In both types of diabetes this process is short-circuited and glucose is left circulating in the bloodstream, causing a high BGL. The body reacts by generating thirst, driving you to drink fluids that will be expelled and carry excess sugar from the bloodstream with it. That’s why the term diabetes mellitus (honeysweet urination) mentioned in Chapter 1 applies to both types. They both result in high BGLs and the resultant expelling of sugar in the urine. But this is where the similarity between Type 1 and Type 2 ends.
Type 1 diabetes is an autoimmune disease in which the body’s own defenses turn against the insulin-producing cells in the pancreas. The cells are killed, wrecking the pancreas’s ability to produce insulin. When a Type 1 eats, glucose enters the bloodstream but the insulin doesn’t get produced to enable the body to use it. The unused glucose stays in the blood.
In Type 2, the pancreas initially works fine. It senses the rising BGLs and produces insulin just like a non-diabetic person. The problem here is called “insulin resistance” because many of the body’s cells don’t allow insulin to unlock them. When a Type 2 eats, the glucose enters the bloodstream and the pancreas produces insulin. But the insulin resistant cells have barred the doors and the sugar stays in the bloodstream.
Insulin resistance doesn’t trigger the Type 2 diagnosis all by itself. Because the body’s cells get increasingly more insulin resistant, the pancreas works ever harder to produce enough insulin to overcome it. Eventually many of the overworked insulin producing cells die, the ability of the pancreas to produce insulin is compromised and high BGLs result. So the immediate cause of a diabetes diagnosis is insufficient insulin production but the underlying cause is insulin resistance that may have been present for years.