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Kindle Notes & Highlights
by
Jason Fung
Read between
June 11 - June 15, 2019
Fatty liver precedes the clinical diagnosis of type 2 diabetes by ten years or more.6 As
In North America, the prevalence of NASH is estimated at 23 percent of the entire population.
Researchers fed overweight volunteers an extra thousand calories of sugary snacks daily in addition to their regular food consumption.19 This sounds like a lot, but it only means ingesting an extra two small bags of candy, a glass of juice, and two cans of Coca-Cola per day. After three weeks, body weight increased by a relatively insignificant 2 percent. However, liver fat increased by a whopping 27 percent, caused by an identical increase in the rate of DNL. This fatty liver was far from benign, as blood markers of liver damage increased by a similar 30 percent.
Producing foie gras in animals and fatty liver in humans is basically the same process.
Randle demonstrated that cells burning glucose could not burn fat and vice versa.
When the body is mostly burning fat, such as during very low–carbohydrate diets or fasting, it cannot burn glucose. Therefore, if you start to eat carbohydrates, the cells temporarily cannot handle the glucose load and your blood glucose levels rise. This phenomenon looks like insulin resistance but is not really the same mechanism at all.
Whereas every cell in the body can use glucose for energy, none can use fructose. Only the liver metabolizes fructose. Whereas excess glucose can be dispersed throughout the body for use as energy, fructose targets the liver like a guided missile.
newer agents, which can reduce both blood glucose and insulin levels, show proven benefits to reduce heart and kidney complications of type 2 diabetes. Nevertheless, these medications, while an important step forward, are clearly not the answer; they do not reverse the root cause of type 2 diabetes—our diet.
Over six months, the two groups showed no difference in the amount of weight and body fat loss between them, but an important difference between their insulin and insulin sensitivity levels.
In the late 1990s, the low-carbohydrate Atkins-styled diets enjoyed a huge surge of popularity. Health professionals like me and most other physicians were aghast, positive that these high-fat Atkins-styled diets would cause heart disease.
Together, we counseled patients, many with type 2 diabetes, on how to follow a low-carbohydrate, high-fat diet. I believed and hoped they would improve their health. The results were a disaster. Nobody lost weight. Nobody got better. A review of my patients’ diet diaries revealed they were eating lots of bread, noodles, and rice. They had misunderstood these foods as being part of a low-carbohydrate diet. Having followed a low-fat diet for most of their lives, this new regimen was entirely foreign to them, and they didn’t know what to eat. I needed to find a simpler solution.