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.

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

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

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...

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...

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....

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.

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...