http://blogs.mercola.com/sites/vita...weetener-Is-Far-More-Deadly--Part-3-of-3.aspx
II. Ethanol Metabolism
Ethanol, or ethyl alcohol, is the favorite carbohydrate of many. But it is also a carbohydrate that undergoes a very different metabolic process, leaving in its wake a trail of toxins a mile long.
Ethanol is an acute central nervous system toxin and a chronic hepatotoxin due to the fact that it must be metabolized almost completely in the liver.
After consuming an alcoholic beverage, 10 percent of the ethanol gets broken down by the stomach and intestine as a “first pass” effect, and another 10 percent is metabolized by the brain and other organs. The fact that ethanol is partially metabolized in your brain is the reason you experience that familiar “buzz.”
The remaining 80 percent hits the liver, where it must be broken down. This is four times the load on the liver as the same number of calories from glucose.
But the metabolic process in the liver is quite different from that of glucose.
This metabolic cascade can be summarized as follows:
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The liver converts ethanol to aldehydes, which produce free radicals that damage proteins in the liver.
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Some of these aldehydes are converted to glucose, but a large amount of excess citrate is formed in the process, stimulating “junk chemicals” that result in free fatty acids (FFAs), VLDL and triglycerides. As compared to the 1 calorie from glucose that was converted to VLDL (see previous section), the same caloric intake from ethanol produces 30 calories of VLDL that are transported to your fat cells and contribute to your obesity, or participate in plaque formation. This is what leads to the dyslipidemia of alcoholism.
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The resulting lipids, together with the ethanol, lead to an enzyme that begins an inflammation cascade, which in turn causes hepatic insulin resistance, liver inflammation and cirrhosis.
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Fat globules accumulate in the liver as well, which can lead to fatty liver disease.
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Free fatty acids (FFAs) leave the liver and cause your skeletal muscles to become insulin resistant. This is a worse form of insulin resistance than hepatic insulin resistance and can lead to type II diabetes.
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After a 120-calorie bolus of ethanol, a large fraction (about 40 calories) can contribute to disease.
Why am I including a discussion of ethanol metabolism in a report about fructose?
Because, in nearly every way, fructose is metabolized the same way as ethanol, creating the same toxins in your body.
III. Fructose Metabolism
Now we finally come to fructose.
When you consume fructose, one hundred percent of it goes directly to your liver to be metabolized. This is why it is a hepatotoxin -- it overloads the liver. Fructose metabolism creates the following adverse effects:
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Fructose is immediately converted to fructose-1-phosphate (F1P), depleting your liver cells of phosphates.
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The above process produces waste products in the form of uric acid. Uric acid blocks an enzyme that makes nitric oxide. Nitric oxide is your body’s natural blood pressure regulator, so when it is blocked, your blood pressure rises -- leading to hypertension. Elevated uric acid levels can also cause gout.
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Almost all of the F1P is turned into pyruvate, ending up as citrate, which results in de novo lipogenesis, the end products of which are FFAs, VLDLs, and triglycerides. The result -- hyperlipidemia.
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Fructose stimulates g-3-p (activated glycerol), which you will recall is the crucial molecule for turning FFAs into triglycerides within the fat cells. Remember, the rate of deposition of fat into fat cells is dependent on the presence of g-3-p. The more g-3-p that is available, the more fat is deposited. Fructose is the carbohydrate most efficiently converted into g-3-p11. In other words, fructose is the most lipophilic carbohydrate.
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FFAs are exported from the liver and taken up in skeletal muscle, causing skeletal muscle insulin resistance.
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Some of the FFAs stay in the liver, leading to fat droplet accumulation, hepatic insulin resistance and nonalcoholic fatty liver disease (NAFLD)[ii][iii].
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Insulin resistance stresses the pancreas, which pumps out more insulin in response to rising blood sugar as your cells are unable to get the sugar out of your bloodstream, and this can progress to type II diabetes.
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As with a bolus dose of ethanol, a 120-calorie bolus of fructose results in a large fraction (again, about 40 calories) that directly contributes to disease.
Do these symptoms sound a bit familiar to you? Hypertension, lipogenesis and dyslipidemia, obesity, inflammation, insulin resistance, and central nervous system leptin resistance?
If you are thinking it sounds a lot like classic metabolic syndrome, you are dead on!
The point to take away is: consuming fructose is consuming fat. Fructose is not really a carbohydrate -- a high fructose diet is a HIGH FAT diet. A high fat diet that creates a vicious cycle of consumption that won’t turn itself off.
You can see by comparing the metabolism of fructose with the metabolism of ethanol that they are very similar. In fact, when you compare the metabolism of 150 calories of soda with 150 calories of beer (a 12 ounce can of each), about 90 calories reach the liver in either case. Fructose causes most of the same toxic effects as ethanol because both come from sugar fermentation.
Both ethanol metabolism and fructose metabolism lead to visceral adiposity (belly fat), insulin resistance and metabolic syndrome.
Studies are accumulating that bear this out.
