Carbs Don’t Cause Insulin Resistance — Dietary Fat Does
Why cutting carbs doesn’t fix the root cause — and why sugar is part of the solution
Obesity, type 2 diabetes, heart disease, and even Alzheimer’s are often packaged under the umbrella of Metabolic Syndrome—a cluster of symptoms unified by one core dysfunction: insulin resistance.
Most clinicians and nutrition ideologies still charge that carbohydrates (especially sugar) are the villains and that eliminating them cures insulin resistance. That narrative is seductive but also misleading—and has likely hurt more people than helped.
From a pro-metabolic framing, insulin resistance isn’t caused by eating too many carbs. It’s caused by your body’s inability to use them properly. That’s a huge distinction—and alters the solution entirely.
Sugar (Carbohydrate) as a Healing Fuel, Not the Enemy
I want to be crystal clear: sugar is not inherently toxic when used in the right context. In fact, in many metabolic healing protocols (e.g. the Ray Peat model), sugar—including from ripe fruit, honey, and even sucrose—is considered one of the most metabolically supportive fuels. The Hadza drink large amounts of honey everyday and have no diabetes.
Key roles sugar (glucose/fructose) plays:
Preferred fuel for liver, brain, and thyroid
Essential for replenishing glycogen in liver and muscle
Potent at lowering cortisol when consumed appropriately
Needed (in many models) for converting T4 → T3
Prevents chronic stress signals by reducing need for gluconeogenesis
Thus the logic: sugar doesn’t trigger insulin resistance—a broken metabolism does.
So why does sugar get blamed? Because almost everyone who suffers from insulin resistance is already operating in a state of metabolic suppression: under-eating, chronic stress, micronutrient deficiency, and chronic exposure to lipid toxins (especially PUFAs / seed oils). Sugar is judged in a terrain already scorched.
What Actually Drives Insulin Resistance
Here’s a refined list (with emphasis) of what I see as primary causal drivers:
PUFA / seed-oil accumulation in tissues
Seed oils (linoleic, linolenic acids) physically embed into mitochondrial membranes, disrupt electron transport, induce lipid peroxidation, and diminish glucose uptake.Excess dietary fat (especially PUFA) load
In ancestral diets, total fat was often low (~10 % of calories). In modern Western diets, fat has ballooned—often 30–40+ %, heavily from PUFAs. The excess free fatty acids interfere with insulin signaling (Randle cycle).Cortisol / catecholamine dominance
Chronic stress (psychological, environmental, or physiological) favors lipolysis, mobilizing fatty acids and impairing glucose uptake.Low thyroid / low metabolic drive
When your metabolic thermostat is turned down, you burn fewer carbs, producing stagnation in glucose utilization.Micronutrient deficiencies (Mg, K, B1, B3)
These are cofactors in glycolysis, Krebs cycle, pentose phosphate, etc. Without them, glucose metabolism bottlenecks.Undereating / substrate starvation (especially of carbs)
If you chronically restrict carbohydrate intake, you force the body into fat oxidation mode, reduce insulin signaling capacity, and further exacerbate metabolic inflexibility.Mitochondrial / oxidative damage
When mitochondria are oxidatively damaged (often via lipid peroxides from PUFAs), their ability to use glucose is crippled.
When your cells are overwhelmed with fatty acids and oxidative stress, they lose their ability to properly respond to insulin. Glucose uptake fails. Insulin levels rise. Over time, receptor resistance emerges. The solution isn’t to eliminate glucose—it’s to restore the cell’s ability to use it.
Muscle Is the Crucible of Glucose Burning (and Healing)
Skeletal muscle is usually the first tissue to lose insulin sensitivity. That matters, because muscle is the body’s primary sink for glucose disposal. If your muscles won’t take glucose, it gets shunted to adipose tissue or stays in circulation.
Low-carb, high-fat diets tend to worsen this: lower thyroid, higher cortisol, suppressed insulin sensitivity, and high intramuscular lipid deposition (IMCL) that blocks glucose flux (again, the Randle cycle).
So the more muscle you have (or improve in function), the better your capacity to burn sugar—and, ultimately, reduce insulin load.
Swampland Metabolism: What Breaks Your System
I like to think of a “healthy metabolism” as a well-drained field. But many people live in a swampy metabolic state—where nutrients stagnate, gradients flatten, signals get mired. What causes this swamp?
PUFA infiltration in membranes
Low mitochondrial reserve
Chronic stress
Low energy flux (low fuel input, low output)
Toxin burden, inflammation, gut dysbiosis
Maladaptive hormonal loops
Once metabolism is in swamp mode, even “safe” foods get misprocessed. The trick to healing is to drain the swamp—restore gradient, flow, and functional capacity.
