It’s the Insulin
An essay on what eight physicians found when they followed the evidence
Danny Cahill won Season 8 of The Biggest Loser, dropping from 430 pounds to 191 pounds. Six years later, he weighed 295 pounds and was still gaining—despite maintaining an 800-calorie daily diet and exercising regularly.
His metabolic rate had dropped by about 800 calories per day. His body was burning dramatically less energy than a person his size should burn. And this wasn’t temporary. The researchers who followed the contestants found that the metabolic suppression persisted for at least six years, showing no signs of recovery.
Cahill wasn’t unusual. Thirteen of the fourteen contestants studied had regained significant weight. The one who kept it off had bariatric surgery.
This pattern—aggressive calorie restriction followed by regain—isn’t a Biggest Loser phenomenon. It’s the predictable outcome of the calorie model of weight loss. When you cut calories, your basal metabolic rate drops by approximately 25%, and for all practical purposes, this drop is permanent. Study after study confirms this: cut calories, lose weight, lose muscle, reduce metabolic rate, regain weight as fat.
The regain phase is particularly cruel. When people regain weight after calorie restriction, they don’t regain the same body. They regain predominantly fat, not the muscle they lost. One physician quantifies it: 40 pounds lost typically means 30 pounds of fat and 10 pounds of muscle. Regain brings back 32-34 pounds of fat and almost no muscle. The person ends up more insulin resistant, metabolically sicker, than before they started dieting.
This is not a failure of willpower. It’s a failure of the model.
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Different Methods, Same Destination
The claim that “it’s not about calories” sounds like diet industry marketing. What makes it worth examining is how many independent lines of investigation point to the same answer.
Dr. Robert Lustig is a neuroendocrinologist and Professor of Pediatric Endocrinology at UCSF who spent decades treating obese children. He came to insulin through the clinical observation that his patients weren’t improving on standard care. His research focus: the biochemistry of fructose metabolism and mitochondrial dysfunction.
Dr. William Davis is a cardiologist who noticed his heart patients kept getting sicker despite following the American Heart Association diet. He shifted his practice toward metabolic health after tracking what actually reversed cardiac risk markers. His method: clinical outcomes and microbiome testing.
Dr. Ben Bikman is a metabolic scientist and professor at BYU. He approaches this through cell biology—studying what insulin does at the cellular and molecular level, running human studies on fat accumulation and fuel partitioning.
Dr. Annette Bosworth (Dr. Boz) is an internal medicine physician who spent her first fifteen years of practice prescribing the standard advice—high fiber, exercise, calorie restriction—and watched her patients get sicker. Her evidence base: thousands of patient outcomes tracked through glucose and ketone measurements.
Dr. Sean O’Mara is a health optimization physician who uses MRI scanning to track visceral fat, heart fat, and muscle fat. He spent seven years volunteering full-time, unpaid, working with over 6,000 patients. His method is imaging—seeing directly where fat accumulates and watching it disappear with intervention.
Dr. Morgan Nolte is a geriatric physical therapist who founded Zivli, an insulin resistance coaching program, after watching elderly patients deteriorate despite following conventional medical advice. Her focus: translating metabolic science into behavioral protocols that patients can actually follow.
Dr. Jason Fung is a nephrologist in Toronto who treats kidney disease—one of the downstream consequences of diabetes. He came to fasting and low-carb protocols by working backward from the organ damage he was seeing. His evidence: clinical reversal of conditions considered irreversible.
Dr. Thomas Cowan is a family medicine physician with 37 years of clinical experience who studied traditional diets through the Weston A. Price Foundation. His approach connects metabolic dysfunction to nutritional deficiencies and food quality.
A cardiologist tracking cardiac outcomes. A cell biologist running metabolic studies. An MRI specialist imaging fat deposits. A nephrologist reversing kidney damage. A pediatric endocrinologist studying children’s biochemistry. An internal medicine doctor measuring ketones. A physical therapist tracking behavioral interventions. A family physician studying traditional diets.
Eight different methodologies. The same variable keeps emerging: insulin.
What Insulin Actually Does
Insulin is a hormone produced by the pancreas. Its primary job is to move glucose from the blood into cells, where it can be burned for energy or stored.
This sounds benign. The problem begins when insulin is chronically elevated.
When you eat carbohydrates, they break down into glucose, which enters the bloodstream. The pancreas releases insulin to deal with this glucose. If you eat carbohydrates frequently—which the modern diet encourages—insulin remains elevated throughout the day.
Insulin is a storage hormone. When insulin is high, the body stores energy. When insulin is low, the body releases stored energy. This is not controversial; it’s basic endocrinology.
