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Insulin resistance is the thread that runs through many chronic afflictions of modern times—obesity, heart disease, and, most conspicuously, type 2 diabetes. All are entangled with diet, and all are linked causally to a dysfunctional response to insulin, the hormone that orchestrates the body's use and storage of nutrients. Elucidating the causes of insulin resistance is one of the most critical endeavors in modern medicine, and two competing theories have now gained wide support. One is that cells essentially become poisoned by fat. This lipotoxicity or lipid overload hypothesis holds that normal processes break down when fat (adipose) tissue cannot store excess fat, and fat accumulates inappropriately in muscle and liver cells. The main rival to this idea, the inflammation hypothesis, holds that as fat cells increase in size with the accumulation of fat, they release inflammatory cytokines and molecules known as adipokines. It's these molecules, so this theory goes, that cause insulin resistance elsewhere in the body. Researchers are now confident that these inflammatory mechanisms play some role in insulin resistance. But they still can't say for sure whether those roles are causal.