Insulin is misunderstood by many, including patients and even physicians. Most physicians think of insulin as a hormone that pushes glucose into the cell by opening a channel. However, the truth is that insulin is primarily a fat-storage hormone and shifts metabolism from fat use as energy to fat as storage. In the absence of insulin, the default is to use fat storage and convert it to usable energy, known as lipolysis. In the presence of insulin, lipolysis stops and lipogenesis starts, converting circulating glucose to lipid (fat) storage.
The higher your insulin, the greater you push circulating glucose to glycogen and then to fat stores. The circulating glucose capacity is approximately 5g. The glycogen storage capacity is 500g. Comparatively, the storage capacity for fat is limitless (exceeding 100,000g). As your fat storage depots fill, they release inflammatory cytokines.
There are two examples of this, both dealing with different types of diabetes. Type 1 diabetics, our first example, have an autoimmune dysfunction that destroys beta cells, stopping insulin production. Type 1 Diabetics produce little to no insulin and are thin until we give them insulin. Once they get excessive insulin, these patients gain weight. The insulin becomes excessive because our dietary guidelines encourage six snacks and meals per day with approximately 40% carbohydrates. We are chasing the blood glucose with insulin because we are overfeeding carbohydrates.
The second example relates to type 2 diabetes. Well over 90% of type 2 diabetics are overweight because they consume too much carbohydrate and produce chronically elevated levels of insulin to compensate. They then become progressively more overweight, and the glycation of the cellular structures leads to rapid aging. This excessive insulin causes excessive fat storage and inflammation as the fat cells swell and leech inflammatory cytokines.