcase for twenty years. Those patients often had dramatic improvements. Medications disappeared. Blood sugars normalized. Some looked as though they had left diabetes behind entirely.

Other patients improved, but not as dramatically.

The difference was often time.

The longer a patient had diabetes, the harder it became to achieve the same degree of recovery. Looking back, that makes perfect sense. If you interrupt the cycle early, many exhausted beta cells are still present. They are overworked, stressed, and functioning poorly, but they are still there. Give them a chance to recover, and they often surprise you.

Wait too long, however, and the story changes. Some cells do not recover, because some cells are gone.

You can give the remaining workers a vacation. You can reduce the workload. You can clean up the factory. But if half the workforce retired ten years ago, production will never return to where it once was.

That observation became one of the strongest evidence that we were not witnessing a miracle. We simply found that mother nature had left us an egg. The earlier the intervention, the more cells remained available to recover.

The longer the disease had been present, cells limited, the more recovery already lost.

For this group of patients, not all the islet cells were dead. Some were exhausted, overworked, and filled with misfolded proteins. In a coma, like those kids in Toronto in 1922.

What I had been watching after surgery was not a miracle. I had not performed CPR on an islet cell. I had rearranged the plumbing.

Somewhere, Gene Wilder is shouting, “It’s alive!”

The remarkable thing was that the beta cells still had enough reserve capacity to recover once the workload fell. The liver didn’t need to export fat. The body required less insulin. The pancreas could finally catch its breath. The cleanup crews inside the cells could start working through the backlog. Some of those exhausted factories reopened for business.

That realization changed the way I thought about type 2 diabetes.

The old model focused almost entirely on blood sugar due to excess weight and insulin resistance. The newer model focuses on the organs producing and responding to insulin. Blood sugar is still important, but blood sugar is the smoke. The fire is happening in the liver, the pancreas, the fat tissue, and the metabolic machinery connecting them.

I must admit there was one casualty.

The continuous glucose monitor salespeople.

Once I became convinced that most postoperative patients were doing well, I stopped recommending CGMs nearly as often. They had served their purpose. The devices I thought would uncover hidden problems had instead helped confirm that recovery was occurring much faster than I had imagined.

The important lesson is not that surgery is magical (those are the surgeon’s hands). The important lesson is that the beta cell is dynamic.

Beta cells probably have a limited lifetime, a Hayflick limit. But unlike muscles, more work does not make the cell live longer. Instead, it will struggle, and over the years, when it cannot clean out the waste material, that cell will die, and the body will replace it with scar tissue. But if you give it a chance to recover, give it a break, many of them respond beautifully.

That raises an obvious question.

If surgery works because it interrupts the cycle, reduces liver fat, lowers insulin demand, and allows beta cells to recover, then do we need surgery to accomplish those goals?

As it turns out, not always.

And that brings us to fasting, low-carbohydrate diets, Mediterranean diets, and eventually GLP-1 medications. Because once we understood the mechanism, we could begin asking a different question.

Not whether the cycle could be interrupted.

But how. And this brings us to the stories of diets, exercise, and GLP-1.

Fasting, Diets, and the hungry cell

Once you understand the twin cycles, many arguments in nutrition suddenly become less interesting.

For decades, we have searched for dietary solutions to diabetes. That should not surprise anyone. Before insulin, diet was the only treatment for type 1 diabetes. It was not a successful treatment, but it was all physicians had. Then Banting, Best, and insulin arrived, and suddenly children who would have died could live.

Type 2 diabetes was a different disease entirely.

We had medications, of course. Metformin remains one of the great drugs in medicine. Eventually, we added sulfonylureas, TZDs, DPP-4 inhibitors, SGLT2 inhibitors, insulin, and a growing alphabet soup of therapies. But dietary interventions never disappeared, because, unlike type 1 diabetes, food was clearly part of the story.

One of the more influential modern approaches came from Jason Fung. Fung took patients with advanced type 2 diabetes, encouraged fasting, reduced carbohydrate intake, and reported something remarkable. Patients lost weight. Blood sugars improved. Medications were reduced. Some patients achieved remission of diabetes.

At the time, people argued endlessly about whether fasting worked because of insulin, carbohydrates, ketosis, autophagy, ancient evolutionary pathways, or some other mechanism. Looking back, the answer appears both simpler and more interesting.

Fasting reduced the workload.

When patients stop eating for prolonged periods, glycogen stores are used. Liver fat begins to decline. Less insulin is required. The pancreas gets a break. Not the dramatic interruption produced by bariatric surgery, but an interruption nonetheless. The factory receives fewer work orders.

Low-carbohydrate diets often produce similar results. The advocates usually identify sugar as the villain. Sometimes carbohydrates become the villain. Occasionally, entire food groups are marched before a nutritional firing squad. Yet many patients lose weight, improve insulin sensitivity, reduce liver fat, and improve blood sugar control.

The more extreme carnivore versions often produce the same early story. Weight falls. Blood sugar improves. Diabetes improves. The mistake occurs when the observation is mistaken for proof of the explanation. Improvement in diabetes does not prove that carbohydrates caused diabetes, but improvement after surgery proves that stapling a stomach cures pancreatic disease.

What matters is that the metabolic workload has been reduced.

The Mediterranean diet arrives at many of the same destinations by a different road. It does not eliminate carbohydrates. It does not require ketosis. It does not require anyone to pretend vegetables are optional. Yet study after study shows reductions in diabetes, cardiovascular disease, and mortality. Patients often lose weight. They eat fewer calories without spending every waking moment thinking about calories. Liver fat declines. Insulin sensitivity improves.

In light of the biology, none of this should be surprising.

The body does not care whether you arrived there through fasting, carbohydrate restriction, Mediterranean eating, calorie reduction, exercise, or surgery. What matters is whether the liver accumulates fat or loses it, whether insulin demand is rising or falling, and whether the pancreas is being asked to work overtime.

The problem is not finding a diet that works. Most diets work. The problem is finding a diet that continues to work after the enthusiasm fades. The ice cream diet sounds great until you are on the second week and find that you have no interest in ice cream at all.

Exercise deserves special mention, because it works through several pathways simultaneously. It improves insulin sensitivity, burns glycogen, preserves muscle mass, and reduces the burden on the pancreas. If exercise were a medication, every physician in America would prescribe it. The problem is not the biology. The problem is adherence.

I know this because I owned a Peloton for two years.

I even used it once.

Yet here I am at sixty-nine, suddenly excited about yoga—I’ve been doing it for four years now—and trying to learn acrobatic planks. The lesson is not that yoga is superior to cycling. The lesson is that the best exercise program is the one you will actually do next Tuesday.

This is one reason exercise improves diabetes, even when weight loss is modest. The muscles become better customers. They take glucose more efficiently, require less insulin, and help reduce the burden placed on the pancreas. In our warehouse analogy, exercise does something diets often struggle to do: it empties the shelves while simultaneously creating room for the next shipment.

Most people know they should exercise. Most people even intend to exercise. Then life happens. Children happen. Jobs happen. Travel happens. Netflix happens. The challenge has never been proving that exercise works. The challenge has always been convincing human beings to keep doing it long enough for the benefits to accumulate.

And that turns out to be true for almost every intervention in diabetes.

This is where nutrition collides with human nature. Some people become loyal followers of Weight Watchers. Others become evangelists for low-carbohydrate eating. Others discover Mediterranean eating and never look back. A few become convinced that mankind evolved exclusively to consume ribeye steaks while contemplating mammoths.

People are wonderfully diverse.

Human nature is remarkably consistent.

The uncomfortable reality is that sustained remission through dietary intervention alone is uncommon. We hear the testimonials because success stories are interesting. We rarely hear from the far larger group of people who quietly regained weight, saw diabetes return, and moved on with their lives.

This is one reason bariatric surgery remained so important for so long. Study after study demonstrated rates of diabetes remission that dietary interventions struggled to match, particularly over the long term. Surgery did not work because it was magical. It worked because it reliably interrupted the cycle. Unlike most diets, patients could not simply quit it on a Tuesday afternoon after a stressful day.

But science had another surprise waiting.

A new class of medications appeared capable of producing many of the same biological effects without an operating room.

And suddenly bariatric surgeons began looking like manufacturers of buggy whips watching the first automobile drive down the street.

The Drug That Shouldn’t Work This Well

Imagine a drug that is remarkably close to bariatric surgery in terms of weight loss.

Now imagine the same drug lowers blood sugar, improves fatty liver disease, reduces cardiovascular events, improves kidney disease, quiets food cravings, and appears to help preserve some of the very beta cells we have spent this entire article discussing.

If I had told you twenty years ago that such a drug was coming, most physicians would have laughed. Many surgeons would have laughed harder.

For most of my career, the most effective treatment for severe obesity and type 2 diabetes involved anesthesia, staplers, operating rooms, and a patient willing to let me rearrange their plumbing. The results were often remarkable. Patients lost weight. Blood sugars improved. Medications disappeared. Fatty livers improved. Some patients achieved long-term remission of diabetes.

When weight loss surgery was compared to any lifestyle or diet, weight loss surgery won that argument again and again. In multiple papers, but here was a drug that did what we couldn’t do - people would take a drug, and less than 2 percent of people eligible for surgery would choose to have an operation.

What fascinated me most, however, was never the weight loss. It was the timing. The diabetes often improved before the weight loss could explain it.

That observation bothered me for years. The hospital records showed it. The glucose logs showed it. The continuous glucose monitors showed it. The pancreas seemed to get the message before the scale did.

Then along came the GLP-1 medications.

The first of these drugs reached the market in 2005. Exenatide was developed from a peptide discovered in the saliva of the Gila monster, which proves that Mother Nature is far more creative than most pharmaceutical companies. The early drugs effects were modest by modern standards. They improved blood sugar control. Patients lost some weight. Insulin sensitivity improved. Beta-cell function appeared to improve.

Interesting, but not revolutionary. The push for better drugs is driven by the marketplace, and weight loss and better diabetic control led to learning more about the GLP-1 pathway, and making drugs that have more effect.

Patients were losing far more weight than expected. Blood sugars were improving more rapidly than expected. Fatty liver disease was improving. Cardiovascular risk was falling. Some patients described something physicians rarely measure and almost never discuss.

