In this lecture, Dr. Bikman presents a framework for understanding the two primary patterns of insulin resistance onset—what he terms “fast” and “slow” insulin resistance.

“Fast” insulin resistance happens quickly and can often be reversed just as rapidly. It’s typically triggered by three major factors: elevated insulin (from frequent carb consumption), stress hormones like cortisol and epinephrine, and inflammation (from infection, injury, or autoimmune activity). These triggers lead to the cellular accumulation of ceramides, which interfere with insulin signaling at the molecular level. The good news, he emphasizes, is that when these triggers are removed, the insulin resistance can often resolve quickly.

“Slow” insulin resistance, on the other hand, develops gradually and is more difficult to reverse. It begins in the fat cell, where prolonged exposure to insulin and excess calories causes hypertrophy—the fat cells get larger. As they grow, they become insulin resistant as a form of self-preservation, but this leads to a damaging cascade: elevated free fatty acids, chronic low-grade inflammation, and disruption of glucose control. Dr. Bikman describes how hypertrophic fat cells become hypoxic, triggering inflammation and impairing surrounding tissues.

Unlike the fast form, slow insulin resistance is rooted in long-term lifestyle habits and takes time to correct. The standard advice to “just cut calories” fails to address the core issue—chronically high insulin. Instead, Ben recommends that people first focus on lowering insulin through carbohydrate restriction, which naturally curbs hunger, boosts energy expenditure, and allows fat cells to shrink in a sustainable way.

He concludes that understanding whether your insulin resistance is fast or slow in origin can help shape more effective interventions. With better insight into the mechanisms—from ceramides to fat cell hypertrophy—comes better, more targeted strategies to improve metabolic health.

Show Notes/References:

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