Get Rid of Insulin Resistance For Good (in 5 easy stages)

DeLauer describes insulin resistance as a state where cells are constantly bombarded with insulin to the point they ignore it. By drastically lowering carbohydrate intake, insulin levels drop, attenuating this noise. He emphasizes that this is pure 'damage control' — the goal is to reset the cellular environment before attempting more complex interventions like mitochondrial repair. He compares it to giving the cells a quiet period so that when insulin eventually arrives, it's a clear signal. The increase in protein and fiber ensures satiety and blood sugar stability during this low-carb phase.

The study DeLauer cites had participants on 19 days of strict bed rest, some doing 30 isometric leg press contractions each morning. The non-exercising group lost 19% of GLUT4 translocation, while the exercising group increased it by 30% above baseline, showing that even minimal muscle contraction reverses insulin resistance at the cellular level. This is crucial evidence that any movement matters, and it allows people in stage one to take an easy first step without needing to go to a gym. It also works for those with mobility limitations. The mechanism is that contraction activates AMPK and calcium signaling that independently trigger GLUT4 vesicle fusion with the membrane.

DeLauer references a European Journal of Sports Science study showing that 6 weeks of HIIT (the described protocol) increased mitochondrial density, efficiency, and overall energy production. He explains that more mitochondria per muscle area means greater capacity to oxidize both glucose and fat, which directly combats the metabolic inflexibility of insulin resistance. Short bursts of intense effort create an energy demand that challenges the electron transport chain, triggering mitochondrial biogenesis through PGC-1α activation. This adaptation makes the system more efficient, extracting more ATP from the same amount of fuel, crucial for long-term metabolic health.

DeLauer explains that stage three specifically targets fatty acid oxidation because having less adipose tissue reduces the inflammatory burden that perpetuates insulin resistance. Zone 2 is the sweet spot where the body predominantly uses fat as fuel, stimulating beta-oxidation pathways. He suggests using a talk test to gauge intensity. By doing this 3x/week, the body becomes more efficient at mobilizing and oxidizing fat, which both directly burns stored fat and improves overall metabolic flexibility, complementing the fasting protocol he also recommends in this stage.

DeLauer details a study published in BBA, Molecular and Cell Biology showing that even short-term fasting alters key enzymes: it reduces lipoprotein lipase, which builds fat; increases adipose triglyceride lipase (ATGL) which initiates fat release from storage; increases hormone-sensitive lipase (HSL) which further breaks down fat into free fatty acids; and decreases acetyl-CoA carboxylase (ACC), which reduces fat synthesis. This enzymatic shift creates a powerful fat-mobilization environment. He recommends 18 hours of fasting three times a week, stating it's 'tremendous' for metabolic flexibility, but warns that if attempted too early, it could be detrimental because the body isn't yet metabolically stable enough to handle the stress.

DeLauer warns that keeping carbs out forever leads to peripheral insulin resistance (loss of glucose tolerance). To restore pancreatic beta-cell health, the body must relearn how to secrete and respond to insulin appropriately. He outlines a phased reintroduction: start with low-glycemic carbs like squash and eggplant, then after a couple of weeks add resistant starches (cooled potatoes, sweet potatoes, overnight oats) which have lower glycemic impact because the starch crystallizes into resistant form. Then implement activity-based carb cycling: on rest days, minimal extra carbs (just veggies); on moderate activity days (strength training), add resistant starches; on high-intensity days, more carbs because glycogen re-synthesis is better. He also discusses carb timing: for sedentary office workers, it may be better to keep carbs low during the day and have them in the evening when they are more active; for physically active jobs, front-load carbs in the morning. This nuanced approach aims to re-establish insulin sensitivity without overwhelming the system.

DeLauer explains that the ultimate goal is to increase the 'rate of flux'—the amount of fuel moving through your mitochondria and cells. By eating more and moving more, you train the system to process larger quantities of nutrients without storing them as fat. He suggests starting by bumping training volume 10-20% and then adding a little more food; then increasing daily activity (not just gym) and eating more. Over time, this could allow someone to eat, say, 5,000 calories while burning 5,000, enjoying a more flexible diet. This stage is only possible after the previous stages have built mitochondrial capacity, fat oxidation capability, and pancreatic health, otherwise the increased input would simply worsen insulin resistance. He warns that if he had introduced this at the start, it could have been detrimental.

He positions this as a powerful maintenance tool that mimics 'the work of many years of dieting' by periodically giving the body a break from feeding, forcing it to tap into stored glycogen and fat. This intermittent stress keeps the enzymatic machinery for lipolysis and ketogenesis active, preventing the metabolic rigidity that often accompanies long-term relaxed eating. He stresses that while it sounds aggressive, doing it just one or two days a week is sustainable and highly effective for preserving gains.

DeLauer argues that insulin resistance is like 'white noise' on cells, desensitizing them to insulin signaling. Stage one is damage control: temporarily removing carbohydrates to reduce the chronic hyperinsulinemic noise so cells can regain insulin sensitivity. Subsequent stages build mitochondrial function, fat oxidation capacity, pancreatic beta-cell health, and finally metabolic flux through increased activity and food intake. This orderly progression prevents the pitfall of adding intensity too soon, which could overwhelm a dysfunctional system, and ensures that each layer of capacity is built before the next is introduced.

He acknowledges that losing fat would help since adiposity drives inflammation, but notes that it's hard to 'swallow that pill initially.' By first doing damage control and mitochondrial repair (stages 1-2), the body is better prepared to efficiently oxidize fats in stage 3 via Zone 2 cardio and time-restricted feeding. This sequencing ensures that the metabolic machinery is functional enough to handle the increased fatty acid flux and that the anti-inflammatory benefits of fat loss can compound without backfiring on a still-insulin-resistant system.

Once mitochondrial density and pancreatic health are improved (stages 2-4), the maintenance phase can incorporate intraworkout carbs to further increase metabolic flexibility. Exercise causes GLUT4 translocation to the cell surface independent of insulin, so consuming a small amount of fast-acting carbs during training allows the muscles to take up glucose without the need for a large insulin response. This trains the body's glucose disposal systems and improves tolerance, potentially making occasional higher-carb intake less problematic in the long run.

DeLauer cites a Journal of Applied Physiology study where subjects on 19 days of bed rest lost 19% of GLUT4 translocation, while those doing just 30 morning isometric leg press contractions gained 30% over baseline. This indicates that muscle contraction itself, not just 'exercise,' is a potent signal to mobilize glucose transporters, suggesting that even during periods of forced inactivity (injury, illness), small isometric movements can maintain or enhance insulin-independent glucose uptake. He uses this to argue that stage one's 'a little bit of movement' is a scientifically rock-solid entry point.