Fork U with Dr. Terry Simpson

In 1990, researchers isolated a peptide from Gila monster venom. Two years later, work from the Bronx VA Medical Center described exendin-4, a molecule that resembled human GLP-1 but lasted far longer in circulation.

Human GLP-1 survives only minutes before the body breaks it down. Exendin-4 resisted that breakdown. That difference changed everything.

Soon afterward, the first GLP-1 receptor agonist reached patients under the brand name Byetta. At the time, physicians used it to treat diabetes. No one called it a weight-loss drug. No one predicted it would reshape obesity medicine.

And yet, the foundation was already in place.

At the Phoenix Indian Medical Center, I performed weight loss surgery in a population with some of the highest rates of type 2 diabetes in the world. Researchers there studied metabolism intensely. The “thrifty gene” hypothesis gained traction in that environment. Scientists asked whether efficient energy storage, once protective in scarcity, became harmful in abundance.

At the same time, I watched something remarkable in the operating room. After gastric bypass, patients’ blood sugars often improved within days, before meaningful weight loss occurred. Hormones were shifting. Physiology was driving outcomes.

Meanwhile, GLP-1 drugs evolved.

Researchers lengthened their half-lives. Chemists modified their structures so they bound albumin and stayed active for days rather than minutes. Clinical trials expanded. Safety data accumulated.

Eventually, semaglutide showed average weight loss approaching fifteen percent of body weight in obesity trials. Then tirzepatide, now marketed as Zepbound for obesity, exceeded 20 percent weight reduction in higher-dose studies. In addition, cardiovascular outcome trials demonstrated reductions in major adverse cardiac events in high-risk patients.

These were not cosmetic results. These were metabolic and cardiovascular outcomes.

Patients rarely talk about receptors. They talk about noise.

Food noise.

The constant internal dialogue about eating. The mental pull toward the pantry. The background chatter that never quite stops.

GLP-1 receptors exist in appetite-regulating areas of the brain, including the hypothalamus and brainstem. These medications act through vagal signaling and through regions where the blood-brain barrier is more permissive. As a result, they modulate satiety and reward pathways.

Consequently, many patients report something simple but profound: the noise quiets.

Not disappears. Quiet.

That distinction matters.

Predictably, not everyone celebrates this shift.

Diet culture thrives on the belief that weight reflects character. Some coaches insist the solution is fewer calories. Others argue for more beef, more butter, more fiber, or stricter discipline. Entire industries depend on the idea that trying harder solves everything.

However, biology does not negotiate with virtue.

Obesity is a chronic, relapsing, neurohormonal disease. No one worked harder at weight loss than many of my surgical patients. Likewise, I do not lack willpower. And I practice culinary medicine. Preaching and eating a Mediterranean diet.

Nevertheless, effort alone does not silence dysregulated signaling.

Calling GLP-1 therapy “cheating” misunderstands the science. These medications restore signaling. They amplify satiety. They reduce excess reward drive. They support physiology.

That is treatment, not moral compromise.

When I began my career, I weighed about 185 pounds. Years later, hospital cafeterias, exhaustion, and irregular meals pushed me to 225. I understood obesity clinically. Then I understood it personally.

In one version of my career, revision surgery remains the answer for weight regain. In this version, I reached for GLP-1 therapy instead.

Today, I weigh what I weighed when Nixon was president.

I am both surgeon and patient.

And your reporter.

GLP-1 medications carry risks as well as benefits. Nausea can occur. Gastric emptying slows. Gallbladder disease risk may increase, although obesity itself already raises that risk substantially. Physicians must monitor dosing carefully.

Therefore, if you consider GLP-1 therapy, work with a trained physician who understands obesity medicine. Avoid quick online scripts. Seek supervision. Demand follow-up.

Metabolic medicine deserves serious care.

I once thought Phoenix was punishment. The heat felt relentless. Even Satan might choose a cooler vacation. Only Canadians brave July—and who can blame them?

However, what felt like exile turned out to be preparation.

In that same desert, I learned surgery. Researchers debated the thrifty gene. A venomous lizard carried a peptide that would become the basis of modern metabolic therapy.

I thought I had been sent to hell. But I found beauty in the desert, and by the time I left Arizona, I missed it terribly.

Little did I know I was sent to the future in Arizona.

Everywhere you look, protein has become a competition.

Scroll long enough and you will believe muscle disappears if you eat less than 150 grams a day. Meanwhile, influencers debate leucine thresholds like they’re trading baseball cards. As a result, ordinary meals now feel like math problems.

However, biology does not require panic.

Protein matters. Yet adequacy differs from excess. And importantly, most people eating real food already meet their needs.

So let’s slow down.

Protein builds and repairs tissue. In addition, amino acids support immune function and hormone signaling. Furthermore, specific amino acids such as leucine trigger muscle protein synthesis.

Nevertheless, once you reach the effective leucine threshold in a meal, adding more protein does not multiply muscle growth. Instead, your body oxidizes the excess.

Therefore, more does not always mean better.

For most healthy adults, about 0.8 grams per kilogram of body weight covers basic needs. Meanwhile, adults over 60 often benefit from 1.0 to 1.2 grams per kilogram to protect lean mass.

Notably, that recommendation does not require heroic intake. In fact, a 75–80 kilogram adult typically lands between 60 and 90 grams per day.

Consequently, many people hit those numbers without even trying.

I do not count protein. I never log grams. Moreover, I do not calculate leucine before breakfast.

Instead, I eat normal meals.

Most mornings, I have a shake. The recipe lives on terrysimpson.com. That shake provides roughly 25 grams of protein. Sometimes I add PB Fit. Occasionally, I include Greek yogurt. As a result, I increase protein slightly without thinking about it.

Later, I eat three to five ounces of chicken breast with Louisiana hot sauce. That adds another 25 grams.

Then at dinner, I often choose salmon and chickpeas. Together, they bring me to roughly 70–80 grams for the day.

Importantly, I have lost 50 pounds and preserved muscle mass. I track muscle periodically. I see no decline.

So what about leucine?

High-quality animal protein contains about 8–10% leucine. Therefore, a 25-gram protein meal delivers about 2 grams of leucine. That amount typically triggers muscle protein synthesis.