How to Actually Reverse Insulin Resistance (Not Just Mask It)
If insulin resistance is a wound, sugar is a tool, not a weapon. The healing process requires:
Adequate caloric intake
Chronic undereating suppresses thyroid, lowers metabolic rate, and elevates cortisol. Many people reversing metabolism—especially women—require 2,000–2,500+ kcal/day (or more, individual) with 50–60 % carbs (or more) during rehabilitation.Low fat, at least during healing
This doesn’t mean zero fat, but keep fat modest while reconditioning insulin sensitivity. For many, fat levels are capped at ~10–15 % of total calories. Focus on saturated fats (coconut oil, dairy fat, butter) in moderated amounts.Pro-metabolic carbohydrates
Favor easy-to-digest carbs: ripe fruit, fruit juice + protein, honey, root vegetables, dairy sugars. Avoid combining high fat + high sugar in the rehealing phase.Target muscle load & movement
Resistive training 2× weekly, combined with daily walking (8–10k steps), primes glucose uptake machinery (i.e. GLUT4). Over time, the more active your tissues, the more carb capacity you regain.Sunlight / circadian support
Morning sun, proper light exposure, regulated sleep help regulate thyroid, cortisol, and mitochondrial signaling.Restorative sleep & cortisol modulation
Use gentle carb + protein bedtime snacks to lower overnight cortisol surges (e.g. warm milk + honey, cottage cheese + jam).Micronutrient support
Ensure adequate magnesium, potassium, sodium, thiamine (B1), niacinamide (B3), etc. In cases of chronic depletion, short-term supplementation may be warranted.PUFA detox / fatty burden reduction
Over time, reduce dietary PUFAs, seed oils, and encourage cycles (fasting, liver support) that help mobilize and clear stored lipid toxins.Avoiding high-fat, re-feeding spikes too early
Be cautious: reintroducing large amounts of fat while metabolism is still fragile often backfires—pulling the system back into swamp mode.
Over time, insulin sensitivity recovers, glucose becomes a safe and useful fuel again, and you start to reclaim metabolic flexibility.
What About Fructose, Fatty Liver, and The “Fat + Sugar” Myth?
Fructose is demonized, but context is everything. When taken in isolation or in a low-fat matrix (fruit, honey with protein), it is typically shunted into glycogen storage (in liver) rather than lipogenesis. In fact, it’s often repackaged as fuel for vital tissues (thyroid, brain, adrenals). The danger arises when fructose is consumed alongside excess dietary fat, especially PUFAs (think: soda + french fries). That mash-up drives lipogenesis and triglyceride elevation—because the liver is overloaded, and fat export pathways are saturated.
So fruit and honey aren’t the enemy—they become part of the repair toolkit, especially when the metabolic swamp is drained.
❤️ Final Takeaway
Insulin resistance is not a carbohydrate problem—it’s a metabolic dysfunction problem. Carbs (and sugars) are not the root of the disease—they’re tools for recovery when wielded strategically.
Healing insulin resistance demands reclaiming metabolic capacity—not by fear, but by fuel, flow, and function. Eat enough. Choose carb-forward, low-fat meals. Move your muscles. Fix your sleep, hormones, and mitochondria. Ditch the fear. Heal the terrain.
Once metabolism is healed, you won’t just survive—you’ll thrive.
References
Sommerfeld, D. et al. Modern Perspective of the Rice Diet for Hypertension and Metabolic Diseases — Historical and clinical overview of Kempner’s Rice Diet and its metabolic impact.
“The Rice Diet and Duke University.” North Carolina Department of Natural and Cultural Resources — Background on Kempner’s work and the Rice Diet’s outcomes.
Kempner, W. Treatment of Massive Obesity With Rice/Reduction Diet Program. JAMA Internal Medicine (1975) — Clinical data on weight loss and insulin normalization using a low-fat, high-carb rice diet.
Scientific Publications of Walter Kempner, M.D. Vol. 2 — Duke University Archives (PDF) — Comprehensive collection of Kempner’s original studies.
“Can the Rice Diet Reverse Type 2 Diabetes?” NutritionFacts.org — Modern review of Kempner’s diet and glucose metabolism outcomes.
Minger, D. “The New USDA Dietary Guidelines: What the USDA Forgot to Mention.” Raw Food SOS (2011) — Denise Minger’s critique of mainstream nutrition science and misinterpretation of carbs vs. fats.
Minger, D. “Industrial Seed Oils: A Hidden Metabolic Disaster.” Raw Food SOS — Discussion of PUFA oxidation, mitochondrial dysfunction, and insulin resistance.
Mercola, J. “Why You Should Limit Unhealthy Fats, Not Healthy Carbs.” Mercola.com (2023) — Overview of emerging evidence connecting excess fat intake with insulin resistance.
“Insulin Sensitivity and Dietary Fat.” Mastering Diabetes — Mechanistic breakdown of how fat intake modulates insulin response in muscle and liver tissue.
“Seed Oil Misinformation.” Wikipedia — Summary of the public debate on PUFA safety, included for balanced context.
