Insulin resistance lies at the heart of a metabolic cascade that can culminate in type 2 diabetes, cardiovascular disease, kidney failure, and more. Dr. Éric Thorin’s insightful article emphasizes that the combination of excess dietary fat—particularly visceral adiposity—and sugar intake triggers inflammatory processes in the body, disrupting normal glucose regulation .
1. How Glucose and Fat Normally Coexist
Glucose regulation: In healthy physiology, blood glucose is tightly maintained at around 4.8 mmol/L (~0.8 g/L) by insulin, which promotes glucose uptake into muscles, liver, and fat cells . Fat as a battery: Beyond glucose, fatty acids supply roughly 60% of daily energy needs, especially during fasting or exercise .
This balance provides metabolic flexibility—switching between glucose and fat based on demand.
2. When Fat Becomes Harmful
Adipocyte hypertrophy: Eating more calories than expended—especially in the form of fats and sugars—leads to enlarged fat cells (particularly in the abdomen) . These cells suffer from oxygen deprivation and cellular stress. Consequently, inflammatory immune cells infiltrate the fat tissue, creating persistent, low-grade inflammation . This chronic inflammation disrupts insulin signaling, meaning more insulin is needed to maintain normal blood glucose—marking the onset of insulin resistance .
3. The Path from Insulin Resistance to Diabetes
Phase 1 (Compensation): Elevated insulin levels keep blood glucose normal—though insulin is surging . Phase 2 (Decompensation): As fat accumulation and inflammation worsen, the pancreas can no longer keep up; both insulin and glucose levels become elevated—signifying type 2 diabetes .
4. The Vascular Toll of High Sugar
Once hyperglycemia sets in, sugar damages the inner lining of blood vessels (the endothelium). This impairs vessel dilation, fosters clotting, and accelerates organ dysfunction—affecting the heart, brain, kidneys, and eyes .
5. Lifestyle Remedies: Prevention & Reversal
Early detection: Measuring insulin, not just glucose, is critical—elevated fasting insulin (>150 pmol/L) with normal glucose indicates early-stage insulin resistance . Fat reduction: Decreasing body fat—especially visceral—reduces inflammation and improves insulin sensitivity. Healthy habits: Balanced nutrition (low in refined sugar and saturated fat), regular physical activity, and maintaining a healthy weight are essential. Timing matters: Action before blood sugar begins to rise makes reversal much more achievable .
6. Evolutionary Mismatch & Society Today
Human biology evolved around intermittent eating and activity—not constant access to high-calorie foods. This mismatch causes chronic adipose expansion and “inflammaging”—low-grade inflammation that accelerates metabolic and age-related disease .
7. Practical Low-Carb+Lifestyle Guidance
As a low-carb high-fat (LCHF) advocate, you can empower readers with strategies to combat this metabolic duel:
Minimize sugar & refined carbs to curb glucose spikes and reduce lipogenesis. Choose healthy fats (avocados, olive oil, nuts) and avoid trans/saturated fats that fuel adipocyte stress. Monitor waist circumference—a simple proxy for visceral fat. Measure fasting insulin if possible—early detection beats late-stage management. Move more—even light daily activity enhances insulin sensitivity. Track progress: Note weight, insulin levels, and how clothing fits, rather than just relying on blood sugar.
✅ Final Takeaway
Insulin resistance isn’t an inescapable destiny; it’s a metabolic warning signal. When excess fat and sugar clash inside the body, they ignite inflammation that derails glucose metabolism and damages organs. But the good news: with timely lifestyle changes—especially LCHF eating and physical activity—you can reverse the process and safeguard long-term health.