Thus, I hit the effective threshold at each meal without obsessing.

GLP-1 medications reduce appetite. Consequently, total intake drops. Because of that, protein intake can fall too.

So yes, people using GLP-1 should pay attention. However, they do not need 180 grams per day. Instead, they need adequacy and resistance training.

Lift something heavy. Spread protein across meals. Preserve lean mass.

Simple.

Protein deficiency remains rare in the United States. By contrast, fiber deficiency remains common.

According to the National Institutes of Health, most adults fail to meet recommended fiber intake levels. In fact, average intake falls far below the 25–38 grams per day recommended for adults.

(Reference: NIH Office of Dietary Supplements – Fiber Fact Sheet)

Meanwhile, high-protein diets often crowd out legumes, whole grains, and vegetables.

So while people panic about protein, they quietly neglect fiber.

And fiber feeds the microbiome. Fiber improves glycemic control. Fiber lowers LDL cholesterol.

Protein builds muscle. Fiber protects metabolism.

Both matter.

Mediterranean-style eating provides protein from fish, legumes, yogurt, and moderate poultry. At the same time, it supplies fiber from beans, vegetables, and whole grains.

Therefore, protein arrives packaged with micronutrients and fermentable substrate.

Unlike protein powders and bars, real food supports multiple systems at once.

Consequently, longevity patterns emphasize diversity, not maximal single-nutrient intake.

Adequate protein preserves muscle. Resistance training drives adaptation. Fiber protects metabolic health.

So before you triple-scoop whey, pause.

Ask yourself whether you lack protein — or whether you lack plants.

Because protein matters.

Panic does not.

And once again, data beats dogma.

Every time someone says Mexican food is unhealthy, I know exactly what they’re picturing.

They aren’t picturing Mexico.

They’re picturing an American taco: a hard shell or a fluffy white flour tortilla, fatty hamburger, sour cream, a thin smear of salsa that contributes almost nothing except salt, and a yellow substance legally allowed to be called cheese.

After eating that, they naturally conclude Mexican food is the problem.

That conclusion doesn’t come from biology. It comes from branding.

Traditional Mexican food looks nothing like that. More importantly, it behaves nothing like that once it hits your body.

So let’s slow down, take a breath, and do what we always do here—follow the evidence, not the vibes.

The American taco stacks the deck against itself.

It leads with saturated fat, piles on refined carbohydrates, and adds dairy on top of dairy. Meanwhile, it offers almost no fermentable fiber. The gut gets nothing to work with. Blood sugar spikes. Inflammation follows.

That taco doesn’t help anyone.

But here’s the key point: it isn’t Mexican food.

It’s ultra-processed American convenience food wearing cultural drag.

By contrast, a traditional taco starts very differently.

It starts with a corn tortilla, not refined flour. Then it adds beans. After that, it layers vegetables, real salsa, and often cabbage. Finally, it finishes with avocado. Sometimes it includes fish. Sometimes it doesn’t. Either way, the structure holds.

And structure matters.

Because when you look at how that meal behaves biologically, it stops looking indulgent and starts looking smart.

First of all, traditional corn tortillas come from nixtamalized corn. That process treats corn with lime, and no, that isn’t trivia.

Instead, nixtamalization improves mineral absorption, improves protein quality, and preserves resistant starch.

As a result, resistant starch passes through the small intestine untouched. Then it reaches the colon, where gut bacteria ferment it. Consequently, those bacteria produce short-chain fatty acids, especially butyrate.

And here’s the important part: butyrate fuels the cells lining your colon. In addition it strengthens the gut barrier. It reduces inflammation. Finally, it improves metabolic signaling.

So no, this isn’t a carb disaster. On the contrary, it’s colon nutrition.

Next, add beans.

At that point, the conversation usually derails, so let’s keep it grounded.

A serving of beans delivers roughly ten grams of fiber. Not one kind — several kinds. Soluble fiber. Insoluble fiber. Resistant starch. Plus protein.

Because of that, beans slow digestion. They flatten glucose curves. They improve satiety. Most importantly, they feed gut bacteria that matter.

Specifically, bean fiber supports Akkermansia, a gut bacterium associated with better insulin sensitivity and a stronger gut barrier.

In other words, beans don’t fill space. Instead, they build infrastructure.

And yes, when you pair beans with rice, you get a complete amino acid profile. Humans figured that out centuries ago, long before protein powders and “ancestral” snack companies tried to monetize it.

At this point, someone inevitably says, “But what about refried beans?”

So let’s clear that up.

First, frijoles refritos does not mean “fried twice.” It means well-fried or thoroughly cooked. Traditionally, people cooked beans, then lightly cooked them again, often mashing them for texture.

So yes — refried beans are traditional. Very traditional.

Moreover, mashing beans does not remove fiber. Cooking beans does not turn them into sugar. Beans remain beans.

So where did refried beans go wrong?

Fat choice.

Historically, many refried beans used lard. That made sense when calories were scarce and undernutrition threatened survival. However, in a modern context, large amounts of lard mean large amounts of saturated fat.

Therefore, when refried beans swim in lard, then get buried under cheese, then land inside a refined flour tortilla, the problem isn’t the beans. The problem is the fat context.

Fortunately, this problem has an easy fix.

Use olive oil or another unsaturated fat. Add onions and garlic. Mash lightly, not into paste. Suddenly, refried beans snap right back into a Mediterranean-style pattern.

And yes — some commercially available refried beans already do this. Look for short ingredient lists. Look for beans, oil, onion, garlic, salt. Skip the lard. Skip the mystery fats. Your gut will notice.

Then comes avocado, which people love to blame for reasons that make no biological sense.

Avocado provides about five grams of fiber and a meaningful amount of monounsaturated fat — the same fat family as olive oil.

More importantly, fat enables absorption of fat-soluble vitamins: A, D, E, and K.

So when you add avocado to vegetables, you don’t ruin the meal. Instead, you make the nutrients available.

In other words, avocado doesn’t cancel vegetables. It activates them.

Meanwhile, real salsa brings tomatoes, onions, garlic, chilies, and cilantro to the table. That means fiber. That means polyphenols. That means fermentable substrate for gut bacteria.

