Episodios

  • Fat Shaming and GLP-1 - It's Biology
    Apr 9 2026
    The Chorus of “Just Eat Less”Spend a few minutes on social media, and you will hear it. On Bill Maher's podcast the other day, I heard it. Two people who know less about GLP-1 drugs than almost anyone, opining about how GLP-1s are horrific.Bill Maher says, “Just eat less.”Jillian Michaels warns that GLP-1 medications are dangerous. Did she even graduate from college?Meanwhile, a rotating cast of gym bros, coaches, and influencers insists that anyone using these medications is taking the easy way out.At first glance, these seem like different voices. A comedian, a fitness personality, a group of online trainers.However, they are all saying the same thing.If you are overweight, this is your fault.If you need help, you are weak.If you use medication, you are cheating.That message travels well. It is simple. It fits into a tweet. It sounds like common sense. Science shows us that fat shaming doesn't work (reference).It is also wrong.Who Is Doing the Shaming—and WhyThe fitness industry has something to lose here, and that part is easy to understand. Entire businesses are built on the idea that weight loss is a matter of discipline. Follow the plan, buy the program, track the macros, and success will follow. If it doesn’t, the explanation is built in.You didn’t try hard enough.However, the criticism does not stop there.When someone like Bill Maher reduces obesity to “just eat less,” it is not about selling a diet plan. Instead, it reflects something else entirely. A kind of cultural impatience with complexity. A belief that if a problem can be described simply, it must also be solved simply.And when that belief meets a condition like obesity, the result is dismissal.If I don’t struggle with this, then it must not be real.If you do struggle, then you must be doing something wrong.That is not analysis.That is a failure of imagination.The Problem with Simple AnswersMedicine has a long history of being wrong in simple ways.We once believed ulcers were caused by stress alone. Then came Helicobacter pylori and antibiotic treatment. We once thought hypertension was simply a matter of salt intake and personality. Then we developed therapies that addressed the underlying physiology.Obesity has followed a similar path, except we have been slower to let go of the old explanation.“Eat less, move more” is not incorrect.It is incomplete.Because it ignores the system that determines how much you want to eat, how often you think about food, and how your body responds when you try to lose weight.The Part I Didn’t AdmitFor years, I saw the damage this thinking caused.I ran support groups for patients struggling with weight. I watched them come in carrying not just pounds, but shame. They believed they were weak, that they lacked discipline, that something about them was broken.We worked to change that.We talked about biology. About appetite regulation. About how the body defends weight. We tried to replace blame with understanding.And yet, I quietly held myself to a different standard.I didn’t blame my patients.I blamed myself.The Surgeon Who Thought He Could Outwork BiologyIf anyone should be able to power through something, it is a surgeon. That is the job. Endure long hours. Stay focused. Push through fatigue. Delay gratification.So I assumed I could do the same with weight.I tried diets. I cleaned things up. I ate vegetables, cut back on certain foods, and experimented with structure. And like many people, I saw results.At first.Weight loss is not the mystery.Weight maintenance is.Because over time, the same thing happened again and again. The body adapted. Hunger increased. Energy dipped. The system pushed back.And eventually, the weight returned.What the Data Shows (and Why It Matters)When you look beyond personal stories and examine long-term studies, the pattern becomes clear.In the Diabetes Prevention Program, participants lost weight early, then gradually regained some of it. In the Look AHEAD trial, an intensive lifestyle intervention produced initial success, but the gap narrowed over time.Observational data suggest that only a small percentage of people—often cited around 3 to 5 percent—maintain significant weight loss at five years.That number should change the conversation.Because it tells us this is not a widespread failure of discipline.It is a predictable outcome of a biological system.The Loop We Keep IgnoringWeight gain does not happen in isolation. It is part of a loop.Sleep worsens, which increases appetite. Movement becomes uncomfortable, so activity declines. Food becomes more rewarding, not less, because it offers relief.Then intake increases.Then the cycle repeats.And yet, into that loop, we continue to insert the same advice.Try harder.What Finally ChangedFor years, I thought I just needed to try harder myself.I was wrong.Today, I am down fifty pounds.Not because I discovered a better diet, but because something changed in the system itself.I started a GLP-1–based ...
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    8 m
  • Menopause: Estrogen Effects Satiety
    Apr 2 2026