The food noise disappeared. As a bariatric surgeon, that caught my attention immediately. At first when someone said that, it was a patient who had a RNY gastric bypass, and now, on some peptide, she said her head was in a better place. I didn’t frankly believe it. But her results were clear. Then came in a patient who wanted a revision because she had regained her weight years after her RNY bypass. I decided to try her on Ozempic, and over the next six months she lost more weight than she had after her initial bypass. But here was the other key, after she gained some, she developed diabetes, something she had not had before, so the Ozempic was for that. But it did more.

Her story sounded familiar. Less food entering the system. Less liver fat, something we could see on our ultrasound. Less insulin demand. More opportunity for exhausted beta cells to recover.

In other words, many of the same biological pathways that had made surgery so effective appeared activated by a weekly injection. And instead of a complex revisional surgery, we had a weekly injection doing the same thing, and in this case better, than her RNY bypass.

What fascinated researchers was that the story did not stop at appetite.

As the studies accumulated, it became clear that GLP-1 drugs were doing far more than helping people eat less. Beta cells survived longer. Some studies suggested new beta-cell formation. Damaged beta cells appeared better able to recover. The mitochondria inside those cells—the tiny power plants responsible for producing energy—functioned better and were protected from some of the metabolic stress that accompanies diabetes.

The liver was changing too.Insulin sensitivity improved. Fatty liver disease improved. The constant export of fat from the liver slowed. The very cycle Roy Taylor had described years earlier appeared interrupted from multiple directions at once.

That was the part that caught my attention.

For years, I had watched surgery improve diabetes before the weight loss could explain it. Now I watched a medication produce many of the same effects. Not identical effects, and certainly not in every patient, but enough similarities that it became impossible to ignore.

A peptide discovered through studying the saliva of a desert lizard was influencing the pancreas, the liver, the gut, the brain, and perhaps even the survival of the very cells responsible for making insulin.

That is not a weight-loss drug, it is a metabolic drug.

And to understand why it works, we need to go back to a discovery that changed how we think about the gut itself.

Because your intestines are not simply a tube that absorbs food.

They are one of the most sophisticated endocrine organs in the human body.

Remember When I Told You Insulin Was a Peptide?

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One of my favorite sayings is that in science, we love to be proven wrong.

Not because we enjoy being embarrassed. Not because we enjoy discovering that years of teaching, research, and clinical experience were incomplete. We love being proven wrong, because whenever nature proves us wrong, she usually has a more elegant solution than the one we started with.

The story of type 2 diabetes is one of those moments. Probably what you think about adult onset diabetes is from our old model. A model that served us well, and still does.

This is not one of those articles that begins with, “Everything you’ve been told is a lie.” Usually when somebody says that, they are about to sell you a supplement, a diet book, or a conspiracy theory.

Instead, this is the story of how medicine changed its understanding of a disease that affects millions of Americans. It is a story of clinical observations, laboratory discoveries, arguments between scientists, and a handful of stubborn facts that refused to fit the model we were using.

Because if you understand how type 2 diabetes actually develops, you won’t be fooled when somebody tells you they can cure it. You’ll understand why bariatric surgery can place diabetes into remission. You’ll understand why GLP-1 medications work so well. You’ll understand why fasting sometimes works, why weight regain can bring diabetes back, and why the word “remission” is usually more accurate than the word “cure.”

Most importantly, you’ll understand why sugar is probably not the villain most people think.

Sugar is more like the person standing over the body holding the knife when the detective walks into the room.

It certainly looks guilty. And blood sugar is involved. But it isn’t the whole story.

For most of my career, the explanation for type 2 diabetes seemed straightforward. People gained weight, became insulin resistant, their pancreas worked harder and harder until eventually it could not keep up. Blood sugars rose. Medications were added. More medications were added. Eventually insulin entered the picture. Lose enough weight and diabetes improved, because insulin resistance improved.

Simple. Elegant. Mostly right.

One of the reasons we performed bariatric surgery on patients with obesity and type 2 diabetes was because we expected exactly that sequence of events. Weight comes down. Diabetes gets better. Lose enough weight and medications can be reduced. Lose more weight, and perhaps the patient no longer needs them.

Even insurance companies eventually accepted that logic. And if you’ve ever worked with insurance companies, getting them to agree to pay for something is roughly equivalent to convincing a Venetian gondolier to install a freeway.

Here comes the mystery, though. My weight loss surgery patients did not follow that model’s timeline. Diabetes was improving before weight loss, and that should not have happened. The entire logic of the model predicted the opposite sequence. Weight loss first. Better diabetic control second. Instead, the body seemed determined to rearrange the order of events.

The Observation

Like most surgeons, I operated on patients with obesity and type 2 diabetes. Some were taking insulin. Some were taking enough insulin that forgetting it on vacation caused more panic than forgetting their wallet. Others were on metformin, a sulfonylurea, and whatever new diabetes medication the pharmaceutical industry had recently named after what sounded like a Scandinavian airport.

But let me separate the weight loss surgery patients from the other patients. In these cases, the operation would go well. They would spend a night or two in the hospital. Like every surgeon, I left orders for blood sugar checks and insulin coverage if needed. Pretty standard stuff.

The moment I realized something strange was happening came early in my career.

I got a call from the emergency room about one of my postoperative patients. She had surgery a few days earlier, went home, followed her instructions, took her diabetes medications exactly as prescribed, and ended up in the ER with dangerously low blood sugar.

At first I thought it was an isolated event. One patient, one strange reaction, one of those things medicine files away under “well, that was interesting.”

Then it happened to another patient.

That is when I stopped automatically telling patients to resume their diabetes medications after surgery. Instead, I told them to watch their blood sugars and only restart medication if the numbers began climbing.

In the hospital, we never order their usual medicines for diabetes. Patients are without food, so they might not be eating enough, or not at all, so we would inadvertently drive their glucose too low. Or events can happen that drive sugar up. So most of the time, we write a sliding scale for our surgical patients, so nurses check the blood glucose and add insulin based on their glucose level. Sometimes our scale is too conservative, and we get a call from the nurses that the blood sugars are high and we need to add more short acting insulin. Rarely the opposite happens. In the hospital, our preference is to go up rather than down. So our scale starts with a small amount of insulin to cover higher blood sugars.

After those two patients had low blood sugars, I noticed that my weight loss surgery patients did not generate calls from the nurses about insulin. That was not the case with patients who had other operations - like colon surgery, or removing a gallbladder. Non weight loss patients with obesity and diabetes, I received calls to adjust the insulin.

Surgeons notice patterns. We especially notice patterns at two o'clock in the morning. Before long, I realized I was sleeping through nights for weight loss surgery patients.

The Review

That seemed like more than a coincidence. So I went back and looked at the data. I reviewed the hospital glucose logs for my surgical patients. I looked at the sliding-scale insulin orders I had dutifully written after surgery.

The funny thing was that the insulin was rarely given for weight loss surgery patients. The orders were there. The insulin was available. The blood sugars were all pretty normal, and the patients didn’t need the short-acting insulin.

The exception was the first 24 hours, as the operation itself raises blood sugar. Surgery is a stress to the body, and cortisol goes up. Stress hormones rise. The body reacts to being operated on in much the same way most people react to seeing their first hospital bill. There is a stress response.

What didn’t make sense was how many patients never needed coverage at all. Then they would return to the clinic. I assumed they would be a bit on the “sweet” side, with higher blood sugars, and need to have medicine restarted. But they didn’t.

Weeks later, many still weren’t taking insulin or metformin. Months later, some still weren’t.

Why Did Diabetes Improve Before Weight Loss

Diabetes improved before weight loss. That didn’t fit the conventional model. Somehow the body had gotten the message before the scale did. The pancreas produced enough insulin, and the cells were sensitive to that insulin long before enough weight had disappeared to explain it.

It is not that my surgical stapler replaced an endocrine organ, although we now call ourselves “Metabolic and Bariatric Surgeons.” It is because the body indeed had a far more interesting role, and diabetes is more interesting than we knew.

In science, we build models to explain nature. Dogma never wants to be wrong. But in science, we love when we are proven wrong. Because that means mother nature has a more elegant solution.

The Hormone That Changed Medicine

To understand why the pancreas got the message before the scale did, we need to understand insulin. And to understand insulin, we need to travel to Toronto in 1922.

Insulin is a peptide, which means it is a chain of amino acids linked together like pearls on a necklace. Yes, a peptide is the same category of molecule that gym bros are trying to sell you out of the back of a truck. Semaglutide is a peptide. Tirzepatide—Zepbound—is a peptide. But long before social media discovered peptides, insulin was the peptide that changed medicine.

Its job is remarkably simple. Insulin acts like a key. When glucose circulates in the bloodstream, insulin tells cells to open the door and let that glucose enter. Once inside, the cell can use glucose to produce energy, repair itself, and perform all the countless little jobs that keep you alive.

Without insulin, the glucose remains trapped outside the cell. Blood sugar rises, but the cells themselves are starving. It is like standing outside a restaurant with your wallet full of cash while every door is locked. There is food everywhere, but you still cannot eat.

This is what happens in type 1 diabetes. Before insulin was discovered, children literally starved to death while surrounded by food. Their blood sugars climbed higher and higher, but the glucose could not get into the cells where it was needed. When blood sugar levels become extreme, the body begins to fail. The brain, which normally runs primarily on glucose, starts shutting down. Patients become confused, then unconscious, and eventually die.

The remarkable thing about insulin is that it is not simply a string of amino acids. Like almost every protein in the body, it must fold into a very specific three-dimensional shape. Imagine some of those amino acid pearls are tiny magnets. Certain parts of the chain attract other parts, causing the molecule to bend, twist, and fold into a very precise structure.

When the folding happens correctly, you get a functional insulin molecule—a key that fits the lock.

When the folding goes wrong, you get something else entirely.

Think of making copies of a house key. One copy is perfect and opens the front door. Another is slightly warped. It looks like a key. It feels like a key. But when you slide it into the lock, nothing happens.

Proteins are the same way.

A properly folded insulin molecule can do its job. A misfolded insulin molecule cannot.