Add corn to the salsa and you add more whole grains and more resistant starch.

Then add cabbage — raw or lightly dressed — and now you feed short-chain fatty-acid producers directly.

Nothing exotic. Nothing trendy. Just food that works.

Now zoom out.

Traditional Mexican food emphasizes whole grains, legumes, vegetables, unsaturated fats, and fermentation. It stays naturally low in saturated fat. It supports the microbiome. It respects digestion.

In other words, it follows the Mediterranean pattern.

Not because it sits near the Mediterranean Sea — but because biology doesn’t care about geography.

The Mediterranean diet is a structure, not a destination.

Whether you eat it in Greece.

Or you eat it in Italy.

But you can eat it wrapped in a corn tortilla.

Processing.

Refining grains.

Deep-frying bases.

Replacing beans with beef.

Replacing water with sugar.

Turning cheese into a load-bearing wall.

Mexican food didn’t fail.

Industrial food did.

A traditional taco — corn tortilla, beans or properly made refried beans, vegetables, avocado, real salsa, maybe fish — fits squarely into one of the healthiest dietary patterns we know.

Different culture.

Same biology.

So the next time someone tells you Mexican food is unhealthy, remember this:

The taco was framed.

And once again — data beats dogma.

Fiber has a public relations problem. Unlike supplements or extreme diets, fiber does not promise instant transformation. Instead, it works slowly, predictably, and quietly. Because of that, people rarely notice it when it’s doing its job well. However, that very boredom is precisely why fiber matters.

When fiber intake is adequate, digestion functions normally, blood sugar behaves more consistently, and bowel habits stay predictable. As a result, there is no drama to post on social media. Consequently, influencers move on. Meanwhile, the science stays exactly where it has been for decades: fiber lowers disease risk over time.

That kind of quiet effectiveness may not sell products, but it saves lives.

Technically speaking, fiber is not an essential nutrient in the classic sense. In other words, there is no disease caused solely by a lack of fiber the way scurvy results from vitamin C deficiency. Because of this, critics often stop the conversation there.

However, medicine does not ask only whether you survive. Instead, it asks whether your risk of chronic disease rises or falls over time. On that front, fiber consistently lowers the risk of colon cancer, improves glucose regulation, reduces constipation, and supports cardiovascular health. Therefore, while you can live without fiber, you do not age particularly well without it.

At the same time, nutrition conversations fixate on protein. Protein goals dominate podcasts, social media, and supplement aisles. Yet, in practice, true protein deficiency in the United States is rare, even among bariatric surgery patients.

In contrast, fiber deficiency is the norm. Roughly 92% of Americans fail to meet recommended fiber intake. As a result, constipation becomes common, long bathroom visits feel normal, and scrolling on a phone in the bathroom gets rebranded as “self-care.” Unfortunately, that normalization hides a real problem.

Years ago, I learned a fiber lesson the hard way. After deciding to increase my fiber intake quickly, I started eating steel-cut oats every morning during a busy meeting week. At first, everything seemed fine. Soon, however, my digestive system made it clear that it had not been consulted in this decision.

By the second day, bloating appeared. By the third day, office etiquette became questionable. Consequently, I lit a candle at my desk. Unfortunately, I turned my back, and papers caught fire. Although the flames were extinguished quickly, the scorch mark stayed for years.

That stain served as a reminder: fiber works best when introduced gradually. Your gut adapts over time. Confidence without patience, on the other hand, leads to unnecessary consequences.

Understanding fiber helps people stop fearing it. Soluble fiber, found in oats, barley, beans, lentils, psyllium, apples, and citrus, forms a gel in the gut. Because of this, it slows absorption, reduces glucose spikes, and lowers LDL cholesterol. Consequently, psyllium appears in clinical guidelines rather than influencer protocols.

Meanwhile, insoluble fiber focuses on mechanics. It adds bulk, speeds transit, and improves regularity. Importantly, this matters even more for people using GLP-1 medications, where slowed digestion often leads to constipation. In that setting, fiber is not optional—it is foundational.

Finally, fermentable fiber feeds gut bacteria. Beans, onions, garlic, asparagus, chicory root, and resistant starch nourish beneficial microbes. As these bacteria grow, they produce short-chain fatty acids, especially butyrate, which supports gut barrier function and immune regulation.

Despite what circulates online, butter does not meaningfully deliver butyrate to your colon. Although butter contains trace amounts of butyric acid, that fat is absorbed in the small intestine long before it reaches the colon. In contrast, the butyrate that protects colon health is produced by bacteria fermenting fiber directly in the colon.

Therefore, if butter were an effective therapy, gastroenterologists would prescribe croissants. They do not.

Fiber supplements can be useful. Psyllium and methylcellulose typically provide four to five grams of fiber, which helps people start. However, that amount represents only about ten percent of a reasonable daily target.

Personally, I use Loam, which provides around twelve grams of mixed fiber in a smoothie. Nevertheless, supplements act as bridges, not destinations. Ultimately, food does the heavy lifting.

Some people with IBS feel worse when fermentable fiber increases too quickly. Because fermentation produces gas, symptoms can flare initially. For that reason, clinicians use FODMAPs as a temporary elimination tool to identify triggers.

However, elimination is not the end goal. Instead, we reintroduce foods within a Mediterranean dietary pattern, which promotes diversity and tolerance. In contrast, Whole30 markets itself as elimination but functions primarily as low-carb restriction. That approach avoids symptoms rather than solving them.

People do not eat grams of fiber. They eat meals. A Mediterranean-style day, such as the 3-Day Mediterranean Diet at terrysimpson.com, delivers fiber incidentally.

Breakfast often includes oats, berries, and nuts. Lunch typically features vegetables, legumes, whole grains, and olive oil. Snacks rely on fruit, nuts, or hummus. Dinner centers on vegetables, whole grains like farro, and fish or poultry. Over the course of a day, fiber naturally reaches 25–40 grams without spreadsheets or stress.

If you currently eat little fiber, the solution is simple but not dramatic. Increase intake gradually. Drink water. Give your microbiome time to adapt. Although you are not fragile, abrupt change can still cause discomfort.