    Menopause, Hunger, and the Brain: Why It Feels DifferentMenopause changes more than temperature control. It reshapes how the brain handles hunger, fullness, and the quiet signals that guide eating. As a result, many women notice something unsettling. The same meals no longer satisfy. Hunger arrives sooner. Food feels louder.For years, we blamed metabolism. We told women their bodies were simply slowing down. While that explanation sounds scientific, it misses the most important part of the story.The brain has changed.A Pattern You Can’t IgnoreDuring my years performing weight loss surgery, about 80 percent of my patients were women. Over time, one pattern became impossible to overlook. When menopause or even perimenopause began, weight gain often followed.Some women had struggled with weight for years. Others had never given it much thought. Yet both groups described the same shift. They weren’t necessarily eating more. Instead, they felt hungrier, less satisfied, and more aware of food throughout the day.Meanwhile, the advice they received rarely evolved. Eat less. Move more. Try harder.However, that advice assumes the system regulating hunger still works the same way. In menopause, it doesn’t.Estrogen and the Appetite Control CenterTo understand what’s happening, we need to look at the hypothalamus. This small but powerful region of the brain regulates appetite, energy balance, and hormonal signaling. Under normal conditions, estrogen helps keep this system stable.Specifically, estrogen supports satiety signals and keeps hunger signals in check. In simple terms, it helps your brain recognize when you’ve had enough.As estrogen declines, that balance shifts. Hunger signals grow stronger. Fullness signals become less reliable. Consequently, the internal experience of eating begins to change.This shift explains why women often say, “I feel different around food,” even before their diet changes.Why Hunger Changes FirstInterestingly, appetite changes often appear before measurable increases in calorie intake. Women report thinking about food more often, feeling less satisfied after meals, and noticing hunger earlier in the day.At first glance, nothing looks different from the outside. Yet internally, the system has already shifted.Because of that, traditional advice falls short. Telling someone to eat less without addressing the change in signaling is like adjusting the thermostat while ignoring the wiring.More Than MetabolismAlthough metabolism does change with age, it does not fully explain the experience of menopause-related hunger. A slower metabolic rate might affect how calories are used, but it doesn’t explain why appetite feels louder or less controlled.Instead, the better explanation lies in the brain. The hypothalamus responds differently when estrogen levels fall. As a result, the signals that guide eating become less precise.In other words, this isn’t just about calories in and calories out. It’s about how the body decides when to eat—and when to stop.The Part We Should Have Addressed SoonerFor decades, menopause care focused on symptoms like hot flashes and bone health. Meanwhile, changes in appetite and weight were often attributed to lifestyle or willpower.Unfortunately, that approach overlooked a key fact. Estrogen plays a direct role in appetite regulation.Because of that, many women were told to push harder when their biology had already shifted. That message wasn’t just incomplete—it was unfair.Estrogen Replacement: A Broader RoleWhen clinicians discuss estrogen replacement, they often focus on symptom relief. However, estrogen also affects brain signaling related to hunger and satiety.In the right patient, hormone therapy may help restore some of that balance. It can improve how the brain responds to fullness and reduce the intensity of hunger signals.Importantly, hormone therapy does not inherently cause weight gain. That belief has persisted longer than the evidence supports.Still, therapy isn’t for everyone. Each patient requires an individualized discussion that considers risks, benefits, and goals.A New Layer: GLP-1 and Appetite ControlMore recently, GLP-1 receptor agonists have added another dimension to this conversation. These medications act on the same appetite centers in the brain, strengthening satiety and quieting hunger.Interestingly, estrogen appears to enhance the effectiveness of GLP-1 signaling. Therefore, menopause may not only reduce estrogen levels—it may also decrease the brain’s responsiveness to satiety cues.This interaction helps explain why some women experience such a dramatic shift in appetite during midlife.What Actually HelpsOnce you understand the biology, the approach changes.Rather than focusing solely on restriction, the goal becomes supporting satiety. Meals should include enough protein, fiber, and volume to sustain fullness. Additionally, sleep deserves attention, as poor sleep amplifies hunger signals. Medication ...
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    7 m
  • Henry VIII, the Brain, and the Obesity
    Mar 26 2026
