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