Fiber does not need hype. Instead, it needs consistency. It works quietly, steadily, and reliably. If bathroom visits require entertainment, the issue is not age—it is fiber.

Food noise does not announce itself politely. Instead, it hums in the background, persistent and exhausting. For years, patients tried to describe it. Meanwhile, medicine largely ignored it. Recently, however, GLP-1 receptor agonists forced the conversation into the open.

I did not understand food noise myself until it stopped.

About twelve hours after my first GLP-1 injection, I stood in my kitchen waiting for baked salmon to finish cooking. Nothing dramatic happened. No emotional moment followed. Still, something felt different. The internal commentary was gone. The negotiations disappeared. For the first time, my brain felt quiet.

At that moment, I finally understood what patients had been telling me for years.

Food noise is not hunger. Hunger serves a biological purpose. In contrast, food noise describes persistent, intrusive thoughts about food that occur regardless of energy needs. People experience rumination, preoccupation, cravings, and mental fatigue—even when they are physiologically full.

Importantly, this phenomenon is now measurable. The Food Noise Questionnaire validates what patients already knew. Specifically, it assesses the frequency of food thoughts, difficulty controlling them, interference with daily activities, emotional distress, and craving intensity. In other words, food noise exists independently of willpower.

Consequently, advice that targets hunger alone inevitably fails.

I eat vegetables. Nevertheless, I have never liked broccoli.

Frankly, if broccoli is air-fried to the edge of carbonization, I will tolerate it. That concession, however, does not transform broccoli into a neurological intervention. Fiber increases fullness. Protein improves satiety. Vegetables slow digestion. None of those actions quiet the reward centers of the brain.

Put simply, broccoli fills the stomach. Food noise lives elsewhere.

Because of that distinction, the “just eat for satiety” argument collapses under scrutiny.

Food noise arises from heightened food-cue reactivity. Visual cues, smells, availability, and anticipation activate reward pathways long before food reaches the stomach. Ultra-processed foods amplify this response. Their engineered combinations of refined carbohydrates, fats, salt, and flavor compounds reliably stimulate the mesolimbic dopamine system.

As a result, ultra-processed foods increase wanting rather than liking.

However—and this matters deeply—removing ultra-processed foods does not automatically restore normal appetite signaling. Once reward circuitry becomes dysregulated, dietary virtue alone cannot reset it. At that stage, telling someone to “just eat whole foods” resembles telling someone with tinnitus to “enjoy the silence.”

Therefore, ultra-processed foods contribute to the problem, but they do not explain it entirely.

GLP-1 receptor agonists act centrally and peripherally. While many people fixate on gastric emptying, the central mechanisms explain the lived experience.

In the hypothalamus, GLP-1 receptor agonists activate satiety-promoting POMC/CART neurons while inhibiting hunger-promoting NPY/AgRP neurons. This dual action reduces homeostatic hunger. Meanwhile, in the brainstem—particularly the nucleus tractus solitarius—GLP-1 signaling integrates gut-brain communication and sustains appetite suppression.

More importantly, GLP-1 receptor agonists modulate reward circuitry. In regions such as the ventral tegmental area and nucleus accumbens, these agents dampen dopamine signaling. Consequently, food becomes less compelling rather than forbidden.

Functional imaging studies confirm this effect. After GLP-1 treatment, brain responses to food cues decrease in the insula, amygdala, orbitofrontal cortex, and related regions. The brain still recognizes food. It simply stops obsessing.

Once food noise quiets, people do not suddenly become disciplined saints. Instead, they become selective.

In my own case, wine lost its appeal. I did not swear it off. I simply stopped wanting it. Eventually, I quit five wine clubs. When a glass tastes mediocre, I put it down and choose iced tea. That behavior reflects altered reward signaling, not moral growth.

Similarly, food choices shift without struggle. People stop eating things merely because they are available. They stop drinking because something is poured. The absence of compulsion creates space for intentional eating.

That distinction explains why GLP-1 therapy feels different from appetite suppression.

The Mediterranean diet improves health. I recommend it. I eat it. Still, it does not cure food noise.

Diet supports metabolic health once interference disappears. GLP-1 therapy removes that interference. Together, they work better than either alone. Pretending otherwise leads to fat shaming disguised as nutritional advice.

Obesity is a disease. GLP-1 receptor agonists treat that disease. Food then becomes nourishment rather than negotiation.

Ultra-processed foods worsen food noise, yes. Yet removing them does not repair dysregulated reward circuitry. Satiety fills the stomach. GLP-1 therapy quiets the brain. Once the noise fades, nutrition finally has a fair chance.

In the end, broccoli keeps my mother from returning from the grave. GLP-1s keep my brain quiet. Both have their place. Only one treats the disease.

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The Journal of the American Medical Association. 2024. Gudzune KA, Kushner RF.

2. The Arcuate Nucleus Mediates GLP-1 Receptor Agonist Liraglutide-Dependent Weight Loss.

The Journal of Clinical Investigation. 2014. Secher A, Jelsing J, Baquero AF, et al.

3. Direct and Indirect Effects of Liraglutide on Hypothalamic POMC and NPY/­AgRP Neurons - Implications for Energy Balance and Glucose Control.

Molecular Metabolism. 2019. He Z, Gao Y, Lieu L, et al.

4. On the Pleiotropic Actions of Glucagon-Like Peptide-1 in Its Regulation of Homeostatic and Hedonic Feeding.

International Journal of Molecular Sciences. 2025. Sayers S, Wagner E.New

5. Glucagon-Like Peptide 1 (GLP-1) Action on Hypothalamic Feeding Circuits.

Endocrinology. 2025. Hwang E, Portillo B, Williams KW.New

6. GABA Neurons in the Nucleus Tractus Solitarius Express GLP-1 Receptors and Mediate Anorectic Effects of Liraglutide in Rats.

Science Translational Medicine. 2020. Fortin SM, Lipsky RK, Lhamo R, et al.

7. GLP-1 Receptor Activation Modulates Appetite- And Reward-Related Brain Areas in Humans.

Diabetes. 2014. van Bloemendaal L, IJzerman RG, Ten Kulve JS, et al.