And that matters a lot, because the cells that make insulin spend their entire lives acting like tiny factories, producing enormous quantities of this protein day after day. The harder those factories are pushed, the more opportunities there are for mistakes, misfolded proteins, and eventually trouble.

Islet of Langerhans - Not A Place to Scuba Dive

The cells that produce insulin are a very specific type of cell found in the pancreas. They are called the Islets of Langerhans, named after Paul Langerhans, a German medical student who spent a lot of time staring down a microscope. Medical students have been doing that ever since, although now they have debt and PowerPoint.

These cells have one primary job: make insulin when the body needs insulin.

Sometimes that need is obvious. Eat a large meal, especially one rich in carbohydrates, and blood glucose rises. The Islet cells respond by producing more insulin, allowing that glucose to move from the bloodstream into cells where it can be used for energy.

Not all of that glucose is burned immediately. Some of it is stored.

The liver takes glucose molecules and links them together into glycogen. Muscles do the same thing. Think of glycogen as the body’s quick-access energy account. If you suddenly decide to run, climb a hill, chase your dog, or flee a bad lecture on nutrition, glycogen can be rapidly broken apart and converted back into glucose.

That is important, because glycogen is easy to mobilize.

Fat is not.

Fat is wonderful for long-term energy storage. If human beings were designed for surviving famines, fat is the pantry in the basement. Glycogen is the snack drawer in the kitchen. When the body needs energy right now, it reaches for glycogen first.

Remember that. The liver and glycogen will become important characters later in this story.

But first, let’s go back to insulin.

In type 1 diabetes, sometimes called juvenile diabetes, the story is very different. In these patients, an autoimmune process destroys the Islet cells. We think viral infections may trigger this process in genetically susceptible individuals. By the time these children come to medical attention, the cells that produce insulin are largely gone.

No insulin.

No backup plan.

No second chance.

Without insulin, glucose remains trapped in the bloodstream, while the cells starve. Children become tired. They lose weight despite eating. They drink enormous amounts of water, because the kidneys desperately try to flush excess glucose out of the body. They urinate constantly. Parents often describe a child who seems exhausted, thirsty, and somehow not themselves.

When they present with type 1 diabetes, the game is essentially over for those Islet cells. The factory has been destroyed. If we do not replace insulin, they die.

That is why the discovery of insulin was one of the great miracles of modern medicine.

Before insulin, physicians could diagnose type 1 diabetes. They could not treat it.

Children were often placed on starvation diets to prolong life for a few months. Parents watched their children waste away, while doctors watched helplessly.

Then along came Frederick Banting and Charles Best. And medicine changed forever.

The idea of insulin was not new.

Scientists already suspected the pancreas produced some mysterious substance that controlled blood sugar. They knew that removing the pancreas from animals caused diabetes. They knew that something coming from the pancreas was essential for life.

The problem was not the theory. The problem was getting the stuff.

The pancreas is a messy organ. Most of it is devoted to making digestive enzymes powerful enough to dissolve food. Mixed among those enzyme-producing cells are tiny islands of hormone-producing cells—the Islets of Langerhans. Somewhere inside those tiny islands was the substance physicians desperately wanted.

Frederick Banting was not trying to invent a new hormone. He was trying to isolate one that nature had already invented.

Working with Charles Best in Toronto, Banting began extracting material from animal pancreases, hoping to separate the life-saving substance from the digestive enzymes that contaminated it. The work was tedious. The extracts were crude. The science was messy. Most breakthroughs look much better in history books than they do while they are happening.

In January 1922, they treated Leonard Thompson, a fourteen-year-old boy dying of diabetes. Before insulin, children like Leonard had only one treatment available: starvation. Physicians would place them on semi-starvation diets, hoping to prolong life for a few months. Everybody knew how the story ended.

The first injection was disappointing. The extract was too impure.

Then biochemist James Collip improved the purification process.

A second injection was given.

This time it worked.

Blood sugars fell. Ketones disappeared. The boy improved.

Word spread quickly.

Soon insulin was being given to children throughout Toronto. Physicians who had spent years watching children waste away suddenly saw them sit up in bed, regain strength, begin eating, talking, laughing, and returning to life. One physician described the transformation as miraculous. Another compared it to watching the dead rise.

It is difficult for us to appreciate what that must have felt like.

Today, insulin is so common that it is easy to forget that before 1922. A diagnosis of type 1 diabetes was essentially a death sentence. Then, almost overnight, it wasn’t.

Few discoveries in medicine have changed the fate of so many people so quickly. The Nobel Prize followed in 1923. Banting was only thirty-two years old, one of the youngest Nobel laureates in history. He shared his prize money with Charles Best because he believed his young collaborator deserved equal credit.

The remarkable thing is that even after insulin was discovered, physicians still didn’t fully understand diabetes.

They had found the key. We still didn’t understand the lock.

History likes heroes, so we remember Banting and Best. What physicians remembered was something else. They remembered walking into silent wards, and finding children sitting up, talking, laughing, and asking for food. The miracle wasn't one child. It was an entire ward returning to life.

The Little Factory That Could

So if Type 1 diabetes is a disease where the factory has been destroyed, what exactly is Type 2 diabetes? For years, we thought we knew the answer. Its rise has paralleled the rise in obesity, and that is hardly surprising. What surprises many people is not finding someone with obesity and type 2 diabetes. The surprise is finding someone who is obese and doesn’t have it.

We know that the Islet cells in the pancreas produce insulin, and we know that people with type 2 diabetes require more insulin than normal. The most common reason is simple: excess calories. Those calories can come from sugar, bread, pasta, steak, butter, or olive oil. The body doesn’t care whether the excess energy arrived wearing a candy wrapper or a cowboy hat. Excess calories require more storage, more processing, and ultimately more insulin.

As more insulin is required, the cells of the body become somewhat resistant to insulin’s effects. That means the pancreas has to produce even more insulin to accomplish the same task. Think of it this way: if insulin is the key that unlocks the cell, eventually the lock becomes a little sticky. The key still works, but you need more effort to open the door.

Now let’s go back to our Islet cells.

Imagine a cardboard box factory. Every day the factory makes boxes. The boxes are folded, inspected, stacked, and shipped out. Life is good.

Then Amazon arrives. Suddenly everyone wants more boxes.

The factory ramps up production. More workers. More shifts. More pressure. Most boxes are assembled correctly, but some are folded improperly. Those defective boxes don’t get shipped. Instead, they get tossed into a corner where the factory can take them apart and recycle them.

At first, that works fine. But demand keeps increasing. More boxes are made. More mistakes occur.

Soon, the corner of the factory is piled high, with defective boxes waiting to be broken down and recycled. Eventually, there are so many bad boxes that the factory cannot function efficiently anymore.

Something similar happens inside the beta cell.

As insulin production increases, more proteins must be folded correctly. Most are. Some aren’t. Those misfolded proteins accumulate inside the cell and create stress on the cellular machinery. The cell activates emergency cleanup systems, attempting to break down the defective proteins and restore order.

For a while, the cell keeps up. Then it doesn’t.

The beta cell becomes dysfunctional. It stops producing insulin efficiently. In some cases, it essentially goes on strike, shutting down production while trying to clean up the mess. In other cases, the stress becomes so severe that the cell dies and the body removes it entirely.

The remarkable thing is that we cannot see any of this happening. Patients don’t feel a beta cell struggling. They don’t feel a protein misfold. Nor do they feel the cellular cleanup crews working overtime. That process uses an inflammatory pathway.

What we see instead is blood sugar slowly creeping upward over years. By the time the diagnosis of type 2 diabetes is made, studies suggest roughly half of beta-cell function has already been lost, and many insulin-producing cells are gone altogether.

Some cells are dead. Others are not functioning because they “are exhausted.” Kind of like my teenager after school, who stops doing work and finds a video game. Those cells are clogged with the cellular equivalent of unfinished paperwork.

The remaining cells simply work harder. That is why type 2 diabetes often progresses quietly for years before anyone notices.

And it raises an important question: if some of those cells are not dead, but merely exhausted, what happens if we can reduce the workload and give them a chance to recover?

So where does that leave us?

We began with a mystery. Why did my patients stop needing insulin before they lost enough weight to explain it? We followed the story from the hospital ward to Toronto, from Banting and Best to the Islets of Langerhans, from insulin itself to the tiny cellular factories that spend their lives trying to produce enough of it.

Along the way, we learned something important. Type 2 diabetes is not simply a disease of high blood sugar. Blood sugar is what we measure. It is not the disease itself.

The real story is happening inside cells. It is happening inside the pancreas. It is happening long before a patient ever receives a diagnosis. By the time type 2 diabetes is recognized, many of the cells responsible for producing insulin have already struggled for years. Some have recovered. Some are exhausted. Some are gone forever.

But that still doesn’t answer the question that started this story. Why did those patients improve before they lost the weight? How could a pancreas that appeared to be failing suddenly begin working better? And what does the liver have to do with any of this?

In Part Two, we’ll follow the next clue in the mystery. We’ll meet the organ that may be doing more to drive type 2 diabetes than most people realize. We’ll look at Roy Taylor’s Twin Cycle Hypothesis, why fasting sometimes works, why low-carb advocates are seeing something real, but not the entire picture, and why the Mediterranean diet may be one of the most effective long-term treatments we have.

Most importantly, we’ll return to the modern mystery: why GLP-1 medications appear to improve diabetes faster than weight loss alone should allow.

Because the pancreas got the message before the scale did.

And we’re finally starting to understand why.

There is a moment that almost every person trying to lose weight encounters. It happens after the excitement of the first few weeks or sometimes months. The scale has been moving steadily down, clothes fit differently, knees hurt less, people start commenting on your appearance, and then one morning you step on the scale and nothing happened.

Or worse, it went up two pounds.

That is the moment panic enters. Patients who were feeling successful suddenly feel as if they failed. They start searching online for metabolic damage, starvation mode, insulin spikes, cortisol surges, hidden carbohydrates, lectins, seed oils, toxic fruit, or whatever the newest nutrition cult is selling this week.

I’ve watched this happen for years as a bariatric surgeon. I watched it after sleeve gastrectomy, after gastric bypass, after lap bands, after medically supervised diets, and now I see it with GLP-1 medications like Zepbound and Wegovy.

