Insulin

Before Banting and Best's breakthrough, they kept a pancreatectomized dog named Marjorie alive for 70 days using their crude pancreatic extract—the first creature to survive without a pancreas. The first human recipient, 14-year-old Leonard Thompson, was near death at 65 pounds when he received the injection in January 1922; within months he'd gained weight and returned to school. The researchers sold their patent to the University of Toronto for $1, believing insulin was too important to humanity to be monopolized, though modern insulin analogs now cost patients hundreds monthly.

Insulin isn't just about blood sugar—it's the master regulator determining whether your body stores or burns, builds or breaks down, even ages fast or slow. When constantly elevated from frequent eating and refined carbs, insulin locks fat inside cells like a one-way valve, simultaneously blocking the release of stored energy and creating the metabolic trap of "hungry but unable to access fuel." This chronic hyperinsulinemia precedes type 2 diabetes by years, making insulin resistance—not high blood sugar—the actual first domino in metabolic disease.

Your insulin sensitivity fluctuates dramatically throughout the day, peaking in the morning and declining toward evening—meaning the exact same meal produces vastly different insulin responses depending on when you eat it. This circadian insulin rhythm explains why eating late or grazing constantly can be metabolically devastating even with "healthy" foods, and why time-restricted eating (compressing meals into 8-10 hours) can restore insulin sensitivity without changing what you eat. Your body expects feast-famine cycles, not the modern 14-hour eating window that keeps insulin perpetually elevated.

Lower insulin levels consistently predict longer lifespan across species, from yeast to mammals, because insulin and its related growth pathway IGF-1 fundamentally accelerate aging at the cellular level. Centenarians typically have exceptional insulin sensitivity and low baseline insulin despite eating normal diets, suggesting that metabolic health may be the most powerful longevity lever we control. The irony: we artificially spike insulin 6-8 times daily through constant eating, overriding the natural low-insulin states where cellular repair, autophagy, and fat-burning occur.

While everyone focuses on carbs and insulin, protein also stimulates significant insulin release—yet somehow doesn't cause insulin resistance or fat storage the way carbs do. The difference lies in glucagon, protein's companion hormone that counterbalances insulin's storage signal with a mobilization command, creating metabolic equilibrium rather than one-way storage. This explains why high-protein diets aid fat loss despite raising insulin, and why the composition of your meals matters more than individual macronutrients in isolation.

Contracting muscles possess a remarkable backup system: they can pull glucose inside without any insulin present, using an insulin-independent transporter called GLUT4 that physically relocates to the cell surface during exercise. A single resistance training session can keep this bypass route open for 48 hours, meaning muscle contraction literally rewires your metabolism to work around insulin resistance. This makes movement the most powerful insulin-sensitizing intervention known—more effective than any drug, and with benefits beginning from the first workout.