 After about age 20, we may have all of the insulin-producing beta cells we're ever going to have in our pancreas, and so if we lose them, we may lose them for good. Autopsy studies show that by the time type 2 diabetes is diagnosed, we may have already killed off half of our beta cells. You can do it right in a Petri dish. Expose human beta cells to fat, they suck it up, and then start dying off. A chronic increase in blood fat levels is harmful as shown by the important effects in pancreatic beta cell lipotoxicity. Fat breakdown products can interfere with the function of these cells and ultimately lead to their death, and not just any fat, saturated fat. The predominant fat in olives, nuts, and avocados gives you a tiny bump in death protein 5, but saturated fat really ramps up this contributor to beta cell death. Saturated fats are harmful to beta cells, harmful to the insulin-producing cells in our pancreas, cholesterol too. The uptake of bad cholesterol, LDL, can cause beta cell death as a result of free radical formation. So diets rich in saturated fats not only cause obesity and insulin resistance, but the increased levels of circulating free fats in the blood, called NEPAs, non-esterified fatty acids, causes beta cell death and may thus contribute to progressive beta cell loss in type 2 diabetes. This isn't just based on test tube studies. If you infuse fat into people's bloodstream, you can directly impair pancreatic beta cell function, and the same when we ingest it. Type 2 diabetes is characterized by defects in both insulin secretion and insulin action, and saturated fat appears to impair both. Insulin secretion showed saturated fat ingestion reduces insulin sensitivity within hours, but these were non-diabetic, so their pancreas should have been able to boost insulin secretion to match, but insulin secretion failed to compensate for insulin resistance in subjects who ingested the saturated fat, and this implies the saturated fat impaired beta cell function as well, again just within hours after going into our mouth. So increased consumption of saturated fats has a powerful short and long-term effect on insulin action, contributing to the dysfunction and death of pancreatic beta cells in diabetes. And saturated fat isn't just toxic to the pancreas. The fats found predominantly meat and dairy— chicken and cheese are the two main sources in the American diet— are almost universally toxic, whereas the fats found in alf nuts and avocados are not. Saturated fat has been found to be particularly toxic to liver cells in the formation of fatty liver disease. You expose human liver cells to plant fat, and nothing happens. Expose liver cells to animal fat, and a third of them die. This may explain why higher intakes of saturated fat and cholesterol associated with non-alcoholic fatty liver disease. By cutting down on saturated fat consumption, we may be able to help interrupt this process. Decreasing saturated fat intake may help bring down the need for all that excess insulin, so either being fat or eating saturated fat can both cause that excess insulin in the blood. The effect of reducing dietary saturated fat intake on insulin levels is substantial, regardless of how much belly fat we have. And it's not just that by eating fat we may be more likely to store it as fat. Saturated fats, independently of any role they have of making us fat, may contribute to the development of insulin resistance in all its clinical consequences. After controlling for weight and alcohol and smoking and exercise and family history, diabetes incidence was significantly associated with the proportion of saturated fat in our blood. So what causes diabetes? The consumption of too many calories rich in saturated fats. Now, just like everyone who smokes doesn't develop lung cancer, everyone that eats a lot of saturated fat doesn't develop diabetes. There's a genetic component. And just like smoking can be said to cause lung cancer, high-calorie diets rich in saturated fats is currently considered the cause of type 2 diabetes.