Here’s what follows: if insulin is always high, you are always in storage mode. You cannot access your fat stores while insulin is elevated. As Lustig puts it: “Insulin is the bad guy in the story.”
Bikman explains the mechanism at the cellular level: insulin-spiking foods promote the accumulation of fat cells. Once those fat cells are full, they become resistant to insulin’s signal—they’re protecting themselves from being overstuffed with more glucose. This is insulin resistance. The body responds by producing even more insulin to overcome the resistance, creating a vicious cycle.
Boz uses a different metaphor: insulin is a “dictator for resources.” When insulin is high, it controls where every molecule of fuel goes. Fat stays locked in storage. Vitamins like D get trapped in fat cells instead of circulating in the blood. Hormones like testosterone become inaccessible.
The body isn’t malfunctioning. It’s responding logically to a hormonal signal that says: store everything, release nothing.
The Storage Problem
The conventional view frames obesity as a calorie problem: too many calories in, too few calories out. The solution, logically, is to eat less and move more.
This model treats the body like a simple container. It ignores the regulatory system that controls what happens to those calories.
Fung offers a clarifying image: imagine a sink filling with water. The conventional approach focuses on the water level. The insulin model focuses on the drain. If the drain is blocked, it doesn’t matter how carefully you control the water coming in—the sink will fill up. Insulin is the drain regulator.
When insulin is chronically high, glucose cannot efficiently enter the cells. It stays in the blood (high blood sugar) or gets converted to fat for storage. Meanwhile, existing fat cannot be released. The cells are simultaneously overfed and starving—flooded with glucose they can’t use efficiently while unable to access stored fat for energy.
This explains the common experience of obese, insulin-resistant people: they feel tired and hungry despite having enormous energy reserves stored as body fat. Their bodies cannot access those reserves because insulin is blocking the exit.
It also explains why calorie restriction fails. When you cut calories without lowering insulin, the body doesn’t release fat stores to make up the difference. Instead, it reduces energy expenditure. You get colder, more tired, less active. Your metabolic rate drops. This is what happened to Danny Cahill and the other Biggest Loser contestants.
The Evidence Converges
Each of these physicians, using different methods, arrived at the same core conclusions:
Insulin—not calories—is the master regulator of fat storage.
Lustig, from biochemistry: “Insulin is where the action is. Insulin is the bad guy in the story.”
Bikman, from cell biology: “Without insulin there can be no weight gain. People who lose the ability to make insulin will never gain weight no matter how much food they eat unless they are supplemented with insulin.”
Boz, from clinical observation: “If I had to put one demon out there for the chronic diseases that have filled my internal medicine clinic for 20 years, insulin wins.”
Three different specialties, three different types of evidence, one conclusion.
Calorie restriction fails because it doesn’t address insulin.
Davis provides the metabolic data: calorie restriction drops basal metabolic rate by 25%, and this persists for at least six years. The body adapts to the reduced intake by reducing output.
Fung provides the clinical observation: “If you give drugs that make people gain weight, your diabetes will get worse. Patients saw it all the time. They’re like, you gave me this insulin. I gained like 30 pounds, and then you gave me more insulin. How is that making me better? It’s not.”
Different types of evidence—metabolic studies, patient outcomes—same finding.
The prevalence of insulin resistance is staggering.
Nolte cites population data: 88% of American adults have some degree of insulin resistance. Lustig places the affected population at 75%—not just diabetics, but everyone with the constellation of conditions called metabolic syndrome: type 2 diabetes, hypertension, dyslipidemia, cardiovascular disease, cancer, dementia, fatty liver disease, polycystic ovarian disease.
These are not separate diseases with separate causes. They are manifestations of a single underlying dysfunction: mitochondria damaged by chronic insulin exposure and fuel overload.
Visceral fat is not inert storage—it’s metabolically active disease.
O’Mara’s contribution is unique because he uses imaging. He doesn’t infer visceral fat from blood tests or waist measurements—he photographs it directly with MRI. His finding: “There is no healthy amount of what is disease.” Visceral fat isn’t just unsightly. It secretes inflammatory compounds, disrupts hormone signaling, and correlates with every chronic disease he’s tracked.
His claim is striking: out of 6,000 patients, not one had chronic disease that didn’t improve as visceral fat was eliminated. And in his AI-assisted review of all available medical records, he found no human being who ever had a heart attack without elevated heart fat.
This is imaging evidence—direct observation—not inference from biomarkers.
Fructose is uniquely harmful.
Lustig has built the biochemical case: “Everything fructose does to the mitochondria is designed to inhibit its functioning.”
