The pancreas, a gland located in your upper abdomen, produces the hormone insulin. Insulin opens gates on the surface of cells to allow glucose to pass out of the bloodstream and into cells. If you don’t make enough insulin, or notably if your cells don’t respond normally to insulin–if they become “insulin resistant” —glucose builds up in your blood, which is what we call type 2 diabetes.
To understand the connection between obesity and type 2 diabetes, you need to examine the difference between type 1 and type 2 diabetes.
Type 1 diabetes is caused by autoimmune damage to the insulin-producing cells in the pancreas, which results in insulin deficiency—simple enough. Type 2 diabetes is more complicated. Patients with type 2 diabetes make plenty of insulin. The problem is their body loses responsiveness to it—they become “insulin resistant.” Consequently, they have to produce as much as five times the normal amounts of insulin to control the level of glucose in their blood. Their blood sugar may rise a little but their insulin levels skyrocket.
The difference between type 1 and type 2 diabetes is that, in addition to the effects of high blood sugar, type 2 diabetics must deal with the effects of high insulin levels, which often cause more problems than high blood sugar. One those problems is obesity.
Excess insulin secretion goes on for years before the blood sugar level rises and doctors diagnose type 2 diabetes. At first the insulin producing cells can keep up with demand, and blood sugar levels remain near normal. However, years of insulin overproduction eventually wear out the insulin producing cells. When production can no longer keep up with demand, blood sugar rises. You might still make plenty insulin, just not enough to keep your blood sugar down.
Not everyone with insulin resistance goes on to develops diabetes. In fact, most don’t. Even though they produce more-than-normal amounts of insulin, their insulin- producing cells keep up with demand. The problem is that high insulin levels keep shunting nutrients out of the bloodstream and into fat, which is why the number of people with obesity has risen along with that of type 2 diabetes.
The Underlying Epidemic: Insulin Resistance
You need insulin to metabolize carbohydrates. If you ate as little carbohydrate as your cave dwelling ancestors did, you wouldn’t have to worry about type 2 diabetes or obesity. Indeed, cutting carbohydrates in the diet helps treat type 2 diabetes. But there’s another problem besides carbohydrates at work here. The amount of insulin your body produces is not only dependent on how much carbohydrate you eat but also on how responsive your muscles are to insulin.
Your muscles are the body’s main consumers of carbohydrate and the target of most of the insulin you produce. If they lose responsiveness to insulin–if they become “insulin resistant,” your pancreas has to secrete more than normal amounts of insulin to control your sugar glucose levels. The reason so many of us these days are overweight and diabetic is that we are being hit by a double whammy: we consume too many carbohydrates—at least compared to cave dwellers–and our muscles lose responsiveness to insulin.
Unlike high blood cholesterol and high blood pressure, which are caused by genetically determined factors we can’t change, insulin production is under our control–in theory. By reducing the amount of carbohydrates in our diet and increasing our muscles’ responsiveness to insulin with exercise, we could reduce the amount of insulin we produce, stop wearing out our insulin producing cells and quit forcing calories into fat. The problem is two realities of modern life that are changeable in theory but in reality prove to be immutable. As hard as we try, we can’t seem to avoid carbohydrates enough and keep our muscles responsive to insulin enough to avoid gaining weight and putting ourselves at risk of type 2 diabetes.
We modern humans consume hundreds of times more carbohydrates than our prehistoric ancestors did because we rely on refined carbohydrates, such as flour, potatoes, rice and sugar, to provide a major portion of our calories. As soon as refined carbohydrates arrive in the intestinal tract they turn to sugar. Our prehistoric ancestors didn’t have to worry about this; there were no refined carbohydrates in their diet. They had no way to process grains or refine sugar. The carbohydrate they consumed—wild fruit, roots, bark and grasses–contained plenty of vitamins, minerals and fiber but yielded little in the way of calories. They got most of their calories from meat, fish and bugs.
But folks in the 1800’s ate plenty of bread, potatoes, rice and sugar. They didn’t gain weight and develop type 2 diabetes because they were more physically active than we are now. Cars and busses hadn’t been invented. People had to walk several miles a day to tend to their needs and spent most of their days doing physical work. Now we rely on cars, busses and trains get around, and most of us work at sedentary occupations. It’s no coincidence that America’s epidemic of obesity and diabetes began around 1915 when Henry Ford started mass producing automobiles. We have built a society around motorized transportation.
Refined carbohydrates are one part of the double whammy that’s making us fat and diabetic, motorized transportation is the other part. The question is what can we do about it? If the answer is not much, then like high blood cholesterol and high blood pressure, we may end up relying on medication. We now have excellent medicines for treating high blood cholesterol and high blood pressure, and the treatment of these conditions has caused deaths from heart attack and stroke to plummet. Until recently there were no medications available that could reliably reverse obesity, but now may be a new day.
Ozempic, Wegovy and Mounjaro counteract the effects of insulin resistance by reducing the amount of insulin the body has to produce to deal with the relatively huge amount of carbohydrates in our diet compared with that of prehistoric humans and with our relatively low physical activity levels compared with that of our 19th century ancestors.
