For years, fructose was considered a benign sweetener because of its low glycemic index.  Fructose was found naturally in fruits.  The problem, as often is the case, is a matter of scale.  Whereas natural fruit consumption contributed only small amounts to the diet, added sweeteners, particularly in the form of sucrose or high-fructose corn syrup (HFCS) added large amounts.

The peak of fructose consumption was reached just before the year 2000, when  people started to become concerned about the relationship between HFCS and obesity.  Adolescents in particular had a high consumption of fructose.  Fructose is the sweetest naturally occurring carbohydrate.  What was wrong with that?

HFCS was developed in the 1960s as a liquid sugar equivalent to sucrose.  HFCS was 55% fructose and 45% glucose compared to the 50-50 split seen in sucrose.  Sucrose was processed from sugar cane and sugar beets.  While not exactly expensive, it wasn’t exactly cheap either.  HFCS, however, could be processed from the river of cheap corn that was flowing out of the American MidWest.

In processed food, HFCS found a natural fit.  It was liquid and therefore easily incorporated into any food.  Indeed, it found its way into almost everything. Pizza sauce, soups, breads, cookies, cakes, ketchup, sauces – you name it, it probably had HFCS.  The advantages didn’t stop there.

• Sweeter than glucose
• Prevented freezer burn
• Helps browning
• Mixes easily
• Extends shelf life
• Keeps breads soft

But there was one overriding benefit to HFCS compared to sucrose.  It was cheap.  Companies cared about that more than anything else in the world.  It was cheap, cheap, cheap.  Given the similarity between HFCS and sucrose, most did not expect any significant difference between HFCS and sucrose.  And it was cheap.  Food manufacturers raced to use HFCS at every chance they had.

The tide began to turn in 2004 when George Bray published a study that showed that the increase in obesity mirrored the rise in use of HFCS.  However, at the same time, there was a significant decrease in the use of sucrose, which was more expensive.  HFCS was merely replacing the more expensive refined sugar in the diet of America.

There rise in obesity really mirrored the increase in the use of sugar.  Whether it was 55% fructose (HFCS) or 50% fructose in sucrose likely did not make a big difference.  The problem was the fructose.

The most important outcome of this furor was the increased scrutiny on the dangers of excess fructose in the diet.  Researchers started to investigate the differences between glucose and fructose.  It turns out that there are many differences.  Glucose can be used by every cell in the body.  Indeed, certain cells can only use glucose.  Red blood cells are often cited as only being able to use glucose.  Skeletal muscles, in need of quick and accessible energy, will preferentially consume glucose as well, but every cell has the ability.  No cell in the body has the ability to use fructose for energy.

Studies into fructose absorption showed that free fructose is poorly absorbed in the human gut.  However, the presence of glucose will significantly increase the amount of fructose absorbed.  Where glucose requires insulin for maximal absorption, fructose does not.  Most cells do not take up fructose and it is really only metabolized in the liver.  Where glucose can be dispersed throughout the body for use as energy, fructose concentrates like a guided missile to the liver.

Fructose rapidly becomes fructose-1-phosphate with no limit.  When an excess of glucose is consumed, the body has a natural rate limiting step that prevents excessive overloading of the metabolic system.  No such system is present for fructose.  The more you eat, the more you metabolize.  This becomes glucose, lactate and glycogen – all concentrated in the liver.  With higher levels of fructose ingestion, it becomes acetyl-CoA which  is needed for fatty acid synthesis.  What this means is that excess fructose becomes fat in the liver.  Fatty liver.  High levels of fructose will cause fatty liver. This fatty liver is absolutely crucial in the development of insulin resistance in the liver.

Think about it this way. Insulin is normally released when we eat.  It directs the glucose to be stored as energy for later use when we are not eating.  In the short term, some of this is stored as glycogen.  However, there is a limited amount of glycogen that we can store in the liver.  The rest of the glucose needs to be stored as fat.  So insulin promotes the production of fat in the liver, a process known as de novo lipogenesis (DNL).  This mean, literally “making fat from new”.  It is the process of turning glucose into fat.  Insulin is the hormone that pushes food energy into storage.

When insulin is low, this process reverses.  Glycogen is broken into glucose (glycogenolysis) and new fat is degraded for energy.  If we balance feeding periods with fasting periods, then there is not net fat gained.  A well designed, well run system.  The blue balloon above depicts the normal situation where it is relatively easy to both put sugar into storage and take it out as well.

But what happens if the balloon is overinflated?  What if the liver, which stores some fat, is crammed full of fat already?  Insulin is trying to cram more fat into a liver that is already completely full of fat.  Just as it is more difficult to inflate an overinflated balloon, insulin has a harder time of trying to shove food energy into the liver.  It takes higher and higher levels of insulin to move the same amount of sugar into the fatty liver.  Another word for this phenomenon is insulin resistance.  The body is now resistant to the efforts of insulin.  Normal levels of insulin will not be able to push sugar into the liver.

The other problem with the over crammed liver is that it takes high levels of insulin all the time to keep the sugar and fat bottled up.  If insulin levels start to drop, then sugar comes whooshing out, just like the overinflated balloon.  This leads to high levels of blood sugar, which the body doesn’t like and will try to oppose with higher insulin levels.  In other words, insulin resistance leads to higher insulin levels.  High insulin level will encourage storage of sugar and fat into the liver.  This causes even more over cramming of fat in the fatty liver causing more insulin resistance.  A classic vicious cycle.

This is true only at the liver.  Skeletal muscle will have normal levels of insulin sensitivity as will the brain (hypothalamus).  Fructose differs significantly from glucose because fructose is 100% metabolized in the liver. It is the difference between pressing down with a hammer and pressing down with a needle point.  You do not need as much pressure if it is all directed onto a single point.  Fructose is all directed at the liver.

Fructose causes fatty liver.  Fatty liver causes insulin resistance.  Why should we care?  Because insulin resistance leads to higher insulin levels.  Higher insulin levels drives obesity.

Continue here with Fructose causes Insulin Resistance – Hormonal Obesity XXXII
Start here with Calories 1 – How Do We Gain Weight?
See the entire lecture – The Aetiology of Obesity 4/6 – The Fast Solution

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By The Fasting Method

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