Unlike glucose, which can be metabolized by any cell in the body, fructose is processed almost exclusively by the liver. In large amounts, it overwhelms the liver and gets converted directly to fat.
Bikman adds human study data: fructose drinks cause visceral fat accumulation; glucose drinks cause subcutaneous fat accumulation. Same calories, different metabolic destinations.
Two types of evidence—biochemistry and controlled human trials—pointing at fructose specifically.
Fasting works because it lowers insulin.
The mechanism is straightforward: when you don’t eat, insulin falls. When insulin falls, the body can access stored fat. Bikman states it simply: “Minute for minute, fasting is going to move the needle the most.”
Fung provides clinical proof: patients on insulin for 20 years got off all insulin within one month using three 24-hour fasts per week. This is faster than bariatric surgery achieves for many patients, without the surgical risks or permanent anatomical changes.
Laboratory mechanism confirmed by clinical outcome.
Where They Diverge
These physicians are not coordinating their recommendations. They’re following different evidence and arriving at different implementation details. The disagreements reveal genuine uncertainty about optimal protocols—and confirm that each is thinking independently.
Carbohydrate thresholds vary widely.
Boz requires 20 total carbohydrates for the first week as a test of commitment. O’Mara eats 95% ruminant meat with only fermented vegetables. At the other end, Nolte provides graduated thresholds: 50 grams for reversal, 75 grams for prevention, 100 grams for maintenance. Cowan recommends 60-70 grams until blood sugar normalizes, then 72 grams for life. Fung suggests that carbohydrate quantity matters less than carbohydrate quality—unprocessed carbs create less damage.
The range is 20 to 100 grams. That’s a fivefold difference.
Fasting protocols differ significantly.
Bikman and Fung emphasize that how you break a fast matters more than how long you fast—bingeing on junk food after a fast undoes the benefit. Fung finds that 16:8 and 24-hour fasts work for most people.
Boz prescribes repeated 72-hour water fasts for severe cases and personally does 60-72 hour fasts weekly. Davis warns that fasting beyond 72 hours reduces metabolic rate.
Nolte takes the most moderate position: she enjoys ketosis but “the type of lifestyle it takes to be in ketosis all the time is not one that I could happily sustain.” She uses intermittent fasting to dip into ketosis without permanent dietary restriction.
Exercise recommendations conflict.
Bikman’s position is pragmatic: “The best exercise to do is the one you will do.” He emphasizes that muscle contraction pulls glucose into cells without requiring insulin, so any movement helps.
O’Mara directly contradicts mainstream exercise advice: “Durational exercise is bad.” He claims marathons and long-distance cycling increase visceral fat while stripping protective subcutaneous fat. He shows MRI images of elite endurance athletes with pathological fat distribution.
Boz recommends Zone 2 training for building new mitochondria. Davis promotes vibration plates, citing studies showing 25% strength increases in weeks. Nolte emphasizes Zone 2 training and post-meal walks for glucose management.
Measurement approaches diverge completely.
O’Mara uses only MRI scanning to track visceral fat, heart fat, and muscle fat. He has abandoned lab testing entirely: “Quit fooling around with your labs. They’re way downstream. A supercomputer couldn’t figure it out.”
Boz wants daily glucose and ketone measurements via finger prick, plus continuous glucose monitoring. She uses the ratio of glucose to ketones as her primary metric.
Nolte recommends fasting insulin as the first test, then the Kraft test (oral glucose tolerance with insulin tracking) for those who want more precision.
Davis uses hydrogen breath testing for SIBO and flow cytometry for microbial analysis.
One physician has abandoned bloodwork entirely; another builds her entire protocol around daily blood measurements.
Specific foods are contested.
O’Mara condemns marbled beef—ribeye, wagyu—as diseased tissue, comparing MRI images of marbled steak to MRI images of fatty human muscle (myosteatosis). He recommends Piedmontese cattle, bred for low marbling.
Davis, Bikman, and Boz make no such distinction. Davis mentions brisket and bacon without qualification.
O’Mara and Davis clash directly on L. reuteri yogurt dosage. Davis recommends half a cup daily of his 36-hour fermented yogurt. O’Mara responds: “Bill, if you’re listening... your face is big and I think your tummy is big.” He uses only 2-3 tablespoons and removes the prebiotic fiber that Davis includes.
The Practical Synthesis
Setting aside the contested details, what would a person actually do based on what converges across these different investigations?
First, understand the goal: keep insulin low.
This is the through-line. Every intervention these physicians recommend achieves its effect by reducing insulin. Carbohydrate restriction, fasting, exercise, eliminating fructose—all lower insulin.
