How? It’s really quite simple. I prescribe you insulin. Insulin is a natural hormone but excessive insulin causes obesity.
Insulin is prescribed to lower blood glucose in both type 1 and type 2 diabetes. Virtually every patient taking insulin and every prescribing physician knows very well that weight gain is the main side effect. This is strong evidence that hyperinsulinemia directly causes weight gain. But there is other corroborating evidence as well. Increasing insulin causes weight gain. Reducing insulin causes weight loss. These are not merely correlations but direct causal factors. Our hormones, mostly insulin, ultimately sets our body weight and level of body fat.
Obesity is a hormonal, not a caloric imbalance.
High levels of insulin, called hyperinsulinemia, cause obesity. But this alone does not cause insulin resistance and type 2 diabetes. The conundrum is why fat becomes stored in the organs such as the liver rather in adipocytes.
How to get fatty liver
Here’s a startling fact. Anybody can get fatty liver. What’s the scariest part? It only takes three weeks! Excessive insulin drives new fat production. If this occurs faster than the liver can export it out to the adipocytes, then fat backs up and accumulates in the liver. This can be achieved simply with overfeeding of sugary snacks. Glucose and insulin levels quickly rise and the liver handles this glut of glucose by creating new fat through de novo lipogenesis.
Overweight volunteers were fed an extra one thousand calories of sugary snacks daily in addition to their regular food consumption. This sure sounds like a lot, but actually only consisted of eating an extra two small bags of candy, a glass of juice and two cans of Coca Cola per day.
After only three weeks on this regimen, body weight increased by a relatively insignificant two percent. However, liver fat increased disproportionately by a whopping twenty-seven percent! The rate of DNL increased by an identical twenty-seven percent. This accumulation of liver fat was far from benign. Markers of liver damage also increased by thirty percent.
Fatty liver is a completely reversible process. Emptying the liver of its surplus glucose, and allowing insulin levels to drift back to normal, returns the liver to normal. Hyperinsulinemia drives DNL, which is the primary determinant of fatty liver disease, making dietary carbohydrates far more sinister than dietary fat. High carbohydrate intake can increase de novo lipogenesis 10 fold, whereas high fat consumption, with correspondingly low carbohydrate intake, does not change hepatic fat production noticeably.