8. Glucagon-Like Peptide 1 and Its Analogs Act in the Dorsal Raphe and Modulate Central Serotonin to Reduce Appetite and Body Weight.

Diabetes. 2017. Anderberg RH, Richard JE, Eerola K, et al.

9. of GLP-1 Therapies for Addiction and Mental Health Comorbidities—Quo Vadis?.

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10. GLP-1 and Weight Loss: Unraveling the Diverse Neural Circuitry.

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11. Mechanisms of GLP-1 Receptor Agonist-Induced Weight Loss: A Review of Central and Peripheral Pathways in Appetite and Energy Regulation.

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Whole milk is back in school cafeterias.

As a result, a lot of people are celebrating. Some are calling it a victory for nutrition. Others are calling it common sense. Meanwhile, a few are even calling it a breakthrough.

However, that excitement misses the point.

Because the biggest problem facing kids in school today is not milk fat.

Instead, the real problem is hunger.

Before we talk about milk, fat, or nutrients, we need to start with something very basic.

Hungry kids do not learn well.

In fact, hunger affects attention, memory, and behavior. As a result, students who do not eat enough struggle to focus. Over time, that struggle shows up as lower academic performance.

Because of that, no change to milk will ever fix an empty stomach.

Therefore, if we want better outcomes, we have to start with food access.

Despite what many people believe, whole milk was not removed from schools in the past.

Instead, schools continued to offer low-fat and fat-free milk.

Importantly, those options provided the same essential nutrients:

1. protein
2. calcium
3. potassium
4. iodine
5. vitamin B12

In addition, vitamin D was added through fortification, regardless of milk fat level.

So, children did not lose vital nutrients.

What they lost was milk fat.

Milk fat is made mostly of saturated fat.

That matters because saturated fat is not an essential dietary nutrient.

If the human body needs saturated fat, it can make it on its own. In other words, there is no requirement to eat it for normal growth or brain development.

As a result, adding more saturated fat to a child’s diet is not necessary.

Here is where biology matters.

The brain is built largely from polyunsaturated fats, not saturated fats.

These polyunsaturated fats keep cell membranes flexible. Because of that flexibility, brain cells can signal, adapt, and learn.

In contrast, saturated fat is rigid. It plays only a small structural role in membranes. If membranes contained too much saturated fat, they would become stiff. When that happens, signaling does not work well.

For that reason, biology uses saturated fat sparingly.

Therefore, less saturated fat in the diet of growing children is actually better for long-term brain and cardiovascular health.

If there is one nutrient that most children lack, it is fiber.

Fiber supports gut health. In addition, it improves insulin sensitivity. Over time, it also reduces cardiovascular risk.

Milk fat does none of those things.

So, if nutrition is the concern, fiber deserves more attention than nostalgia for saturated fat.

While milk is being discussed, something else is happening quietly.

Food assistance programs are being reduced.

That matters because programs like SNAP do more than help families buy groceries. They also help children qualify for free school meals.

When eligibility is reduced, fewer children qualify. As a result, schools receive less funding for lunch programs. Consequently, some schools serve fewer meals. In certain communities, programs disappear entirely.

Therefore, the outcome is simple: fewer kids eat at school.

Some states have shown a different approach.

When children receive meals consistently, attendance improves. At the same time, concentration improves. Over the long term, educational outcomes improve as well.

This result has been seen repeatedly.

Because of that, feeding kids is not charity. Instead, it is an investment in education, health, and future productivity.

Whole milk is fine.

If families enjoy it, they can drink it. If schools offer it, that is acceptable.

However, whole milk is not an innovation.

Feeding children is.

Ultimately, school meals should not be treated as a budget line to debate each year. Instead, they should be treated as part of what a functioning society does for its kids.

For readers who want the science behind membrane fats and brain function, this review explains it clearly:

Stillwell W, Wassall SR.

Docosahexaenoic acid: membrane properties of a unique fatty acid.

Chemistry and Physics of Lipids. 2003;126(1):1–27.

This paper explains why polyunsaturated fats keep membranes flexible and why saturated fats play only limited roles.

Every few years, nutrition gets a makeover.

First comes a new graphic.

Then comes a new slogan.

Soon after, we hear claims that this time, someone finally figured it all out.

Recently, that makeover arrived in the form of a “reverse food pyramid” and the cheerful phrase “Eat Real Food.” On the surface, that message sounds reasonable. In fact, many doctors have said the same thing for decades.

However, the real problem isn’t the slogan.

Instead, the problem lies in who is now shaping nutrition advice—and who is not.

To be clear, let’s start with agreement.

Eating real food helps health.

Limiting added sugar makes sense.

Reducing ultra-processed foods improves outcomes.

Importantly, none of this is new.

Doctors, dietitians, and public-health researchers have said these things for years. Because of that, when influencers now say, “See, we were right,” a serious issue appears.

They didn’t discover this information.

They copied it.

At first glance, agreement sounds harmless.

Nevertheless, agreement becomes dangerous when it turns into ownership.

Once someone believes they have discovered basic nutrition truths, they often assume they can rewrite everything else. As a result, bad ideas slip in quietly, wrapped in confidence instead of evidence.

That shift matters.

At this point, we need to say something clearly.

We cannot afford to replace scientists with influencers.

Nutrition science didn’t come from podcasts or social media. Instead, it came from metabolic ward studies, long-term population research, and randomized trials. Moreover, real scientists accept uncertainty. They change their minds when the data changes.

By contrast, influencer culture rewards certainty.

Even worse, confidence often replaces humility.

There is no “Mediterranean diet influencer community.”

Likewise, there is no “DASH diet movement.”

Those dietary patterns exist because scientists studied them, tested them, and measured outcomes over time.

On the other hand, a loud low-carb and carnivore influencer ecosystem does exist. That ecosystem includes brands, supplements, coaching programs, and a strong contrarian identity. Because of that structure, influence—not evidence—often drives the message.

If you want to know whether someone understands nutrition science, ask a simple question:

Which matters more—fiber or saturated fat?

Influencers often say, “Fiber isn’t an essential nutrient.”