And now, being on a GLP-1 myself, I understand the psychology of it even better.

The plateau feels personal. It feels like betrayal. But biologically, plateaus are normal. In fact, they are expected.

Weight loss is not a slide. It is a staircase.

You lose weight, then pause. Lose again, then pause. Those pauses become the landings on the staircase, and the farther down you go, the longer the landings tend to become. Early weight loss often includes glycogen depletion and water loss, especially when appetite changes dramatically. Later, some glycogen and water return. One salty dinner, alcohol, poor sleep, travel, constipation, or simply eating later than usual can move the scale several pounds overnight.

Glycogen is a way to store energy in your muscles that is more readily available than fat. If you look at glycogen, it is simply one molecule of glucose strung to another. Your body can break this down quickly to get the fast energy it needs for almost anything. You store this in your liver, your muscles, and your heart. When you first lose weight and your body needs energy, it breaks down glycogen. With gram of glycogen, you break down, and you also lose slightly more of that in water, as the glycogen is stored in water. This is why you get fast weight loss on low-carb diets. It isn’t fat, it is breaking down glycogen.

That is not fat.

The human body is not gaining three pounds of fat because you had sushi on Saturday. But if you had a lot of soy sauce with the sushi, that extra salt doesn’t just urinate away overnight.

I wish more people understood this, because modern diet culture has convinced people that every fluctuation is either virtue or failure. It isn’t. It is physiology.

This is why I like regular weigh-ins. Daily or weekly is fine if you understand what you are looking at. I personally use a Withings scale, because I like watching trends in fat mass and lean mass, rather than obsessing over a single number. If body weight stays stable, but muscle mass improves while fat mass decreases, that is a victory. If you are walking farther, climbing stairs easier, sleeping better, or fitting into smaller clothes, those count too.

The scale is a tool. It is not a morality test.

What I have learned over the years is that the biggest issue during a plateau is usually not what people are eating.

It is how they are eating.

One of the clearest signs a GLP-1 dose may need adjustment is speed. How fast are you eating? I do not mean compared to a competitive eater. I mean compared to a normal human sitting at a table. Patients often tell me their medication stopped working, and then I watch them finish an entire meal in under ten minutes.

That is not medication failure. That is outrunning your biology.

GLP-1 medications help slow gastric emptying and amplify satiety signals, but those signals are not instantaneous. If you eat rapidly, you can overshoot fullness before your brain catches up. You can overwhelm the system.

And this is where I have learned something important both from patients and myself: if the medication tells you to stop, people stop. But if the medicine isn’t having an effect on people tend to stop when the plate is empty, rather than hearing that simple signal in the brain.

People often say, “I felt full, but I kept eating.”

That sentence contains the entire problem.

The best part of food is the first or second bite. You get the flavor, the texture, the little reward of a new bite. But after that you are either eating to feel “full” or until it runs out.

With GLP-1, after that first bite, the food becomes less interesting, less rewarding, so stopping sooner is pretty easy. But if that food tastes great you can eat past where a GLP-1 medicine tells you to “slow down and walk away.” If food is becoming less interesting, if the urge to continue fades, if you feel pressure, fullness, or simply loss of desire for the next bite, then the medication is working. The mistake is treating fullness as a suggestion instead of an endpoint.

You do not have to finish the plate, because the restaurant gave you too much food. You do not have to “get your money’s worth.” You do not have to clean your plate because of some childhood guilt left over from another generation.

First Box it Up. Then Eat less. Walk away. Box it up.

You can always return later.

Most of the time, you won’t.

One of the biggest mistakes people make during plateaus is falling back into all-or-none thinking. One high-calorie meal becomes “I blew it.” One weekend away becomes “I’m off the wagon.” Then suddenly a temporary fluctuation becomes a month-long spiral because shame entered the equation.

I try to teach patients to stop moralizing food. Dessert is not evil. Rice is not poison. Bread is not a biochemical assassination attempt.

Asians eat rice.
Italians eat pasta.
Mediterranean cultures eat bread with olive oil, and still historically had far lower obesity rates than modern America.

Meanwhile, I watch people order giant steaks dripping in butter, while fearing a side of risotto because someone on social media told them carbohydrates are the problem.

Calories still matter. Portions still matter. Hyperpalatable foods still matter.

And perhaps most importantly, food environments matter.

The average restaurant meal today is essentially three meals, pretending to be one. Soft textures, endless chips, sugary drinks, giant portions, engineered foods that barely trigger satiety — we created an environment that disconnects people from fullness. GLP-1 medications help restore the volume on satiety signals, but they do not magically change the environment around you.

Contrary to some myths, GLP-1 will not force you to stop, if it does, you’ve really eaten too much. But it will give you a soft signal. But setting yourself up for success means, when you go out, box up a bit of food before you start.

I can eat the 600 calorie burger, it is delicious. But if I eat half, then I am just as satisfied and if not, I can eat more. This is an old “diet” trick, but in this case it is more. Because if you keep thinking about that burger, or really feel the urge to eat the rest - you need to up the dose of your GLP-1. Remember you can feel “full” on a GLP-1 and still eat more. The GLP-1 is not your mom telling you to stop eating (and that never worked either).

Grazing: The Quiet Way Calories Sneak Back In

One of the reasons people plateau on GLP-1s is not giant meals.

It is grazing. Mindless eating. Unconscious bites. A handful here. A few chips there. Finishing the kids’ fries. Walking through the kitchen and grabbing something because it is there.

The problem with grazing is that it often bypasses awareness. You never feel like you “ate a lot,” because there was never a formal meal attached. There was no plate, no pause, no decision point. Just continuous low-level eating throughout the day.

Bariatric surgeons learned this years ago. Patients could sometimes eat around surgery by constantly grazing soft foods. Tiny amounts at a time still add up if there is never a stopping point.

GLP-1s help with this, but they do not completely eliminate it.

And this is where mindfulness actually matters. Not mindfulness as some wellness cliché. Mindfulness as paying attention.

The medication gives many people something they have not had in years: enough quiet around food to actually notice what they are doing.Use that.

If you sit in front of the television with snacks and scroll your phone while half-reading emails, you can still eat far beyond what you intended, because your brain never fully registered the experience.

Eating becomes background noise.

So one of the most powerful things you can do is surprisingly simple:

When you eat, just eat. Put the phone away - a rule in the Simpson house. My 15 year old son would love to keep his phone on and text his buddies. But instead phones are not allowed. Not at the table. Family time to catch up.

Turn off the endless scrolling. Stop reading. Pay attention to the conversation if you are with people.

Pay attention to the taste if you are alone. Notice the bites. Even if it isn’t a Michelin Star restaurant, you can and should strive to enjoy food.

Notice when the excitement of the first few bites fades. That is important, because most pleasure from food occurs early. After that, many people are simply eating out of momentum.

Slow down enough to notice when satisfaction appears before fullness.

That distinction matters.

One of the hidden gifts of GLP-1 medications is that they can help people rediscover the experience of eating instead of consuming food mechanically. Taste becomes more important than volume. A few good bites become more satisfying than endless quantity.

That is why many patients naturally drift toward foods with stronger flavor, texture, freshness, and balance. They stop chasing sheer volume and start appreciating quality.

And honestly, that may be one of the healthiest psychological shifts these medications create.

You still have to participate.

Now, after years of doing this, people often ask me what diet I recommend. The funny thing is that I usually end up moving people toward a Mediterranean style of eating, without ever calling it Mediterranean.

I do not hand people a laminated Mediterranean Diet pyramid and tell them to memorize it.

Instead, I say simpler things.

Eat something green every day.

That’s it. Something green. A salad, broccoli, asparagus, green beans, spinach, zucchini, Brussels sprouts, herbs, avocado, whatever works for you. Green foods tend to slow you down, fill space in the stomach, provide fiber, micronutrients, texture, and satiety. They also crowd out some of the ultra-processed foods that dominate modern eating.

Yes, everyone online screams “more protein” and “more fiber,” and they are not entirely wrong. Protein matters. Fiber matters. But people often hear those messages as supplements, powders, bars, or strange engineered foods.

I would rather people start by learning to eat actual meals again.

Meals with vegetables. And yes, sometimes I have to hide them from myself.
Meals with beans. Once you start cooking with beans and chickpeas and lentils you find a great source of satisfying meals that have a lot of fiber.
Meals with fish occasionally.
Meals where olive oil appears more often than industrial sauces.
Meals where dessert is enjoyed but not worshipped.

The goal is not perfection.

The goal is normal.

Food Noise or Head Hunger is Real and Persistent Nagging

And perhaps the most important thing I have learned from being on a GLP-1 myself is understanding food noise. Before these medications, many people lived with constant mental chatter about food and assumed that was normal. Thinking about the next meal while eating the current one. Opening the refrigerator repeatedly. Negotiating with yourself about snacks. Seeing dessert menus before the entrée arrives. Watching television while mentally inventorying the pantry.

Then the medication works, and suddenly patients say something fascinating:

“The noise got quiet.”

That may be one of the most profound effects of these medications.

This is why I do not love obsessive food tracking during plateaus. Tracking every calorie often becomes old diet behavior. It shifts people back into punishment instead of awareness.

What I care about more is whether the noise is returning.

Are you thinking about food all day again?
Are desserts becoming mentally louder?
Are grocery cravings returning?
Are you opening delivery apps at night?
Are you bargaining with yourself constantly?

For me personally, one clue is embarrassingly simple: when I start thinking about ice cream more often, and suddenly it appears on the grocery list again, I know the medication effect may be fading. Last time I skipped a dose of Zepbound, and in my freezer there were a selection of Dove bars and Ice Cream sandwiches. No idea where they came from, they magically appear when my Zepbound wears off. What is odd is that as magically as they appear, my brain knows they are there, and in a day I can have three of them just because they are there. With my dose of Zepbound, I know they are there, but they don’t call to me.

That is useful information.

Not failure.
Not weakness.
Information.

To Up the Dose or Not?

And sometimes the answer is not necessarily a huge dose increase. Some people simply metabolize these medications differently and notice the medication wearing off before the next injection. By day six, food becomes louder, hunger increases, and grazing returns.