    The Madness of King Henry VIII—and What We Got Wrong About ObesityThe King We ForgotThere is a moment in history that most of us think we understand. King Henry VIII—large, immobile, temperamental—has become almost a caricature of excess. We picture a man who simply ate too much, moved too little, and paid the price. It is a tidy story. Unfortunately, it is also likely the wrong one.Before the 1530s, Henry was something very different. He was athletic, charismatic, and energetic. He hunted, he jousted, he played sports, and he carried himself like the Renaissance ideal—educated, capable, and physically impressive. His armor, still preserved today, tells that story clearly. Narrow waist. Broad chest. Built for motion.The Fall That Changed EverythingThen everything changes.In January of 1536, Henry was thrown from his horse during a jousting match. The horse fell on him. He was reportedly unconscious for hours. Not minutes—hours. Even by modern standards, that is a significant traumatic brain injury.Soon after, in May of that same year, Anne Boleyn was arrested and executed. She was accused not only of adultery but also of witchcraft. That detail matters. Prior to this period, Henry was not known for superstition. He was a rational thinker. Yet suddenly, accusations of witchcraft become part of the story. It is tempting to say this was political theater. It may have been. Still, the timing is difficult to ignore.Meanwhile, his body begins to change.The Story We Told OurselvesAt first, historians explained this in simple terms. He ate more. He exercised less. Calories in, calories out. That explanation sounds neat. It fits what we like to believe. Even so, the math does not hold up.To gain over 200 pounds, you need a massive and sustained excess of calories. A reduction in physical activity alone does not explain that. We measure activity in METS—metabolic equivalents—and even a dramatic drop in activity would not account for that level of weight gain. In other words, you cannot outrun the math.Yet every January, gyms fill with people who are told exactly that. Move more. Try harder. Burn it off. By February, most of those gyms are empty again. If exercise alone solved obesity, we would not still have the problem.The Organ in ChargeSo what did we miss?The answer sits deep in the brain, in a small but powerful structure called the hypothalamus. It regulates hunger, satiety, hormones, and stress. When it works, eating feels normal. You get hungry, you eat, you stop. No drama. No constant thinking.However, when the hypothalamus is disrupted—by injury, disease, or chronic metabolic stress—that quiet system becomes loud. Hunger no longer behaves like a signal. It becomes a drive.This is not theory. Modern medicine has a name for it: acquired hypothalamic obesity. After traumatic brain injury, some patients develop rapid weight gain, persistent hunger, and changes in impulse control. Studies show that nearly half of patients with significant brain injury gain weight over time. The strongest predictor is not inactivity. It is hyperphagia—an abnormal increase in appetite.In simpler terms, the problem is not how much people move. It is what their brain is telling them to do.What Patients Taught MeThat pattern feels familiar if you have ever sat with patients. I have. Years ago, working with former NFL players, we noticed something striking. The players who struggled most with weight often had long histories of concussions. Not all of them gained weight. Yet those who did described the same experience—something they had never felt before.Food noise.Not hunger. Noise. A constant suggestion that does not go away.At first, I understood that as a physician. Later, I understood it as a person.When the World Went QuietAbout twelve hours after my first injection of Zepbound, something changed. The world became quiet. For the first time, I realized how much of my thinking had been shaped by that background noise. It did not disappear dramatically. It simply stopped.Since then, I have lost fifty pounds. More interesting than the weight loss is what happens between doses. As the medication wears off, the noise returns—subtly at first. A thought here. A reminder there. Even my stress levels rise slightly, something I can see on my WHOOP device. Then, a few hours after the next injection, it quiets again.That experience changes how you see patients. It changes how you see history.Looking Back at HenryBecause now, when we look back at Henry, we are not just looking at excess. We are looking at a possible disruption of the system that regulates behavior itself.There are hints of this even in his own time. A French ambassador noted that Henry’s chronic leg pain troubled him often and that he compensated by eating and drinking more. Later reconstructions suggest large meals, heavy in meat, along with substantial alcohol intake. Those numbers are estimates, not precise measurements. Even so, the pattern is...
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    12 m
  • The Carnivore Priesthood
    Mar 19 2026
    When Beef Becomes Belief: The Carnivore PriesthoodNutrition debates rarely begin with money. Yet money almost always explains how they spread.That fact explains much of the modern carnivore movement.At first glance, the carnivore diet appears to be a radical nutritional idea: eat beef, organs, and animal fat while avoiding vegetables, grains, legumes, and most fruits. Advocates often present the idea as a return to ancestral eating. According to the story, prehistoric humans thrived on meat, and modern illness appeared only after plants and processed foods entered the menu.However, once you look past the rhetoric, another pattern appears. The carnivore movement did not grow out of decades of clinical research. Instead, it grew out of a very modern ecosystem: social media, podcasts, influencer culture, and supplement companies.And once that ecosystem forms, the incentives become clear.First, someone declares that conventional nutrition science has misled the public. Next, they present a dramatically simple solution. Afterward, they build a community around that solution. Eventually, products appear—supplements, coaching programs, special meat boxes, laboratory panels, and branded lifestyle advice.In other words, the diet becomes the marketing engine.And beef becomes the sacrament.Why Simplicity SellsExtreme diets succeed for a reason. Complexity frustrates people, while simplicity reassures them.