Which causes which: extra fat or the hormone driving it

Everyone assumes they know the order of events: you eat too much, you gain fat, and that fat makes you insulin resistant. Benjamin Bikman doesn't deny that this happens. But he lays out a stack of evidence suggesting the arrow can just as easily point the other way, and untangling which direction matters more changes what actually helps.

Start with two versions of diabetes that sit at opposite extremes of insulin. Type 1 diabetes means almost no insulin at all, and people with it, unless they inject insulin, simply cannot get fat, no matter what or how much they eat; some who want to stay thin dangerously underdose their injections on purpose. Type 2 diabetes means too much insulin, and when patients are prescribed insulin injections to control their blood sugar, they gain weight, sometimes even while eating less, because the extra insulin is pushing their bodies to store rather than burn fuel. In both directions, insulin, not the food itself, decides where the calories go.

Then there's a study Bikman cites that followed children over roughly a decade. Kids who started out at similar weights but had the highest insulin levels were up to thirty-six times more likely to become obese as adults than kids with lower insulin, even though their earlier body weight looked the same. The hormone showed up before the fat did.

The clearest illustration might be a class of diabetes drugs called thiazolidinediones. These drugs work by forcing fat cells to multiply, creating more, smaller fat cells rather than a few overstuffed ones. Patients on them typically gain weight, yet their insulin sensitivity improves. If excess fat were simply the villain, more fat should mean more resistance. Instead, the opposite happens, because, Bikman explains, individual fat cells have a size limit, sometimes called a personal fat threshold. A fat cell that hits its ceiling stops responding well to insulin and starts leaking fat and inflammatory signals into the blood, whether the person is technically thin or overweight. That's why some lean people carry serious insulin resistance hidden as fat packed around their organs, while some heavier people, whose fat cells can still divide and expand, remain insulin sensitive.

None of this erases the fact that, over time, excess fat clearly does worsen insulin resistance too; Bikman is careful to say the relationship runs both directions. But treating obesity as a simple case of willpower against calories misses half the story, and it explains why two people eating the same diet can end up on completely different metabolic paths.

Start by checking where your fat actually sits: grab it and see if it jiggles, since that's less concerning than a hard, protruding belly, which points toward fat packed around your organs. Measure your waist-to-hip ratio and aim to keep it below roughly 0.9 if you're a man or 0.8 if you're a woman. Resist the urge to assume a lean frame means a clean metabolic bill, and take risk markers seriously even at a low body weight. And when you're choosing how to eat, weigh whether the approach actually lowers insulin, not just how many calories it restricts, since the hormone may be steering the scale more than the arithmetic does.