In some patients, taking the medication every six days instead of every seven may smooth out those fluctuations — under the guidance of their physician.

But even then, the medication remains a tool, not a replacement for awareness.

That has been true in bariatric surgery for decades. Surgery works well, but patients can still eat past restriction. They can graze around the operation. They can override fullness. The patients who do best long-term are rarely the most obsessive or rigid. They are usually the ones who learn to recognize the moment they have had enough and consistently stop there.

The same is true with GLP-1s.

The greatest skill in weight loss is not calorie counting. It is not avoiding carbohydrates. It is not buying expensive supplements from influencers with suspiciously perfect lighting and absolutely no endocrinology training.

The real skill is learning to stop when your body says:
“That’s enough.”

GLP-1 medications help people hear that signal.

Weight loss surgery amplifies it.

But neither can force you to respect it.

That part still belongs to you.

And honestly, after years of treating obesity, performing surgery, studying nutrition, and now living with these medications myself, I think that is where long-term success actually lives — not in perfection, not in punishment, and certainly not in fear of food, but in finally learning how to hear your body without all the noise drowning it out.

Those who say this is about willpower have never had that constant brain loop. And once that noise is quieter, or quieter, it is easy to make some better choices.

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Practical Things to Do When the Plateau Arrives

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The headline this week came from Italy.

Two humanitarian workers returning from Uganda were isolated in Lombardy after developing symptoms concerning enough to trigger Ebola protocols. Both were transferred to infectious disease specialists at Sacco Hospital in Milan, one of Europe’s premier bio-containment centers. Officials stress Ebola remains unconfirmed, and severe malaria remains a strong possibility, but emergency containment protocols were activated immediately.

That matters.

Because in infectious disease, you do not wait for certainty before you act.

You move early, or the outbreak moves faster than you do.

Meanwhile, the World Health Organization warned this week that the Ebola outbreak in the Democratic Republic of Congo is now “outpacing” response efforts. Cases continue to spread regionally, while healthcare systems in affected areas remain strained by insecurity, delayed diagnosis, attacks on treatment facilities, and population movement.

And yes, this outbreak is now affecting sports and international travel.

The Democratic Republic of Congo’s World Cup preparations have already been dramatically altered. The national team canceled planned events in Kinshasa and moved preparations to Europe because of U.S. entry restrictions connected to the outbreak. Several reports now confirm the team is effectively undergoing a 21-day isolation period before entering the United States for tournament play.

That sounds alarming until we remember something important:

Ebola is not spread through the air like influenza or COVID.

You do not catch Ebola by sitting near someone at a soccer stadium.

Transmission still requires close contact with infected bodily fluids, caregiving exposure, contaminated medical settings, or handling bodies during burial practices.

So despite dramatic headlines, the World Cup itself is extraordinarily unlikely to become a “spreading event.”

That distinction matters, because modern media often collapses all infectious disease into one emotional category: panic.

But biology matters.

The reason COVID became a pandemic is because respiratory viruses spread incredibly efficiently through the air. Ebola does not behave that way.

At the same time, this outbreak is serious for another reason: geography.

There are roughly ten neighboring countries surrounding the DRC now considered at elevated regional risk due to cross-border movement and fragile healthcare infrastructure. WHO has already classified the outbreak as a Public Health Emergency of International Concern.

Still, elevated regional risk is not the same thing as the imminent global pandemic.

Those are very different epidemiologic realities.

Public Health Only Looks Excessive When It Works

The United States now routes travelers from affected regions through enhanced airport screening, particularly through Washington Dulles, while CDC teams expand monitoring efforts.

And predictably, some people immediately begin mocking those precautions.

Until they need them.

Nobody notices:

• the outbreak that never occurred,

• The transmission chain quietly interrupted,

• Or, airport screening that prevented one infected traveler from entering a crowded emergency department.

Public health succeeds invisibly.

And the uncomfortable truth is that outbreaks like this expose how fragile those systems have become after years of political attacks, funding cuts, distrust, burnout, and institutional erosion.

Viruses are ruthlessly indifferent to ideology.

Fatty Liver Is Not “Just a Liver Problem”

Another major study this week reinforced something clinicians increasingly understand:

Fatty liver disease is not simply about the liver.

Patients with fatty liver showed dramatically higher rates of heart attack, hospitalization, and cardiovascular death.

The liver packed with fat often acts as a visible marker of systemic metabolic dysfunction:

• insulin resistance,

• inflammation,

• abnormal lipid handling,

• and vascular injury.

The liver may simply be the first organ to wave the white flag loudly enough for us to notice.

And this connects directly to another major study this week showing that diabetes significantly increases dementia risk.

The worse the metabolic disease, the worse the risk.

That should finally end the outdated idea that the brain somehow exists independently from the rest of the body.

Your neurons are fed by blood vessels.
Metabolism affects your blood vessels.
Metabolism therefore affects your brain.

The same inflammatory injury damaging kidneys and coronary arteries also affects cognition.

The Teenage Brain Was Not Built for Infinite Scroll

Nearly half of adolescents in a major national study used phones between midnight and 4 a.m. on school nights.

Predictably, this gets turned into a morality lecture about weak kids or bad parenting.

But let us be honest.

Teenagers evolved for:

• novelty seeking,

• emotional reinforcement,

• social learning,

• reward sensitivity,

• and risk taking.

Then we handed them glowing devices engineered by billion-dollar companies specifically designed to exploit those neurologic pathways indefinitely.

Asking why teenagers cannot stop scrolling at 2 a.m. is like asking why moths struggle around porch lights.

The teenage brain was not built for infinite scroll.

And sleep deprivation affects far more than grades:

• depression,

• anxiety,

• obesity,

• appetite regulation,

• memory,

• impulse control,

• and accident risk
  All worsen with chronic sleep loss. —

And I have a 15 year old. Yes, his screen time is monitored and limited.

Smoke, Pollution, and the Air We Pretend Not to Notice

I live in an area where wildfire smoke drifts into homes during fire season.

Many urban residents also live under chronic exposure to particulate pollution.

People assume that if they cannot smell smoke anymore, the danger is gone.

Unfortunately, some of the most dangerous particles are invisible.

PM2.5 particles penetrate deep into the lungs, trigger systemic inflammation, worsen cardiovascular disease, aggravate asthma, and increasingly appear associated with cognitive decline and dementia.

Your lungs are not perfect filters.

Some of these particles cross into the bloodstream itself.

So yes:

• close windows during smoke events,

• Replace HVAC filters,

• Use HEPA filtration when possible,

• and pay attention to air quality reports.

Preventing inflammation is often smarter than medicating the damage afterwards.

Exercise Is Good. “Industrial Quantities” of Exercise May Be Something Else

One of the more fascinating studies this week looked at extreme endurance runners and found unexpectedly high rates of advanced colon polyps.

Important caveat:
This study does not prove that marathon running causes colon cancer.

But it raises an important possibility:
Extreme endurance exercise may biologically differ from ordinary healthy movement.

A 30-minute walk and a 100-mile ultramarathon are not simply different amounts of the same thing.

Extreme endurance exercise can involve:

• oxidative stress,

• intestinal ischemia,

• inflammation,

• and repeated tissue injury.

Humans evolved to move frequently.

We did not necessarily evolve to perform industrial quantities of exercise.

The Supplement Industry’s Favorite Fantasy

And finally, medicine delivered another uncomfortable reminder this week:

Calcium and vitamin D supplements are not magical anti-fracture pills.

A large review in The BMJ found routine supplementation had surprisingly little effect on fractures or falls in average community-dwelling adults.

Now before social media transforms this into:
“Vitamin D is useless,”
Let us maintain our sanity.

Deficiencies matter.
Bariatric patients become deficient.
Institutionalized elderly patients may absolutely require supplementation.

But fracture prevention is not solved by sprinkling calcium tablets onto biology like lawn fertilizer.

Bone health is a systems problem:

• muscle strength,

• balance,

• movement,

• protein intake,

• neurologic health,

• and physical activity.

Exercise tells bone that there is still a reason for it to exist.

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Ebola, Trust Collapse, and Why Modern Public Health Feels So Fragile

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Not intentionally wrong. Not manipulated. Just incomplete in the way outbreak numbers often are early on, especially in regions where laboratory confirmation takes days, transportation is limited, and many people die before ever reaching a formal medical system. The current outbreak in Congo and Uganda has already pushed the WHO to declare an international public health emergency. Officials are now discussing nearly 750 suspected cases and 177 suspected deaths, but even WHO officials are acknowledging the outbreak likely began months before detection. Testing shortages, delays in specimen transport, and unsafe burials mean the real numbers are almost certainly higher than the official count.

And burial practices matter enormously with Ebola.

One of the cruel realities of Ebola is that the dead can remain highly infectious. Families naturally want to wash bodies, touch loved ones, hold funerals, gather. Those rituals are human. They are ancient. They are also how Ebola spreads. This week there were reports of clashes with authorities after families were denied access to bodies. One treatment center was reportedly attacked and burned after tensions over burial restrictions.

That is how outbreaks accelerate quietly at first. A few funerals. A few infections. A few people traveling before symptoms become severe. Then suddenly epidemiologists realize the visible outbreak is only the shadow being cast by a much larger one.

And reading those reports this week brought me back to 2014.

In August of 2014, Ebola felt like the monster at the edge of the map. Distant, terrifying, and unpredictable. About 1,100 people had died at that stage of the West African outbreak, and American hospitals suddenly realized that if even one patient arrived unrecognized, an emergency department could become a transmission event.

So we prepared.

And I mean really prepared.

Our Hospital Was Going to be the regional hospital for Ebola

I was at a large regional hospital. We were not a trauma center, which oddly made us more attractive as a potential Ebola intake facility. The thinking at the time was that trauma centers were already overloaded with catastrophic emergencies. Gunshots. Crashes. Strokes. Ruptured aneurysms. If Ebola arrived, a busy regional hospital with physical space and operational flexibility might actually be safer than a Level 1 trauma center already drowning in chaos.

So our hospital became one of the regional preparedness sites. As Chairman of Surgery I was tasked to get our department up to speed, as well as having to attend endless meetings.