Second, restrict carbohydrates—especially fructose.
Start with added sugars and high-fructose corn syrup. Then reduce or eliminate sugary fruits (bananas, grapes, pineapple). Then processed carbohydrates (chips, crackers, bread). Then starches (potatoes, rice). Berries are relatively safe. Beans and legumes are debated but generally tolerated because their fiber content slows glucose absorption.
The exact threshold depends on how insulin resistant you are. Severely metabolically damaged individuals may need the strict end of the range (20-50 grams). Those preventing future problems can likely tolerate more (75-100 grams).
Third, add fasting.
The baseline, Fung notes, should be at least 14 hours overnight—which was normal eating in the 1970s. Twelve hours “is just regular eating.” For therapeutic effect, extend to 16:8 (16 hours fasting, 8 hours eating) or one meal a day (OMAD).
How you break the fast matters. Don’t spike insulin immediately with carbohydrates. Break with protein and fat.
Fourth, change breakfast.
Bikman emphasizes this as the highest-leverage single change: “When we wake up in the morning, insulin has finally come down over the night. The last thing we want to do is spike our insulin up.” A high-carb breakfast creates a roller coaster that keeps insulin elevated all day.
Either skip breakfast (extending the overnight fast) or eat protein and fat only.
Fifth, move after eating.
Fung cites studies showing that walking after meals significantly reduces glucose spikes. Muscle contraction pulls glucose from the blood without requiring insulin. A walk after dinner may be more valuable than a workout in the morning.
Sixth, prioritize protein and fat.
Boz recommends 80% of calories from fat in the initial phase for severely insulin-resistant patients. Bikman notes that in nature, protein always comes with fat—never isolated. The modern invention of fat-free protein (protein shakes, lean chicken breast) is unnatural and potentially counterproductive.
Don’t fear fat. Fear the absence of fat, which drives hunger and leads to carbohydrate consumption.
Seventh, fix the gut.
Davis, O’Mara, and Bikman all emphasize fermented foods. Davis estimates that 50% of North Americans have small intestinal bacterial overgrowth (SIBO), which disrupts metabolism and nutrient absorption. His protocol involves specific bacterial strains fermented into yogurt.
O’Mara goes further: adults should not consume unfermented dairy at all. Only fermented dairy (yogurt, kefir, aged cheese) is appropriate for adult digestion.
Why This Matters
The metabolic diseases now affecting 75% of the population are not mysteries. They are the predictable result of a food environment that keeps insulin chronically elevated, combined with medical advice that ignores insulin entirely.
The conventional approach—eat less, move more, take medications to manage symptoms—has failed for fifty years. Obesity rates continue to climb. Diabetes rates continue to climb. The patients who try hardest often suffer most, as Danny Cahill’s story demonstrates.
The physicians examined here offer a coherent alternative framework. They disagree on details, sometimes sharply. But following different types of evidence—clinical outcomes, cellular biology, MRI imaging, biochemistry, population data—they arrive at the same mechanism: insulin controls fat storage, and any intervention that doesn’t lower insulin is addressing symptoms while ignoring the cause.
This is not fringe science. It’s well-established endocrinology, ignored by mainstream dietary advice for reasons that have more to do with institutional inertia and food industry influence than with evidence.
The good news is that insulin resistance reverses. Fung’s patients got off decades of insulin medication in weeks. O’Mara’s patients eliminated visceral fat and saw chronic diseases improve. Boz’s patients recovered metabolic flexibility.
The protocol is not complicated: stop spiking insulin with constant carbohydrate consumption, give the body time without food to access stored energy, and provide the protein and fat needed for satiety and tissue repair.
The difficulty is that this requires rejecting advice that comes from every official source—the dietary guidelines, the medical establishment, the food industry, the well-meaning family members who push low-fat foods and warn against skipping meals.
Eight physicians using eight different methods found the same answer.
The methods are the evidence.
References
Bikman, Ben. “If You DO THIS Your Insulin Resistance Will Be Normal FAST!” The Jesse Chappus Show, December 29, 2021. YouTube.
Bosworth, Annette (Dr. Boz). “You’ll NEVER Reverse Insulin Resistance if You IGNORE THIS...” The Jesse Chappus Show, November 5, 2025. YouTube.
Cowan, Thomas. “Treating Diabetes: Practical Advice for Combatting a Modern Epidemic.” Wise Traditions (Weston A. Price Foundation), Winter 2003.
Davis, William. “1/2 Cup per Day to Fix Insulin Resistance & Shrink Belly Fat.” The Jesse Chappus Show, December 10, 2025. YouTube.