“Eat a balanced diet rich in vegetables, whole grains, legumes, fish, and moderate meat” may represent excellent advice supported by decades of research. Unfortunately, that advice does not travel well on social media.By contrast, statements such as “plants are poison” or “fiber is unnecessary” spread rapidly. Bold claims generate engagement. Engagement produces followers. Followers create revenue streams.Consequently, the carnivore diet does not function only as a nutritional recommendation. It functions as a brand.Once someone builds that brand, they must defend it.The Prophets: The Case of the Liver KingEvery belief system eventually develops its prophets, and the carnivore world found one in a man who called himself Liver King.He appeared online with an enormous beard, an even larger physique, and a simple message: modern men had grown weak because they had abandoned the practices of their prehistoric ancestors. According to his message, people should eat raw organs, train like cavemen, reject modern foods, and adopt “ancestral living.”Conveniently, the ancestral lifestyle also included supplements he sold through his company.The marketing proved effective. The image of a muscular barbarian rejecting modern science attracted millions of followers and produced a supplement business worth tens of millions of dollars.Unfortunately, the story collapsed in 2022 when leaked emails revealed the Liver King spent more than $10,000 per month on anabolic steroids and other performance-enhancing drugs. Shortly afterward, he admitted publicly what physicians suspected from the beginning.Raw liver did not build that physique.Pharmacology did.Nevertheless, the episode illustrates the economic logic of the carnivore movement. First comes the doctrine. Then comes the identity. Finally, come the products.The Theologians: Paul SaladinoMovements rarely survive on prophets alone. They also require theologians—people who explain the doctrine with intellectual confidence.Within the carnivore community, one of the most prominent interpreters has been Paul Saladino, a physician originally trained in psychiatry who later rebranded himself as Carnivore MD.For several years, his message remained uncompromising. Plants contained toxins. Vegetables acted as chemical weapons. Humans thrived best on meat, organs, and animal fat. His book The Carnivore Code argued that modern civilization misunderstood nutrition and that health required a return to meat-centered eating.However, the human body eventually entered the conversation.After spending years on a strict carnivore diet, Saladino described several physiological problems: poor sleep, heart palpitations, muscle cramps, and hormonal changes. Consequently, the diet evolved.Fruit appeared. Honey appeared. Raw dairy appeared.Today, the diet carries a new label—an “animal-based diet.” In practice, that means meat accompanied by carbohydrates from fruit and honey.In other words, the diet rediscovered sugar.This pattern appears frequently in nutrition movements. Early stages emphasize purity and certainty. Later stages quietly reintroduce flexibility when biology refuses to cooperate.Also, Paul is partners with Liver King.The Economic EngineThe economic component remains impossible to ignore.Carnivore influencers rarely restrict themselves to books and podcasts. Instead, they build supplement companies that sell freeze-dried organs, nutrient capsules, and other “ancestral” products. The marketing narrative follows a familiar path.Modern food supposedly lacks ...
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    12 m
  • Minnesota Starvation Experiment: Food Noise, Science
    Mar 5 2026
    The Minnesota Starvation Experiment: What Hunger Does to the Human MindEvery few years, someone announces the solution to weight loss.Eat less.Fast longer.Cut carbs.Cut fat.Cut something.Naturally, the advice usually comes with a tone of moral certainty. If you are hungry, the implication goes, you simply lack discipline.However, long before social media, diet influencers, and the phrase food noise entered the modern vocabulary, scientists ran an extraordinary experiment that revealed something profound about hunger.Rather than speculate about appetite, they studied it directly.In the middle of World War II, researchers deliberately starved healthy young men.The results changed how we understand hunger forever.Why the Experiment HappenedDuring World War II, much of Europe faced severe food shortages. Cities were bombed, farms disrupted, and supply chains shattered. Consequently, millions of civilians were suffering from malnutrition and starvation.Yet another problem quickly emerged. Refeeding starving populations turned out to be complicated. If nourishment returned too quickly, dangerous metabolic complications could occur. Doctors needed to understand not only starvation but also recovery from starvation.Therefore, the U.S. government supported research designed to answer a simple but critical question:What happens to the human body and mind when calories are severely restricted for long periods?The scientist leading that effort was Dr. Ancel Keys at the University of Minnesota.Today, Keys is often remembered for his later work on diet and heart disease. Nevertheless, his wartime research produced one of the most remarkable studies ever conducted in