Isolation rooms were identified immediately. Separate emergency department pathways were developed. Dedicated ICU beds were assigned. We even had a dedicated surgical suite identified for a potential Ebola patient should emergency surgery somehow become necessary.

PPE stations appeared everywhere.

Protocols multiplied weekly.

There were meetings upon meetings upon meetings.

Who transports the patient?

Who draws blood?

What elevator do they use?

Which hallway is cleared?

Where does contaminated waste go?

What if they need intubation?

What if they arrest?

What if the ventilator becomes contaminated?

Who cleans the room afterward?

Every one of these cases is important, critical, and had to have a decision ahead of any patient that might arrive. When facing these threats you want protocols in place. You do not want to have to think about.

Drill Baby Drill

For us this was not about oil, it was about every potential staff member from the person who greets you in the ER to the janitor needed to know what to do.

And because this was before everybody became an amateur epidemiologist on social media, most of us took it extremely seriously. We drilled constantly because everybody understood something simple: hospitals are systems, and infections spread when systems fail.

Not because doctors are stupid. Not because nurses do not care.mBecause systems break under stress.mSo we practiced. Putting on PPE. Taking off PPE.

Watching one another remove gloves so nobody accidentally touched their face. Simulating transfers. Simulating codes. Simulating contamination events.

Federal Money and Mandates Came into play

The federal government funded much of this preparation. Hospitals received money because preparedness was considered infrastructure. Nobody complained much about spending the money because the images coming out of West Africa were horrifying enough that preparation felt rational.

Then Ebola faded from the headlines.

And slowly the machinery of preparedness drifted into the background. And all of us took a collective sigh. The containment program put forth by the Obama administration kept Ebola contained. They had built new hospitals in Africa, sent morticians to help bury the dead, and set up testing facilities so that Ebola could quickly be diagnosed instead of waiting days.

We did have some come back from Africa with Ebola, the most famous being the nurses in Texas. But we dodged a bullet and after endless drills, quietly forgot those lessons.

Then COVID arrived.

And suddenly we discovered we had prepared for containment, not scale. I had moved to California and was in two hospital systems. While many there remembered the Ebola scare, what we did not believe was how many COVID patients would arrive at our doorstep.

Ebola was terrifying because it was lethal. COVID was devastating because it was everywhere.

The Ebola model assumed a small number of highly isolated patients. COVID turned every hallway, every ICU, every emergency room, every recovery area, and eventually every exhausted nurse into part of the infectious disease system simultaneously.

At first some of our Ebola preparation helped. We understood isolation. We understood PPE. We understood exposure reduction. We understood negative pressure rooms and contamination zones.

But none of us were prepared for the volume. Nobody was.

Anticipating Covid since February there was no Federal Preparation

The PPE disappeared almost immediately. Masks became precious. Gowns were reused. Equipment designed for single use suddenly became multi-day use because there simply was no replacement available. And then we discovered something that should have frightened every policymaker in America: much of our PPE manufacturing had been outsourced overseas, particularly to China. When the entire world needed protective equipment simultaneously, supply chains collapsed almost overnight.

We had protocols to reuse N-95 masks. Usually involved baking the masks in an oven at 350 degrees for an hour. We didn’t have enough. And what was available in the public was quickly bought out by people.

The patients came in waves. We didn’t just get a few in our Emergency rooms, we got dozens a day. We saw them coming and we had to stop all elective surgeries. There was no room in the hospital and we thought we would need the ventilators. And we did.

Hospitals hemorrhaged money. ICUs overflowed. And health care workers aged visibly in real time.

Brutal Burnout

That is the part I think the public still underestimates. COVID did not simply overwhelm hospitals physically. It exhausted them psychologically. The people who attended all those Ebola preparedness meetings in 2014 were already burned thin by 2021. Some retired. Some left medicine entirely. Some simply stopped believing the country had the attention span necessary to sustain preparedness.

I remember during the height of COVID I would go to the hospital, change into scrubs, get into what look like spacesuits, and start rounding on ICU patients. We had, at one time, over 200 ICU patients in one hospital, most on ventilators. You are never used to people dying in the ICU, some die, but this was a scale that we could not imagine. Every patient who lived and got off the vent we celebrated. And the too many who died slayed us.

Yes, sometimes we danced, made silly videos, and yes our parking lots were empty because we were not allowing visitors. We held the hands of patients dying, holding up iPads so families could give the last words.

Then many of us would go home and on Facebook have people tell us that the hospitals were empty, this was just the flu, and I’d just come home after 12-18 hours working trying to save. Many died.

We were overwhelmed. A medical school classmate of mine, Howard Markel, described flattening the curve. By getting people to shelter in place we could take the strain off our hospitals. Most states instituted it - I remember when California was ordered to shelter in place. The first time I saw the 405 without traffic. We did it, I would go to work with no one else on the street.

Many of my colleagues, both physicians, nurses, respiratory techs, and others retired, quit, or moved into something else.

Here We Go Again

And now here we are again. Another viral outbreak.

Another round of discussions about surveillance, isolation, travel screening, testing delays, and public health response.

Except this time the system feels older.More brittle. More cynical.

During Ebola in 2014 there was still a broad assumption that preparedness was worth funding even if the disaster never fully materialized here. COVID changed that politically. Now every discussion about preparedness immediately becomes a culture war argument about spending, mandates, expertise, and distrust.

But viruses do not care about ideology. They care about opportunity. And outbreaks are always easier to stop early than late.

National Defense is Being Prepared

In January of this year we exited from the World Health Organization, and with it was 15% of the WHO funding. I’ve heard that the WHO was a lot of wasted money. Perhaps that is true, but so is the Defense Department that has all of those planes, missels, tanks, and other equipment just sitting around. The $600 toilet seats, the $150 hammers. We don’t blink an eye.

More people have died in war from infectious disease than any spear, bullet, bomb, or weapon ever killed.

Like the shiny firetruck at the fire station. No one thinks it is a waste of time. You hear about a fire on the other side of town, and you are happy to be prepared. If that fire comes closer to you then you want more fire trucks.

That is how we need to look at being prepared for any world wide epidemic.

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One future is hopeful: precision cancer drugs once thought impossible are extending lives. Telemedicine continues to reshape healthcare delivery, and even simple habits like walking are more powerful than wellness influencers often admit.

The other future is darker: Ebola spreading through central Africa without an approved vaccine for the circulating strain, hantavirus clusters triggering international monitoring efforts, and public-health systems weakened after years of political exhaustion and distrust.

Medicine always lives in this tension.

Scientific progress moves forward while public confidence lurches backward.

And increasingly, the systems that quietly protect modern civilization are only noticed when they begin to fail.

WHO Declares Ebola a Global Health Emergency

The World Health Organization officially declared the Ebola outbreak spreading through the Democratic Republic of Congo and Uganda a “Public Health Emergency of International Concern” — the organization’s highest warning level short of declaring a pandemic.

That phrase sounds bureaucratic. It is not.

It means the world’s leading infectious disease experts believe this outbreak poses enough international risk to require coordinated global action before it spreads further.

And there are reasons for concern.

This outbreak appears to involve the Bundibugyo strain of Ebola, rather than the classic Zaire strain responsible for previous outbreaks.

That matters enormously, because the currently licensed Ebola vaccines were designed against the Zaire strain.

At this moment, there is no approved vaccine specifically for Bundibugyo Ebola.

The outbreak is also occurring in one of the most difficult environments imaginable for infectious disease control: eastern Congo, a region fragmented by militia violence, poor infrastructure, displaced populations, weak healthcare systems, and ongoing humanitarian instability.

Getting supplies into these regions is extraordinarily difficult.

Protective equipment travels through conflict zones. Refrigeration chains fail. Roads disappear in heavy rains. Laboratory samples may take days to move safely. Communication between rural clinics and national authorities can collapse entirely.

And a heroic doctor does not stop outbreaks holding a syringe.

They are stopped by logistics.

Fuel. Gloves. IV fluids. Refrigeration. Mobile labs. Contact tracers. Burial teams. Secure transport routes. Community trust.

Containment is infrastructure.

During the 2014–2016 West African Ebola epidemic, the United States and WHO aggressively intervened. CDC teams entered outbreak zones. Mobile laboratories were built. Field hospitals were established. Teams were deployed to safely handle and bury the dead, because Ebola remains highly contagious after death.

I remember this personally.

At the time, I was chairman of surgery, and we held meetings preparing for Ebola’s possible arrival in the United States. Isolation rooms were designated. PPE stockpiles were checked. Protocols were rehearsed. We were told to expect Ebola.

The reason widespread transmission never happened here was not luck.

It was intervention.

We helped contain the outbreak there before it became catastrophic here.

That infrastructure is weaker now.

The United States withdrew from WHO and cut funding to the organization that historically coordinated international outbreak response. CDC staffing has also been substantially reduced. The institutions that once served as the backbone of epidemic response are now politically controversial.

Viruses do not care.

This is where many Americans first learned about Dr. Craig Spencer, the New York physician who survived Ebola after treating patients in West Africa. He recently discussed the emotional and physical reality healthcare workers face when confronting dangerous pathogens firsthand and why preparation matters before panic begins.

One of the recurring themes of infectious disease is that humans consistently misunderstand risk.

We fear cinematic catastrophes while ignoring ecological realities.

Hantavirus is fundamentally an ecological disease. Rodent populations expand after favorable climate conditions. Humans encounter contaminated droppings in cabins, garages, sheds, campsites, barns, and poorly ventilated spaces. Exposure happens quietly and accidentally.

And once again, prevention comes down to boring but essential infrastructure:

• surveillance,

• laboratory capacity,

• environmental monitoring,

• communication systems,

• rapid testing,

• and coordinated public-health response.

The same systems that detect Ebola in central Africa help identify unusual respiratory clusters in Colorado, Nebraska, or Illinois.

Public health is interconnected.

Hantavirus and the Ecology Problem

Public health officials are also continuing to monitor the multinational hantavirus cluster linked to the MV Hondius cruise ship outbreak.