Fung, Jason. “Get Rid of Diabetes Once and for All.” The Jesse Chappus Show, September 28, 2022. YouTube.
Lustig, Robert. “You’ll NEVER Reverse Insulin Resistance Until You FIX THIS...” The Jesse Chappus Show, June 14, 2023. YouTube.
Lustig, Robert. “The REAL Cause of Insulin Resistance & How to FIX IT!” The Jesse Chappus Show, August 20, 2025. YouTube.
Nolte, Morgan. “How to ELIMINATE Insulin Resistance Once and for All (COMMON Early Signs).” The Jesse Chappus Show, December 25, 2024. YouTube.
O’Mara, Sean. “This Fat Is the Root of Chronic Disease (Doctors Aren’t Measuring It).” The Jesse Chappus Show, July 29, 2025. YouTube.
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Author's note:
The essay focused on where eight physicians converge. Several readers rightly noted what it doesn't address.
Sarcopenia. Ray Falciola pointed out that older adults face age-related muscle loss while trying to implement these protocols. The physicians emphasize muscle as metabolically protective, but none directly addresses how to build muscle when biology is working against you. This is a real gap.
Long-term sustainability. Janet and others report that carb restriction worked initially, then failed—or caused harm—over years. The essay presents these protocols without discussing failure modes. Worth noting: the physicians themselves disagree on how restrictive to be. Nolte recommends 100g carbs for maintenance. Fung emphasizes food quality over strict carb limits. The essay could have made this range clearer.
Individual variation. What reverses one person's insulin resistance may destabilize another. The essay presents a fairly universal framework when the reality is messier.
The historical question. Kay and yantra asked why there was no obesity epidemic 60-70 years ago when people also ate sugar and processed foods. This suggests the insulin model may be incomplete—or that something else has changed (food composition, meal frequency, seed oils, environmental factors) that the essay doesn't explore.
These questions deserve their own essays. Thank you for the pushback.
Most of these diets the doctors talk about above are not optimal. Like Keto and carnivore etc. THEY JUST BECOME CALORIE RESTRICTED DIETS IN TIME TOO, WITH NO GLUCOSE OR LITTLE TO SUPPLY ENERGY ANYWAY. DUH. The protein and fat are very satiating so you just drop calories eventually because you are not eating. You get off toxic food—a big reason it seems to be working. Have no appetite eventually. Fat is not magic. This is not virtuous. This is garbage and they are too. Quacks. It works for a long time and then your energy, metabolism and thyroid crash. Insulin resistance becomes center stage. I’ve been 21/2 years to heal from this nonsense. I’m in a group of hundreds recovering from carb restriction, keto, carnivore. OMAD, IF, fasting, afraid of FRUIT For God’s Sake. Fruit is a combination of glucose and fructose. There is not much food we eat that IS pure fructose. Lustig fed his famous sad mice just fructose. Let me give you a little hint. On this nonsense, You use stress hormones to make glucose your body needs. Gluconeogenisis.. These stress hormones cortisol, adrenaline etc use another pathway—your liver to make energy.Plus takes from organs ,tissue, bones—I.e. scavenges your own body to make the fuel you can just eat. Glucose or glucose and fructose . You are not just burning fat. You do lose muscle. I went back to a sort of paleo eating and added some more fruit, good sugars just no bread and grains. They affect me. Added back carbs very very slow. There is some value to a fast here and there and always good to remove toxic modern food. That’s when I lost weight at first. Ditched the poison. The best thing you can do. But after the low carb thing screws you up, it’s much harder to get back where you belong.
They are wrong and I’m disgusted this is here to fool people, again. I did this 5 years and it all fell apart while eating this way. Sleep tanked (Yoo-hoo—stress hormones) broken bones, anxiety, crazy cardio doesn’t help. Weight gain. Big time. You can’t “do it harder” when it quits working. Restricting more isn’t the answer. Cutting out important glucose is not the answer. Running 24/7 on cortisol and adrenaline ? I don’t see any lions around these days needing quick energy. I feel much better now, my thyroid is healing. I get real nutrition from adding fruit and potatoes. Some rice. Even Paul Saladino, noted carnivore, has added fresh fruit and honey. I’ve started losing a little weight with increased energy and a healing metabolism. Restrict carbs to basically nothing and you will regret it, some sooner than later. . The science backs this. Just a warning. Check out Jay Feldman on YouTube or others raising the alarm. I read Kate Deering’s book first. Jay has 100 videos helping and explaining the real science.others are making changes. The post above is falling.