nutrition science.The results were eventually published in a monumental two-volume work titled:“The Biology of Human Starvation.”This massive text, published in 1950, remains one of the most detailed examinations of hunger ever written.KEYS, ANCEL, JOSEF BROŽEK, AUSTIN HENSCHEL, OLAF MICKELSEN, HENRY LONGSTREET TAYLOR, Ernst Simonson, Angie Sturgeon Skinner, et al. The Biology of Human Starvation: Volume I. University of Minnesota Press, 1950. https://doi.org/10.5749/j.ctv9b2tqv.The VolunteersTo conduct the study, Keys recruited 36 conscientious objectors.These men had refused military service during World War II for moral or religious reasons. Nonetheless, they still wanted to contribute to the war effort. Participating in this experiment became their way of helping.Importantly, the volunteers were healthy young men. They had normal body weight, good physical fitness, and no significant psychological problems. In other words, they were ideal research subjects.Furthermore, they understood the risks.They would experience months of severe caloric restriction.Even more remarkable, the experiment took place beneath the University of Minnesota football stadium, turning an athletic facility into one of the most important laboratories in nutrition history.The Structure of the ExperimentThe study unfolded in three distinct phases.First came the baseline period. For several months, the men ate normally, consuming approximately 3,200 calories per day. Researchers measured body weight, metabolism, and psychological health to establish a stable starting point.Next came the central part of the experiment: six months of semi-starvation.During this period, calorie intake dropped to roughly 1,500 calories per day. That number may sound familiar because many modern diet programs recommend similar intake levels.The food itself resembled wartime rations. Participants ate simple meals consisting primarily of potatoes, bread, macaroni, turnips, and small amounts of dairy.Although the men remained physically active, their energy intake was cut in half.Finally, the experiment concluded with a refeeding phase designed to observe how the body recovers after prolonged starvation.The Unexpected Psychological EffectsResearchers expected weight loss.What surprised them was the dramatic change in the men’s relationship with food.Gradually, the volunteers became completely preoccupied with eating.First, they began collecting recipes. Soon afterward, they spent hours reading cookbooks.Remember that this was long before television cooking shows or the Food Network. Nevertheless, these men read cookbooks the way other people read novels.Additionally, food became the center of conversation. Participants talked about meals constantly. They debated cooking techniques and discussed ingredients in remarkable detail.Meanwhile, eating itself changed dramatically.Many men developed elaborate food rituals. Some cut meals into tiny pieces to make them last longer. Others chewed gum continuously to quiet hunger. Still others drank large amounts of water or coffee simply to fill their stomachs.Eventually, several participants reported dreaming about food every night.At that point, hunger had completely dominated their mental landscape.When Hunger Changes PersonalityAlongside this intense food...
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    12 m
  • From Gila Monster to GLP-1 Revolution
    Feb 26 2026
    Meanwhile, in a Laboratory

    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.


    While I Was Operating

    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.


    Food Noise

    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.


    Diet Culture Pushback

    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.


    My Parallel Universe

    When I began my career, I weighed about 185 pounds. Years later, hospital cafeterias, exhaustion, and irregular meals pushed me to 225.

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    13 m
  • Protein Panic: How Much Do You Really Need?
    Feb 19 2026
    Protein Panic: How Much Do You Really Need?

    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.


    First, What Protein Actually Does

    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.


    How Much Is Enough?

    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.


    Here’s What I Actually Do

    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.


    Now Let’s Bring In GLP-1

    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.


    Here’s the Real Deficiency

    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

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    8 m
  • Mexican Food Is Healthy. The Taco Took the Blame.
    Feb 12 2026
    Why Traditional Mexican Food Is Healthy — and How America Got It Wrong

    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.

    First, Let’s Talk About the Taco America Put on Trial

    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.


    Now Let’s Look at a Real Taco

    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.


    Corn Tortillas Aren’t the Villain — They’re the Foundation

    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.


    Beans Do the Heavy Lifting — And They Always Have

    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.


    Now Let’s Deal With Refried Beans — Because This Is Where People Panic

    At this point, someone

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    10 m