The latest CDC updates emphasize that there are currently no confirmed U.S. cases of the Andes hantavirus strain responsible for the outbreak, and public risk remains very low. (CDC)

Still, dozens of Americans are being monitored after exposure during the cruise outbreak. (American Hospital Association)

The Andes strain matters because unlike the North American Sin Nombre strain typically seen in the United States, Andes hantavirus can occasionally spread person-to-person through prolonged close exposure. (Reuters)

The Supreme Court and the Quiet Telemedicine Revolution

This week, the Supreme Court also allowed continued access to mifepristone by mail, while litigation continues in lower courts.

That may sound like a narrow abortion story.

It is also a telemedicine story.

COVID permanently accelerated one of the largest shifts in healthcare delivery in modern history: medicine partially leaving buildings and entering digital space.

Patients now routinely receive care remotely. Prescriptions arrive by mail. Mental-health visits happen virtually. Chronic diseases are managed online. Geographic barriers matter less than they once did.

And regardless of political views about abortion, this case highlights a deeper unresolved question:

What happens when healthcare no longer respects state borders the way old medical systems assumed it would?

Technology has already changed medicine.

The legal system is still catching up.

A Pancreatic Cancer Breakthrough Once Thought Impossible

And amid all the anxiety this week, there was also extraordinary news from cancer research.

An experimental drug called daraxonrasib significantly prolonged survival in patients with advanced pancreatic cancer.

That is an astonishing sentence in oncology.

Pancreatic cancer has long been one of the most lethal and discouraging diagnoses in medicine. For decades, scientists unsuccessfully targeted a protein called KRAS, which drives many pancreatic, colon, and lung cancers.

Researchers referred to KRAS as “undruggable.”

And then science did what science occasionally does best: it proved its own assumptions wrong.

After decades of failures, publicly funded NIH research, academic laboratories, and biotech companies slowly identified vulnerabilities in KRAS that eventually allowed a drug to disable it.

Patients receiving daraxonrasib survived a median of more than 13 months, compared with less than seven months for chemotherapy patients.

That is not a cure.

But in pancreatic cancer, it is enormous progress.

And it is also a reminder that scientific progress often looks inefficient right up until the moment it changes lives.

Ice Cream, Metal Fragments, and Why Food Safety Matters

Meanwhile, Straus Family Creamery voluntarily recalled several organic ice cream flavors after concerns about possible metal contamination in certain production batches.

No injuries were reported.

Which is exactly the point.

Modern food safety systems work because they identify problems before many people are harmed. The FDA, epidemiologists, manufacturing oversight, traceability systems, and recall infrastructure are all part of the same invisible public-health architecture most people never notice.

Milk used to routinely kill people.

Foodborne outbreaks once devastated communities.

Now we complain when a company voluntarily recalls ice cream before anyone gets hurt. Yes, I love ice cream–if only my intestines had more lactase.

That annoyance is actually evidence of success.

Maybe Walking Still Works Better Than Biohacking

And finally, one of my favorite studies of the week.

Researchers found that people averaging roughly 8,500 steps daily during weight-loss programs were significantly more successful at maintaining weight loss long term.

Not 30,000 steps.

Not cold plunges.

Not wearable optimization systems.

Walking.

There is something wonderfully humbling about that.

Modern wellness culture often swings between extremes: either obsessive optimization or complete resignation. But most durable health improvements still emerge from remarkably ordinary behaviors repeated consistently:

• walking,

• sleeping,

• resistance training,

• social connection,

• eating fewer ultra-processed foods,

• spending time outside.

The body still responds beautifully to consistency.

And increasingly, obesity medicine and GLP-1 science are reinforcing something many physicians quietly suspected for years:

The best intervention is often the one people can actually continue doing. You can measure your steps with almost any device, but once you have the route you will travel, just keep doing it. This is about 4 miles of walking.

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The Larger Story

The larger story this week is not merely Ebola, hantavirus, cancer drugs, abortion pills, food recalls, or walking studies.

It is the strange contradiction of modern medicine itself.

We are simultaneously:

• more scientifically capable than ever,

• and more socially distrustful than ever.

We are sequencing viruses faster while questioning epidemiology.
We are developing molecular cancer therapies while dismantling pieces of public-health infrastructure.
We expect miracles from medicine while growing suspicious of the institutions that produce them.

And yet medicine keeps moving forward anyway.

Sometimes awkwardly.
Sometimes politically.
Sometimes inefficiently.

But forward nonetheless.

The danger is not simply that dangerous viruses exist.

The danger is that societies begin mistaking the absence of catastrophe for proof the systems preventing catastrophe were unnecessary all along.

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What Ebola Actually Looks Like on the Ground

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In the first episode of Dr. Simpson Unfiltered MD, weight loss surgeon Dr. Simpson and his producer April discuss his personal experience taking Zepbound for about a year and a half, including his fear of needles, a 50‑pound weight loss, minimal side effects, improved sleep, reduced “food noise,” decreased alcohol interest, refined taste for food and coffee, and lower measured stress. He shares his long history of weight fluctuations and diets, why he didn’t pursue bariatric surgery for himself, and explains GLP‑1 history and testing, including the Gila monster connection and long-standing clinical data. They address common concerns such as constipation/diarrhea, nausea, bone and muscle loss with weight loss, gallbladder disease vs pancreatitis risk, “Ozempic face,” thyroid cancer fears, and cautions about compounded GLP‑1s, emphasizing seeing an obesity medicine specialist and registered dietitian.

Just when you think we can relax from a viral epidemic: Ebola.

The Democratic Republic of Congo confirmed another Ebola outbreak. Current estimates suggest roughly 246 suspected infections and at least 65 deaths. Early sequencing suggests this may not be the classic Zaire strain — the one for which we already have an approved vaccine. That matters. A great deal.

Because Ebola is not just another “bad flu.” It is one of the most lethal viruses modern medicine encounters. Depending on the strain, mortality can range from 25% to nearly 90%.

And yet what struck me reading the reports was not merely the outbreak itself. It was the uneasy realization that ten years ago, we were far more prepared for this moment than we are now.

During the West African Ebola epidemic of 2014–2016, the United States anticipated that Ebola could reach our shores. Public health agencies trained hospitals. Isolation units were prepared. Airports screened passengers. The CDC mobilized rapidly. Scientists collaborated internationally. The military assisted with logistics. The WHO coordinated surveillance.

I was chairman of surgery at the time, and we had meetings about Ebola. We were told to expect Ebola in the United States. We put protocols in place, had isolation rooms ready. We taught signs and symptoms and had PPE gear ready and stored for when Ebola hit our shores. The reason it didn’t was because of the intervention we did through WHO and the CDC that kept Ebola in Africa. We did bring home several Americans infected, but not contagious.

There was anxiety, certainly. But there was also infrastructure.

Today we have something very different: exhaustion, fragmentation, and political contempt for public health itself.

We cut expertise and then congratulate ourselves for “saving money.” We withdrew from international partnerships and then pretend viruses require passports. We lost experienced personnel from the CDC and global surveillance networks precisely as the world became more interconnected than at any point in human history.

Viruses do not care about ideology. Ebola certainly does not.

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What Ebola Actually Is

Ebola is caused by a filovirus — a long, filament-shaped RNA virus. Unlike DNA viruses, RNA viruses mutate relatively quickly. They are sloppy copiers. That biological chaos is part of why outbreaks can evolve unpredictably.

The natural reservoir is believed to be fruit bats. Humans usually become infected through contact with infected animals or contaminated bodily fluids from infected individuals.

And this is important: Ebola is not airborne in the way measles or COVID can be.

It spreads primarily through direct contact with blood, vomit, stool, sweat, saliva, semen, breast milk, and contaminated surfaces or medical equipment. Caregivers and healthcare workers are at particular risk when protective systems fail.

That distinction matters, because it means Ebola is both terrifying and containable — if you have functioning public health systems.

The virus causes fever, weakness, vomiting, diarrhea, rash, and in severe cases, bleeding and organ failure. The immune system becomes overwhelmed. Blood vessels leak. Clotting systems collapse.

It is a brutal disease.

And unlike many respiratory viruses, Ebola can persist in survivors long after recovery. The virus has been detected months later in semen, ocular fluid, and even the central nervous system. Survivors may clear symptoms, yet still harbor reservoirs of infection.

That is one reason outbreaks can reignite unexpectedly.

What We Did Last Time — And Why It Worked

During the major West African Ebola outbreak, the world did not simply sit back and hope for the best.

The United States deployed CDC teams directly into outbreak zones. Epidemiologists tracked chains of transmission village by village, patient by patient. Mobile laboratories were established so that viral testing could occur in hours instead of weeks. Military logistics teams helped move supplies, personnel, and protective equipment into areas with almost no infrastructure.

Field hospitals and specialized Ebola treatment units were rapidly constructed. Healthcare workers were trained in infection-control procedures that most hospitals in the developed world take for granted, but are extraordinarily difficult to implement in resource-poor settings, wearing layers of suffocating protective gear in tropical heat.

And then came one of the hardest realities: burial practices.

Ebola remains highly infectious after death. Traditional funeral rituals involving washing and touching the body became major amplifiers of spread. International teams worked with local communities to establish safe burial protocols that still respected cultural traditions, while preventing further transmission.

That meant trained mortuary teams. It meant protective equipment. It meant vehicles, refrigeration, disinfectants, and personnel willing to do emotionally devastating work under dangerous conditions.

At the same time, the World Health Organization coordinated international surveillance, funding, and communication between countries. Wealthier nations provided emergency resources because everyone understood a simple truth: stopping Ebola in central Africa was far cheaper — and far safer — than allowing it to spread internationally.

This was not charity. It was intelligent self-defense.

And that is the part many people forget.

Public health only looks “expensive” until you compare it with the cost of failure.

Today, many of those systems are weaker. Funding has been reduced. International partnerships have frayed. Experienced personnel have left. Support for WHO coordination has become politically controversial. Outbreak preparedness has increasingly been treated not as national security, but as optional bureaucracy.

Viruses exploit exactly that kind of complacency.

What Has Changed Since The Last Ebola Crisis

During the last major Ebola response, the United States was the logistical backbone of global outbreak containment.

Today, that backbone is weaker.

