The Bad and the Ugly Regarding High Fructose Corn Syrup
Okay, we hear about it day in and day out. First it’s good – how can it not be? It’s made from corn, right? Then it’s bad. How can that be true? Well, I’m about to take some of the confusion out of the HFCS debate so that you, the consumer, can decide for yourself what’s healthy and what’s …. well ….. not so much.
First, a little background on high fructose corn syrup. It was invented in Japan in 1966 and introduced to the United States in the mid-1970s. It became a big seller in response to the fat-free fad, as it was mostly used to make fat-free foods taste better. When the American Heart Association and the USDA reduced their recommended dietary level of fat from 40% to 30% of your diet, the use of HFCS went through the roof because now just about everyone was consuming processed foods that were either low-fat or non-fat in order to avoid obesity and heart disease. While everyone thought that they were being health conscious, little did they know that the results of this low-fat, high fructose diet would be metabolically devastating! Not all sugars were created equal, after all. I will now explain a little bit about the differing metabolic reactions of various forms of sugar.
Every living thing needs glucose to survive. It is the primary energy source for our brain and it is a product of photosynthesis. It is found in rice, corn, and grains that make up bread and pasta. In this case, imagine that you have just eaten two pieces of bread. 80% of the glucose from that bread is used for energy by each and every cell in your body. The remaining 20% travels to the liver where it is metabolized and stored as glycogen (sort of like a temporary, non-toxic packaged form of glucose; able to be converted to energy easily and quickly when the need arises).There is no limit on the amount of glycogen that can be hanging out in the liver, waiting.
At the same time, a small amount of pyruvate is produced and converted to ATP (the chemical storage form of energy) along with Carbon dioxide. A very tiny amount of citrate is then produced through the process of “de novo lipogenesis” – less than 1 calorie from 2 slices of bread . This ends up as VLDL (Very Low Density Lipoprotein) which is bad and causes plaque formation.
Insulin is now released by the pancreas in response to increased blood glucose levels. It provides the key to unlocking the doors of each cell to allow the glucose to enter and get the heck out of the bloodstream. The bottom line: when you consume 120 calories of glucose, less than 1 calorie contributes to adverse metabolic outcomes.
This carbohydrate goes through a very different metabolic process that leaves a long trail of toxins in its wake. Not only is it an acute central nervous system toxin (think “drunk”) but it is also a chronic hepatotoxin due to the fact that it is almost totally metabolized in the liver. Let’s imagine that you have just consumed one alcoholic beverage. What happens? Well, 10% of the ethanol is broken down by the stomach and intestines, 10% is metabolized by the brain and other organs, and the remaining 80% is processed by the liver. This represents about four times the load on the liver as the same number of calories coming from glucose!
Once ethanol arrives in the liver, the toxin production begins! It is immediately converted to aldehydes, which produce free radicals that damage proteins in the liver. Now some of these aldehydes convert to glucose, but most become citrate, resulting in FFAs (Free Fatty Acids), VLDL (Very Low Density Lipoprotein), and triglycerides.
It’s important to note that fat tissue is metabolically active in its own right. FFAs are constantly moving in and out of cells, across cell membranes, whereas triglycerides (consisting of 2 FFA molecules and 1 glycerol molecule) are too big to cross the cell membranes. So, fat enters and exits as FFAs but is stored as a triglyceride until energy is needed. At that point the triglyceride is broken down into FFAs and burned as fuel. The glycerol molecule within the triglyceride actually comes from what is called g-3-p and originates from the metabolism of glucose. The more g-3-p that there is available, the more fat will be deposited.
So, back to ethanol: basically, whereas only 1 calorie from glucose was converted to dangerous VLDL, 30 calories from ethanol was converted to VLDL, contributing to obesity and heart disease. Not only that, but the lipids mixed with the ethanol create an inflammation-causing enzyme that leads to hepatic insulin resistance, a precursor to fatty liver disease and Type 2 Diabetes.
The reason that ethanol metabolism is so important is that it basically illustrates exactly what happens after you ingest fructose or high fructose corn syrup.
One hundred percent of fructose is metabolized in the liver, making it a hepatotoxin. Forgive me if some of the following is repetitive. Like I said, the metabolism of fructose is very, very similar to that of ethanol.
First, in the liver, fructose is converted to F1P, which serves to deplete liver cells of phosphates. This process is nasty, as it produces the waste product Uric Acid, which blocks the enzyme that makes the body’s natural blood pressure regulator, nitric oxide and also leaves you prone to gout. Almost all of the F1P turns into pyruvate, ending up as citrate. This is where the metabolic process most resembles ethanol – de novo lipogenesis occurs, the end products of which are FFAs, VLDL and triglycerides.
Next, the fructose stimulates g-3-p that turns FFAs into triglycerides in your fat cells. Ironically, fructose is the carbohydrate that happens to be most efficiently converted into g-3-p. Remember, the more g-3-p there is, the more fat there is. The FFAs that leave the liver go to the skeletal muscle and cause skeletal muscle insulin resistance. The FFAs that stay in the liver, on the other hand, accumulate as fat droplets causing hepatic insulin resistance and nonalcoholic fatty liver disease. The pancreas pumps out insulin to help the sugar out of your bloodstream and into your cells, potentially leading to Type 2 Diabetes. Bottom line: About 40 calories out of 120 calories of fructose contributes directly to disease. Consuming fructose is basically consuming fat.
There’s more. If the nasty stuff going on with fructose metabolism wasn’t enough to turn you off to this carbohydrate, there are several other downsides to its consumption.
Keep in mind that the hormones leptin and insulin cause your brain to send you signals to stop eating. Fructose undermines these signals, causing you to eat more. How? First, fructose does not stimulate an increase in leptin in the first place. Next, although glucose suppresses ghrelin (the hunger hormone that makes you want more food), fructose does not. Also, because fructose raises triglyceride levels, the amount of leptin crossing the blood-brain barrier is reduced, almost like a vicious cycle. Lastly, the increased insulin levels caused by fructose interfere with the communication between leptin and the hypothalamus, so pleasure signals aren’t extinguished. Your body senses starvation and tells you to eat more. Finally, nearly all HFCS is made from genetically modified corn, the danger of which is still unknown.
There are alternatives out there, the best one being Stevia, an herb that is much sweeter than sugar and has no effect on insulin response. And, it’s actually got many other beneficial qualities. Otherwise, use organic cane sugar or organic raw honey in moderation. And if you have to eat sugar, eat some fiber at the same time to offset the negative metabolic effects, similar to eating a piece of fruit.
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