On the carbohydrate-insulin model, insulin resistance keeps the weight the body defends elevated. What’s the only reliable way to break this resistance?
The Short Answer
On the model’s account, time without insulin elevation. Extended periods of low insulin (time-restricted eating, intermittent fasting, or simply not eating constantly) may improve insulin sensitivity beyond what eating less alone does, though the evidence is mixed. Across six randomized trials comparing intermittent against continuous restriction, weight loss was the same in all six, and two found intermittent restriction cut insulin resistance far more, independent of the fat lost; a review of these regimens finds the reductions in insulin resistance comparable overall.[1] None of these trials compared it against medication or exercise.
Something to Sit With
On this model, your body isn’t broken. It’s responding rationally to a hormonal environment of chronically elevated insulin. Change the hormonal environment, and the body responds.
On that view, the question isn’t how much you eat. It’s how often, and how long you let insulin stay low.
Learn More
What Insulin Resistance Actually Is.
Insulin is a hormone that tells cells to take up glucose from the blood. When you eat (especially carbohydrates), blood glucose rises, insulin is released, and cells absorb the glucose. This is normal.
Insulin resistance occurs when cells stop responding properly to insulin’s signal. The body compensates by producing more insulin. For a while this works: higher insulin overcomes the resistance. But over time, insulin levels stay chronically elevated even when you’re not eating.
This creates problems:
An elevated defended weight, on this model: the body defends a higher weight because it is constantly in storage mode. Insulin signals “store energy as fat.” Chronically high insulin means chronically active fat storage.[2]
Blocked fat burning: Insulin inhibits lipolysis, the breakdown of stored fat for energy.[2] When insulin is high, you can’t efficiently access your fat stores. You have plenty of stored energy, but it’s locked away.
Increased hunger: A dip after high insulin (reactive hypoglycemia) is one proposed route to renewed hunger. Kishimoto found that people with subclinical reactive hypoglycemia had a median snacking frequency six times higher than those without: 0.9 against 0.15 times a day.[3] The cycle is the review’s proposal rather than a demonstration.
These three claims are the carbohydrate-insulin model of obesity. That insulin drives storage and blocks fat release is not disputed; whether elevated insulin is the primary cause of human weight gain is, and that evidence is inconclusive.[2]
Why Eating Less Doesn’t Work.
The intuitive solution, which is just to eat less, often fails long-term. The Minnesota Starvation Experiment showed why: thirty-six men entered and thirty-two completed twenty-four weeks on about 1,570 calories a day, roughly half their normal intake, and basal metabolic rate fell about 40%.[1] That is severe, prolonged restriction, not an ordinary diet: read the size of the drop against those conditions.
Crucially, eating regularly means insulin is still being triggered regularly.[4] You’re eating less, but you’re still eating. Every meal, every snack produces an insulin response. The cells never get a break from the insulin signal, which, on Fung’s argument, is how they lose sensitivity.
On that argument, this is why calorie restriction so often produces temporary results followed by regain. How it feels is on firmer record. The Minnesota men’s recorded symptoms were apathy, obsessive food thoughts, depression, and irritability, alongside a small decrease in body temperature: the book’s own word for it, and much the smaller change beside the cardiac and respiratory ones.[1]
Why Time Works.
Fasting, meaning extended periods without eating, works differently. When you stop eating, insulin drops. On this account, when insulin stays low for long enough, cells begin regaining sensitivity.
Research by Zauner and colleagues measured resting energy expenditure rising by up to ~14% during short-term fasting, alongside norepinephrine more than doubling: eleven lean subjects, across 84 hours. A larger trial of twenty-nine found a smaller rise that faded by 72 hours and did not reach significance in men at all.[5] The claim both support is the one this page needs: short fasting does not slow the metabolism down. This is the opposite of what happens during calorie restriction. The same evidence records a limit: past roughly sixty hours expenditure does fall, around 11% in a sixty-hour fast.[5]
On Fung’s account, the hormonal environment differs completely:[1]
- Calorie restriction: Insulin stays present (triggered by regular eating), metabolism drops
- Fasting: Insulin falls, counter-regulatory hormones rise, metabolism maintains or increases
One caution from the study his figures come from: Zauner’s paper reports that insulin did not change across its fast, where the book reports a fall.[1]
Jason Fung argues in The Obesity Code that constant stimulation of insulin eventually leads to insulin resistance, and that fasting works with the body’s hormonal switches rather than against them.[4] That is an argument in a trade book, not a measured finding.
What “Breaking Resistance” Looks Like.
Breaking insulin resistance is gradual. Here is what the account above predicts from consistent periods of low insulin, rather than what anyone has measured:
- Fasting feels easier (less hunger)
- Energy stabilizes (fewer crashes)
- Cravings diminish as blood sugar stabilizes
The trial evidence is for the sensitivity change, not for that sequence.
The set point, the weight the body defends, would gradually lower as insulin sensitivity returns, if the model above is right. On that model, you’re not fighting your biology anymore; you’re resetting it.
Practical Approaches.
On this model, any approach that gives you extended low-insulin periods may help:
- Time-restricted eating: Eating within an 8-10 hour window, fasting 14-16 hours
- Intermittent fasting: 24-hour fasts once or twice weekly
- Longer fasts: 36-72 hours periodically (with appropriate guidance)
- Eliminating snacking: Even three meals with no between-meal eating may help
On this model, the key is consistent time with insulin low. Occasional fasting surrounded by constant eating doesn’t accomplish much. The pattern matters.
Further reading:
- Fung J, The Obesity Code[6] (2016) — On insulin and fat metabolism
- Ludwig DS & Ebbeling CB, “The Carbohydrate-Insulin Model of Obesity”[7] — JAMA Internal Medicine, 2018
- Zauner C et al., “Resting energy expenditure in short-term starvation is increased as a result of an increase in serum norepinephrine”[8] — American Journal of Clinical Nutrition, 2000
- Kishimoto I, “Subclinical Reactive Hypoglycemia with Low Glucose Effectiveness”[9] — Metabolites, 2023
Written by AI, directed and approved by me. How this is made →