Technically, that statement is true in the narrowest sense.

However, context matters.

Fiber supports a healthy gut microbiome.

Additionally, fiber improves insulin sensitivity.

Furthermore, fiber lowers cardiovascular risk.

Finally, fiber supports colon health.

Because fiber feeds beneficial gut bacteria, entire fields of microbiome research depend on it.

Now compare that with saturated fat.

Saturated fat is truly non-essential.

Your body can make all it needs.

No deficiency disease exists from avoiding it.

Even more importantly, excess saturated fat raises LDL cholesterol and worsens artery health. Over time, that increases cardiovascular risk.

So ask yourself this:

Why dismiss fiber as optional while quietly promoting saturated fat?

That choice reflects ideology, not biology.

Here’s another reality check.

Your brain—the most important organ you own—relies heavily on polyunsaturated fats. These fats support cell membranes, nerve signaling, and blood flow.

Ironically, these same fats often get labeled “seed oils” and dismissed.

Meanwhile, saturated fat does not belong in high amounts in brain tissue. Worse still, saturated fat can clog the arteries that supply the brain.

Biology does not respond to marketing.

Physiology does not care about popularity.

Another issue deserves attention.

After influencers step into the spotlight and claim credit for old science, they often step away from responsibility. Then they tell the public to “figure it out.”

That approach ignores reality.

Many Americans live in food deserts.

Even more rely on school meals.

Lots of Americans work multiple jobs.

Many lack time, money, or kitchens.

Public health exists because willpower alone does not scale. Without system-level support, advice turns into abandonment.

Recently, debates around nutrition have highlighted this pattern clearly.

Some influencers argue that because they agree with basic nutrition advice, they deserve authority over the rest of the science. Unfortunately, agreement does not grant expertise.

Copying conclusions does not mean you earned them.

Science rewards method, not confidence.

Yes, eat real food.

And clearly, limit added sugar.

Most definitely, reduce ultra-processed foods.

Doctors have said this for years.

However, flipping a pyramid does not change biology.

Likewise, sidelining scientists does not improve health.

Finally, promoting saturated fat while dismissing fiber misleads the public.

People do not fail diets.

Systems fail people.

When we trade evidence for influence, health suffers.

This article provides general education, not personal medical advice. Always talk with your healthcare professional about individual nutrition needs.

At Your Doctor’s Orders, we believe data matter more than dogma, and evidence matters more than trends.

Because when it comes to health, confidence without science is not bold.

It’s risky.

Ultra-processed food has become the villain of modern nutrition.

Scroll through social media, and you’ll hear that it’s poisoning us, wrecking our gut, and driving the obesity epidemic all by itself.

At the same time, other voices dismiss the entire idea as fear-mongering.

According to them, processing doesn’t matter at all.

Neither extreme tells the full story.

So instead of slogans, let’s talk about what ultra-processed food actually means, why people want to blame it, where the science is strong, and where it starts to drift into storytelling.

The obesity epidemic is real.

Rates have climbed for decades, and people understandably want answers.

Human biology didn’t suddenly change in the 1980s.

Willpower didn’t vanish overnight.

Something in our environment shifted.

Food is an obvious suspect.

Because food changed, many people assume there must be a single culprit hiding in the ingredient list.

That belief leads to bold claims.

Some say Europe bans certain additives and therefore avoids obesity.

In reality, obesity rates continue to rise across Europe as well.

Others argue that specific ingredients damage the gut, letting in more calories or triggering metabolic chaos.

Those ideas sound scientific, especially when they involve complex biology.

However, when a problem is large and complicated, humans naturally want a cause that feels simple and controllable.

Blaming one ingredient feels easier than confronting patterns of eating, stress, time pressure, and convenience.

Biology, unfortunately, rarely offers cinematic villains.

To understand the debate, definitions matter.

Researchers use the NOVA classification system to describe food processing.

NOVA does not rate healthfulness.

Instead, it categorizes food by how manufacturers produce it.

The system includes four groups.

First come whole or minimally processed foods, such as vegetables, beans, eggs, and fish.

Next are culinary ingredients like oil, sugar, salt, and flour.

Then come processed foods, including bread, cheese, yogurt, and canned vegetables.

Finally, NOVA defines ultra-processed foods as industrial formulations.

These products often combine refined ingredients with additives, stabilizers, emulsifiers, and flavor systems that home cooks rarely use.

Here’s the crucial point.

Ultra-processed food is defined by how it is made, not by what it does in the body.

That distinction often gets lost.

As a result, soda and whole-grain bread can fall into the same category, even though they behave very differently nutritionally.

At this point, many discussions take a wrong turn.

Instead of asking how people eat, the conversation focuses on what to ban.

Ingredients become the enemy.

Yet most claims about additives rely on animal studies using doses far higher than what humans consume.

Human data remains limited and inconsistent.

Meanwhile, the bigger picture often gets ignored.

Ultra-processed food correlates with stress, long work hours, poor sleep, and limited time for cooking.

Those factors influence eating behavior regardless of ingredients.

When people feel rushed and overwhelmed, they don’t just eat differently.

They eat faster, snack more often, and rely on foods that require little effort.

That context matters.

Instead of chasing villains, one researcher asked a much simpler question.

Do people eat more when food is ultra-processed, even when nutrition looks the same on paper?

That question led to the most important experiment in this entire debate.

At the National Institutes of Health, Kevin Hall conducted a tightly controlled feeding study.

Participants lived in a metabolic ward.

Researchers controlled the environment, the meals, and the measurements.

Each participant ate two diets.

One diet consisted mostly of ultra-processed foods.

The other relied on minimally processed foods.

Importantly, researchers matched calories, protein, fat, carbohydrates, sugar, and salt.

People could eat as much as they wanted.

The result surprised almost everyone.

On the ultra-processed diet, participants consumed about 500 extra calories per day.

Yet, they didn’t report more hunger.

They didn’t feel less full.

However, they simply ate more.

This finding matters because it avoids speculation.

No ingredient theories appear here.

No gut damage claims drive the conclusion.

Ultra-processed food made it easier to eat more calories without noticing.

Sometimes the most powerful answers are also the least dramatic.

