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Visceral fat deposited in and around the organs4 is the main contributor to high insulin resistance. The very first place this fat starts to accumulate, often before insulin resistance becomes noticeable, is the liver.
Too much sugar and
insulin, over too long a period of time, leads to fatty liver.5
As shown in Figure 7.2, the cycle proceeds as follows: 1.Hyperinsulinemia causes fatty liver. 2.Fatty liver causes insulin resistance.
3.Insulin resistance leads to compensatory hyperinsulinemia. 4.Repeat cycle.
Fat inside the liver, rather than overall obesity, is the crucial stepping stone toward insulin resistance and diabetes.
Fatty liver is the clearest sign that hyperinsulinemia and insulin resistance are developing, and one of the earliest. Fatty liver precedes the clinical diagnosis of type 2 diabetes by ten years or more.6 As the liver slowly accumulates fat it becomes increasingly insulin resistant. Fatty liver can be diagnosed by ultrasound,
but an increased waist circumference or waist-to-height ratio is an important clue to its presence.
More importantly, the new recognition of NAFLD confirmed the extraordinarily close association between obesity, hyperinsulinemia/insulin resistance, and fatty liver.
Furthermore, NASH has become one of the leading causes of end stage liver disease, known as cirrhosis, and one of the top indications for liver transplant in the Western world. In North America, the prevalence of NASH is
estimated at 23 percent of the entire population.
This is a truly frightening epidemic. In the space of a single generation, non-alcoholic fatty liver disease has gone from being unnamed and completely unknown to being the commonest cause of abnormal liver enzymes and chronic liver disease in the Western world.16 This is the Rocky Balboa of liver diseases.
In short, the fattier the liver, the higher the insulin resistance.
Fatty liver is the harbinger of insulin resistance, but it is only the beginning. The fat within other organs, including the skeletal muscles and the pancreas,23 also play a leading role in this disease.
Sugar is toxic.
Fructose is the sugar naturally found in fruit, and it is the sweetest-tasting naturally occurring carbohydrate.
Eating fructose does not appreciably change the body’s blood glucose level, since they are different sugar molecules. Neither does fructose produce much insulin response directly.
Other dietary sugars, like fructose or lactose (the sugar found in milk), do not raise blood glucose levels appreciably and therefore have correspondingly low glycemic index values.
Fructose, which raises neither blood glucose nor insulin, was considered more benign than other sweeteners for many years. An all-natural sweetener found in fruit that didn’t raise the glycemic index sure sounded healthy. But it had a hidden dark side that was not obvious for many decades. The toxicity of fructose was invisible when looking at the blood glucose; it only became apparent by looking at the slow accumulation of fat in the liver.
THE DOSE MAKES THE POISON
That is, anything can be harmful in excessive amounts, even if it is typically considered beneficial.
high-fructose corn syrup (HFCS),
FRUCTOSE AND FATTY LIVER
Fructose overfeeding can increase DNL fivefold,6 and replacing glucose with a calorically equal amount of fructose increases liver fat by a massive 38 percent within only eight days. This fatty liver plays a crucial role in the development of insulin resistance.
Since fatty liver and the resultant insulin resistance is a key contributor to hyperinsulinemia and obesity, this means that fructose is far more dangerous than glucose. A back-of-the-envelope calculation shows that, for an average 170-pound
pound person, fructose would be approximately 34 times (170 divided by 5) more likely to cause fatty liver and thus obesity and insulin resistance.
FRUCTOSE AND INSULIN RESISTANCE
What happens after decades of high fructose consumption? The result is a diabetes disaster—precisely the one we are experiencing right now.
FRUCTOSE AND THE GLOBAL DIABETES EPIDEMIC
DATA FROM MORE than 175 nations links sugar intake inextricably to diabetes, independent of obesity. For example, Asian sugar consumption is rising at almost 5 percent
per year, even as it has stabilized or fallen in North America. The result has been a tsunami of diabetes. In 2013, an estimated 11.6 percent of Chinese adults had type 2 diabetes.11 Yet the Chinese being diagnosed with diabetes have an average body mass index of only 23.7, which is considered in the ideal range. By contrast, American diabetics average a body mass index of 28.7, well within the overweight category.
This situation presents an apparent paradox since the Chinese diet has traditionally been based upon white rice. Yet, despite such a high intake of refined carbohydrates, the Chinese have suffered little obesity or type 2 diabetes. The reason for this apparent protection is that they ate almost no sugar, as Figure 8.2 shows. Refined carbohydrates, such as white rice, are composed of long chains of glucose, whereas table sugar contains equal parts of glucose and fructose.
In the late 1990s, the INTERMAP study compared the diets of the U.K., U.S., Japan, and China.12 Chinese sugar consumption has steadily increased since the time of that study, and diabetes rates have moved in lockstep. Combined with their original high-carbohydrate intake, the Chinese are facing their current diabetes disaster.
The traditional Chinese diet: High carbs, low sugar, no diabetes
Diabetes correlates strongly to sugar, not other sources of calories. Fructose overconsumption directly stimulates fatty liver and leads directly to insulin resistance. Consumption of high-fructose corn syrup, which is chemically almost identical to sugar, also shows the same tight correlation to diabetes.
But this toxicity is not easily recognized. In the short term, fructose has few obvious health risks since it affects neither blood glucose nor
insulin levels. Instead, it exerts its toxicity mainly through long-term effects on fatty liver and insulin resistance, which may take decades to manifest. Short-term studies, often focusing on insulin, blood glucose, and calories, miss this long-term effect, just as short-term studies of cigarette smoking miss the long-term cancer risk.
The 2005 National Cholesterol Education Program (NCEP) Adult Treatment Program III (ATP III) defines metabolic syndrome as three of the following five conditions1: 1.Abdominal obesity, measured by waist circumference: men over 40 inches, women over 35 inches; 2.Low high-density lipoprotein (HDL): men less than 40 mg/dL or women less than 50 mg/dL or taking medication; 3.High triglycerides: over 150 mg/dL or taking medication;
4.High blood pressure: over 130 mmHg systolic (top number) or over 85 mmHg diastolic (bottom number) or taking medication; 5.Fasting blood glucose > 100 mg/dL or taking medication.
To their surprise, hypertriglyceridemia was not caused by eating too much fat; instead, it resulted primarily from excess dietary
carbohydrates and the subsequent hyperinsulinemia.
This emphasizes again that the problem is not obesity per se, but abdominal obesity.
FROM FATTY LIVER TO METABOLIC SYNDROME
THESE NEWLY CREATED triglycerides are made from the substrate glucose, not from dietary fat. This distinction is important because fats made by DNL are highly saturated. Eating dietary carbohydrates, not dietary saturated fat, increases saturated fat levels in the blood. Saturated fats in the blood, not the diet, are highly associated with heart disease.
Dr. Reaven showed that hyperinsulinemia and fructose shared responsibility for most of the rise in blood triglyceride levels.
Simply put, higher insulin levels and fructose ingestion produce higher blood triglyceride levels. There’s just too much sugar.
What is clear, however, is that the lipid profile typical of the metabolic syndrome—high triglycerides and low HDL—results from the excess of VLDL,25 which ultimately stems from hyperinsulinemia, which ultimately stems from eating too much glucose and fructose. Again, too much sugar.
Figure 9.2. Hormonal obesity VII: Fatty liver → low HDL
Abdominal obesity
This abdominal, or visceral, fat is the most important predictor of metabolic syndrome.26 Surgical removal of visceral fat reverses insulin resistance,27 whereas removal of subcutaneous fat has no such metabolic benefits.28