The United States formally completed its withdrawal from the World Health Organization after halting funding and pulling personnel from WHO operations. The U.S. had historically been WHO’s single largest contributor, providing roughly 15% of the organization’s budget — hundreds of millions of dollars annually that funded outbreak surveillance, laboratory support, emergency response teams, vaccination campaigns, and field coordination in low-resource nations.

That funding mattered.

WHO is not simply a building in Geneva issuing press releases. It coordinates disease reporting between nations, deploys emergency teams, organizes vaccine campaigns, tracks outbreaks in real time, and helps fragile countries respond before local epidemics become international crises.

At the same time, the CDC itself has undergone significant contraction.

Recent reports estimate the CDC has lost more than 3,000 employees — roughly a quarter of its workforce — during the current administration’s reductions and reorganizations. Proposed federal budgets would reduce CDC funding by more than 50%, while cutting staff by over 40%.

And these are not abstract bureaucratic positions.

The cuts have affected global health units, outbreak analytics teams, disease detectives in the Epidemic Intelligence Service, surveillance specialists, laboratory personnel, and experts who historically deployed to outbreaks involving Ebola, Marburg, mpox, measles, and hantavirus.

During the previous Ebola crises, CDC teams traveled directly into outbreak zones. American experts helped establish field hospitals, train healthcare workers, set up mobile labs, trace contacts, and coordinate safe burial practices.

That response infrastructure is now diminished.

The danger is not merely that another Ebola case could appear. The danger is delay. Delay in detection. Delay in sequencing. Delay in reporting. Delay in deploying trained personnel before chains of transmission expand.

Outbreaks are controlled in the first days and weeks. Once exponential spread begins, medicine becomes far more difficult and far more expensive.

And perhaps the most dangerous change is psychological.

After COVID, much of the political world stopped treating preparedness as essential infrastructure and began treating it as unnecessary overhead. Public health workers became targets, not assets. International cooperation became politically toxic. Expertise itself became suspect.

But viruses do not negotiate with ideology.

Nature does not care whether a government believes in public health. Ebola will replicate perfectly well regardless of who wins an election.

And that is the uncomfortable truth beneath all this: we are entering a more dangerous biological era with fewer defenses than before.

The Lesson We Refuse To Learn

Every outbreak follows the same emotional cycle.

First comes denial.

Then comes mockery of experts.

Then comes sudden panic.

Then comes revisionist history, where everyone claims they “always knew” it was serious.

COVID should have taught us humility. Instead, it taught many people arrogance. They emerged from a once-in-a-century pandemic convinced not that preparedness matters, but that preparedness itself was somehow the enemy.

That is madness.

The world is getting smaller. More humans are traveling into remote ecosystems. More forests are being disrupted. More animal reservoirs are being encountered. More viruses are crossing species barriers.

The next pandemic will not politely announce itself on cable news before arriving.

And the cruel irony is that the systems required to stop outbreaks early are relatively inexpensive compared with the cost of uncontrolled spread. We casually approve trillion-dollar defense budgets, while hollowing out institutions that defend us from organisms we cannot bomb, sanction, or negotiate with.

A virus needs no navy. It only needs an opening.

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There may be no phrase in modern nutrition more ridiculous than this:

“Real food protein bar.”

And yet here we are.

Recently, internet nutrition personality Paul Saladino introduced what he described as his best “real food” protein bar. While I have nothing personal against the man, I admire the confidence required to sell twelve protein bars for forty-four dollars while talking about ancestral living.

Because let’s be honest for a moment.

Protein bars are the modern candy bar.

They simply come wrapped in better fonts, cleaner branding, and enough wellness language to make people feel morally superior while eating what is essentially an overpriced Snickers bar with collagen.

Now, before the internet decides I am anti-protein-bar, let me say something clearly.

I actually like Aloha bars.

They are expensive, but they say the right words to me. More importantly, they taste better than many bars pretending to be nutrition while having the texture of compressed drywall. Besides, life is busy, airports exist, traffic exists, and there are absolutely days where convenience wins.

Still, pretending industrial engineering untouched these foods is fantasy.

And honestly, fantasy is part of the problem.

Breakfast Used to Be a Moral Lecture

To understand how we got here, we need cereal, because cereal explains almost everything about modern food.

The earliest cereals in America were basically granolas—dense grain mixtures that required chewing, preparation, and patience. While nobody was dreaming about them at night, they solved a real problem because they stored well, traveled well, and provided calories in a rapidly industrializing country.

Then came John Harvey Kellogg.

Now Kellogg was brilliant, eccentric, controlling, deeply moralistic, and profoundly suspicious of pleasure. He believed rich foods, spicy foods, meat, and almost anything enjoyable stimulated dangerous passions, and among those passions he was particularly terrified of masturbation, which he considered one of the great threats to civilization.

So his answer was blandness.

Very blandness.

Little sugar. Little stimulation. Little excitement.

The original cereal movement was not designed around pleasure.

Instead, it was designed around suppression.

In many ways, those cereals were crunchy moral discipline.

Fast forward a hundred years, and the cereal aisle becomes the exact opposite of Kellogg’s vision. Sugar increases, crunch becomes engineered, mascots appear, colors explode across the box, and breakfast slowly transforms into dessert with vitamins added.

And importantly, none of this happened because someone woke up wanting to destroy public health.

That part matters.

Food Engineering Solved Real Problems

Before obesity became the dominant nutritional problem, the real challenge facing humanity was hunger.

For most of history, people worried about:

• starvation

• spoilage

• crop failures

• transportation

• and simply getting enough calories

Modern food engineering changed that reality.

Shelf-stable foods mattered.
Affordable calories mattered.
Transportation mattered.
Refrigeration mattered.

And honestly, millions upon millions of lives improved because of those innovations.

It is very easy for people with stocked refrigerators and grocery delivery apps to romanticize the past, but the past involved tremendous amounts of malnutrition and uncertainty.

So modern food systems were not evil.

They were revolutionary.

Then We Solved One Problem and Created Another

However, once calories became cheap, portable, stable, and endlessly available, the challenge changed.

The problem was no longer finding enough food.

The problem became stopping.

And this is where modern biology collides with the modern grocery aisle.

Our brains evolved in environments where calorie-dense food was rare and valuable. Suddenly, within only a few generations, we found ourselves surrounded by foods engineered to be affordable, repeatable, convenient, and highly rewarding.

That mismatch matters.

Now medications like GLP-1 help many people—including me—regain balance and reality in a food environment our biology was never designed to navigate.

Extrusion Changed Everything

Most people have never heard the word extrusion, even though it may be one of the most important food technologies in modern life.

The process is simple.

Take grains, starches, or protein powders. Apply heat and pressure. Force them through machinery.

Suddenly you have:

• cereal

• crackers

• cheese puffs

• protein snacks

• breakfast bars

And here is the important part: extrusion changes texture, and texture changes satiety.

When food crunches perfectly, dissolves quickly, and slides down effortlessly, people consume more of it before fullness has time to register.

That is not conspiracy.

It is simply biology interacting with engineering.

Natural Selection Entered the Grocery Store

Food companies did not necessarily set out to create hyper-palatable foods.

Instead, they followed what sold.

And what sold was what people returned to repeatedly.

So over time, the grocery aisle became a form of natural selection.

Products survived because they effectively triggered pleasure.

Foods that did not simply disappeared.

And I will confidently say something controversial:

Reese’s sells better than Brussels sprouts.

I will die on that hill.

Now yes, Brussels sprouts can be wonderful roasted with olive oil and balsamic, and somewhere right now a chef in Brooklyn is shaving them raw onto handmade pottery while explaining their emotional complexity.

Still, Reese’s triggers something primal.

Sweetness.
Fat.
Salt.
Texture.

And your brain immediately says:

“Yes. More of that.”

For some people, comfort food is a tamale. For others, it is lefse. Meanwhile, many people find comfort in peanut butter cups or a Dove Bar.

Food is culture.

Food is memory.

Food is emotion.

The grocery aisle evolved around those realities much faster than human biology evolved to manage them.

The Wellness Fantasy

There is another uncomfortable reality that nobody on wellness Instagram likes to admit.

To feed a hungry planet, we cannot all live on pasture-raised beef, farm-fresh eggs gathered from cheerful backyard chickens, and organic kale harvested by a local poet-farmer wearing linen.

That is not a food system.

That is a lifestyle catalog.

The modern world has eight billion people.

Food has to:

• travel

• survive droughts

• survive wars

• survive supply chain failures

• and feed cities that no longer produce their own calories

Engineered foods are not going away.

Nor should they.

Yes, Even on Mars

When human beings eventually colonize Mars, we are not putting cattle on the rocket ship.

Nobody is building a space ranch outside Olympus Mons.

Likewise, we are not stocking the moons of Jupiter with artisanal grass-fed herds wandering beneath methane clouds.

Instead, we will use engineered foods and lab-grown proteins because they will be:

• efficient

• reproducible

• resource-conscious

• and eventually taste just as good

That future is not dystopian.

It is practical.

Even here on Earth, whole foods are fragile. Fresh food spoils quickly, transportation breaks down, ports close, and supply chains fail. Consequently, long-term food storage matters, distribution matters, and preventing malnutrition still matters.

The challenge today is different.

We no longer live in a world where most people fear starvation.

Instead, we live in a world where many people are simultaneously overfed and undernourished.

Calories are abundant.

Satiety is not.

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Food Is Not the Enemy

Food is not evil.

Engineering is not automatically bad.

Convenience matters, and sometimes a protein bar is perfectly fine.

However, pretending heavily processed convenience foods become “real food” because someone added collagen, and an Instagram strategy does not help anyone understand the real issue.

The goal is not perfection.

Awareness is the goal.

We need food systems that:

• reduce malnutrition

• prevent shortages

• improve satiety

• and avoid creating environments where obesity becomes the default outcome of modern life

Because feeding humanity was one of civilization’s greatest achievements.

Now we simply have to figure out how to do it without overwhelming the biology that got us here in the first place.

🎙️ Listen to the Podcast Version

This topic will also be featured on my podcast FORK U, where we make sense of the madness of food, medicine, culture, and the strange world we built around eating.

And if you enjoy topics like this—food engineering, GLP-1s, obesity science, history, nutrition myths, and why the modern grocery aisle looks the way it does—please subscribe to FORK U wherever you get your podcasts

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