That study helped fuel widespread interest, including the success of Ultra-Processed People: The Science Behind Food That Isn't Food by Chris van Tulleken.

Van Tulleken, a British physician, took a personal approach.

He ate a diet dominated by ultra-processed foods and documented the effects.

Weight gain followed.

Hunger became harder to regulate.

Energy and mood shifted.

The book resonated because it made an abstract concept feel personal.

It also highlighted how modern foods often prioritize shelf life, softness, and convenience.

Stories like this help people recognize patterns they already sense in daily life.

However, a compelling narrative does not replace careful interpretation.

Ultra-processed food is not one thing.

It does not act through a single mechanism.

The research faces several challenges.

First, heterogeneity clouds interpretation.

Grouping soda and yogurt together creates confusion rather than clarity.

Second, confounding remains a major issue.

People who eat more ultra-processed food often face structural barriers that affect health in many ways.

Third, additive panic oversimplifies biology.

Mouse data cannot stand in for long-term human outcomes.

Ultra-processed food may contribute to health problems, but it rarely acts alone.

Rigid rules tend to fail.

Real eating happens in real life.

Instead of asking whether a food qualifies as ultra-processed, better questions help guide choices.

Does the food contain fiber?

How will it contribute protein or micronutrients?

Finally, will it replace a balanced meal or help create one?

Can you eat it mindfully and stop when satisfied?

Foods like yogurt, tofu, olive oil, canned beans, and frozen vegetables often break simplistic rules.

Yet they support healthy eating patterns when used well.

Processing did not ruin our food.

Confusion did.

People want a villain because villains feel actionable.

Science, however, often points toward behavior rather than ingredients.

Ultra-processed foods encourage faster eating, softer textures, and higher calorie intake.

That pattern explains a great deal without invoking conspiracies.

Understanding that reality empowers better choices than fear ever could.

Hall KD, Ayuketah A, Brychta R, et al. Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial. Cell Metabolism. 2019;30(1):67–77.e3.

For decades, I started every New Year the same way.

In January, I promised myself this would be the year.

By February, I tried harder.

Every spring, I adjusted the plan.

And by summer or fall, the weight crept back.

That cycle repeated not because I lacked knowledge, discipline, or effort. Instead, it repeated because I misunderstood biology — at least when it came to myself.

This year is different.

For the first time since Ronald Reagan was first elected, weight loss is not at the top of my New Year’s resolution list. Not because I stopped caring, but because I lost 45 pounds with the help of Zepbound over the last year. More importantly, however, I learned something that reshaped how I think about obesity, healthspan, and shame.

Before anything else, let me be clear: this is not medical advice. This is a story. Anecdotes are not evidence, even when the anecdote is from a physician. Nevertheless, stories help us understand science when data alone fails to move us.

And this story matters.

For years, people told me — and millions of others — the same thing: move more and eat less. At first glance, that advice sounds logical. After all, calories matter. Energy balance matters.

However, reality is more complicated.

To begin with, I am a surgeon. Surgical training requires extraordinary willpower. Moreover, I’ve logged food meticulously, cooked Mediterranean-style meals, exercised consistently, and followed every evidence-based recommendation I’ve ever given patients.

Meanwhile, Oprah has willpower. Olympic athletes have willpower. Yet obesity persists.

Sure, willpower works briefly. In fact, go on a liquid protein diet, and the weight will fall off quickly. Unfortunately, the food noise remains. Eventually, biology wins. Always.

In the same way you cannot positive-think your way out of hypertension, cholesterol, diabetes, cancer, or heart disease, you cannot willpower your way out of obesity. Obesity is a disease. It is not a moral failure.

Ironically, I knew this intellectually. Nevertheless, I failed to apply it to myself. We have a name for that: cognitive dissonance.

The real turning point did not come from reading another study. Instead, it came from listening to people I trusted.

One colleague quietly lost weight on a GLP-1. Another friend told me something more striking: the food noise stopped. Alcohol lost its appeal. Smoking no longer called.

That phrase — food noise — suddenly explained decades of struggle.

To illustrate, think of sleeping near Lake Shore Drive in Chicago. At first, traffic noise dominates your awareness. Eventually, it fades into the background. Only when you leave the city do you realize how loud it was.

Food noise works the same way.

When GLP-1 therapy quieted that background signal, eating slowed naturally. Meals ended without effort. Desire changed without rules. Biology shifted.

Notably, calories did not lower my stress. Calories did not improve my sleep. Calories did not stop snoring. Biology did.

Interestingly, weight loss was not the first change I noticed.

Sleep improved almost immediately. Stress dropped dramatically. Commutes that once registered hours of physiologic stress now barely registered minutes. Appetite normalized. Eating slowed.

These changes matter because sleep and stress directly affect inflammation, metabolic health, appetite signaling, and long-term disease risk. In other words, healthspan improved before the scale reflected anything meaningful.

That observation alone reframed the entire experience.

Along the way, something else happened.

Friends noticed.

Predictably, they asked the same question everyone asks: What diet is working? After I answered honestly, several started their own journeys.

Soon enough, we formed an informal support group. People texted. Others called. Questions surfaced: Is this normal? Should I eat this? Does this feeling pass?

Support did not mean coaching. Rather, support meant context. Shared experience reduced anxiety. Honest conversations prevented unnecessary panic.

Not surprisingly, patterns emerged. People still loved great food. Wine interest decreased naturally. Travel did not end. Joy remained intact.

Support mattered because isolation amplifies shame.

Equally important, practical realities surfaced.

Eating less means needing micronutrients, not fewer of them. Unfortunately, some vitamins fail when appetite drops. In fact, the only time I vomited was after taking a vitamin on an empty stomach. That lesson mirrored decades of bariatric follow-up experience.

For me, AG1 worked. No sponsorship exists here. Nevertheless, cost raises questions. With a background in culinary medicine, developing a better formulation makes sense. Thiamine deficiency, for example, causes devastating neurologic consequences. This is not theoretical.

Similarly, bowel habits change. Less intake means less output. Fewer bowel movements do not equal constipation. Fiber still matters. Mediterranean-style eating naturally solves most of this problem.

Understanding physiology prevents fear.

At some point, frustration turned into obligation.

Recently, a physician who has never used a GLP-1 published a book about eating on GLP-1 therapy. That bothered me more than it should have.

Given my background — weight-loss surgery, culinary medicine, and lived experience — I realized I had to write this book. Not to sell diets, but to explain reality.

The working title?

Willpower Is B.S.

Subtlety has never been my strength.

This book will focus on biology, food ideas, micronutrients, behavior, and healthspan. Above all, it will remove shame from the conversation.

Incidentally, my literary agent retired long ago. Therefore, if you know someone who understands medicine, food, and honesty, I’m back in the market.

At the same time, conversations kept expanding beyond weight loss.

Healthspan matters more than thinness. Longevity depends on sleep, stress, nutrition, social connection, and movement. Accordingly, the Mediterranean Healthspan Cruise was born.

This is not a weight-loss cruise. Instead, it’s a learning experience. We will discuss food, medicine, science, and aging. Yes, there will be a GLP-1 support session. Equally, there will be conversations for everyone.

Learning works best in a community.

As I write this, I’m preparing to inject my 7.5 mg dose of Zepbound. I still hate needles. Some things never change.

Nevertheless, this is only part one of the journey.

Science progresses when we admit what we got wrong.

This time, I listened.

1. Jastreboff AM, Aronne LJ, Ahmad NN, Wharton S, Connery L, Alves B, Kiyosue A, Zhang S, Liu B, Bunck MC, Stefanski A; SURMOUNT-1 Investigators. Tirzepatide Once Weekly for the Treatment of Obesity. N Engl J Med. 2022 Jul 21;387(3):205-216. doi: 10.1056/NEJMoa2206038. Epub 2022 Jun 4. PMID: 35658024.
2. Rubino F et al. Joint international consensus statement for ending stigma of obesity. Nature Medicine, 2020.

My Whoop tells me I’m eight years older than I actually am.

Naturally, that raises a question.

Does that mean I’m going to die eight years sooner?

Is my watch quietly chiseling a new date onto my tombstone?

Fortunately, the answer is no.

Still, confusion around biologic age has exploded.

Wearables promise insight.

Apps offer scores.

Some even whisper about your future health, as if destiny lives on your wrist.

So let’s slow this down and talk about what biologic age really is — and why it matters far less than you think.

Every tombstone has two numbers.

One marks when you were born.

The other marks when you died.

However, the most important part isn’t either number.

It’s the dash in between.

That dash represents your life.

It reflects your health, mobility, independence, and curiosity.

When we talk about longevity, we shouldn’t obsess over the second number.

Instead, we should focus on making those two numbers far apart — and keeping the dash strong for as long as possible.

That’s healthspan.

Biologic age is not a prophecy.

It isn’t a death clock.

It doesn’t predict how long you’ll live.

Instead, biologic age is a model.

It estimates how your body is functioning right now based on things like:

• resting heart rate
• heart-rate variability
• sleep duration and consistency
• activity and recovery patterns
• sometimes weight or blood pressure

Different devices use different inputs.

As a result, they often give different answers.

In other words, biologic age reflects recent stress and behavior, not your destiny.

Think of it as feedback — not fate.

Earlier in the Fork U longevity series, we talked about telomeres.

Those shorten slowly over decades, one cell division at a time.

Your wearable isn’t tracking that.

Instead, devices like Whoop measure physiology, not DNA.

They detect how hard you’ve been living lately, not how much time you have left.

A bad week of sleep, travel, stress, or alcohol can push your biologic age higher.

A calm, consistent routine can bring it back down.

That’s not aging.

That’s load management.

Here’s a trick I tried.

I told Whoop I was younger than I actually am.

Guess what happened?

Suddenly, my biological age dropped below my real age.

That alone tells you everything.

Whoop isn’t predicting where you’re going.

It’s comparing how you’re doing relative to the age you told it you are.

Once again, that’s feedback — not destiny.

I use multiple devices because, frankly, I’m a nerd.

However, I tend to prefer Withings for one simple reason.

They don’t try to scare you.

Instead of telling you how old you “really” are, Withings focuses on things that actually improve your life today:

• blood pressure trends
• body weight and composition
• heart rhythm
• sleep duration
• long-term consistency

More importantly, they ask better questions.

Are you sleeping better?

Is your blood pressure improving?

Are your habits trending in the right direction?

That’s medicine.

Not numerology.

And no — Withings didn’t pay me to say that.

Many people treat biologic age like a grade.

Others see it as a moral judgment.

When the number drops, they feel virtuous.

When it rises, they panic.

That framing misses the point.

The only question that matters is this:

Is it moving in the right direction over time?

One bad week doesn’t define you.

One good week doesn’t either.

Trends matter.

Moments don’t.

No wearable can tell you:

• when you’ll die
• whether you’ll get cancer
• if you’ll have a stroke
• how many years you have left

Anyone claiming otherwise is selling fear — or subscriptions.

Technology can guide behavior.

It cannot predict destiny.

If you want to improve your biologic age — and more importantly, your healthspan — start here:

Sleep better and more consistently.

Build and maintain muscle.

Move your body every day.

Eat a Mediterranean-style diet.

Lower stress where you can.

Spend time with people you enjoy.

Do those things, and most metrics improve on their own.

Your watch is not your destiny.

Chronological age is fixed.

Healthspan is not.

Biologic age is adjustable, responsive, and reversible.

Use it as feedback.

Ignore it as prophecy.

And remember — the goal isn’t to beat time.

The goal is to live well while time keeps moving.

1. Levine ME. Modeling the rate of senescence: Can estimated biological age predict mortality more accurately than chronological age? J Gerontol A Biol Sci Med Sci. 2013.
2. Belsky DW, et al. Quantification of biological aging in young adults. Proc Natl Acad Sci USA. 2015.
3. Blackburn EH, Epel ES, Lin J. Human telomere biology: A contributory and interactive factor in aging, disease risks, and protection. Science. 2015.
4. WHOOP Team. Understanding Recovery, HRV, and Physiological Load.
5. Withings Health Institute. Longitudinal tracking of cardiometabolic health markers.