Fructose (also levulose or laevulose) is a simple reducing sugar (monosaccharide) found in many foods and is one of the three important dietary monosaccharides along with glucose and galactose.

Honey, tree fruits, berries, melons, and some root vegetables, such as beets, sweet potatoes, parsnips, and onions, contain fructose, usually in combination with glucose in the form of sucrose. Fructose is also derived from the digestion of granulated table sugar (sucrose), a disaccharide consisting of glucose and fructose, and high fructose corn syrup (HFCS).

Crystalline fructose and high fructose corn syrup are often mistakenly confused as the same product. The former is simply pure (100%) fructose. The latter is composed of nearly equal amounts of fructose and glucose.

Nutrition and Health

We have one primary appetite-control centre in our brain called the hypothalamus. It reacts to four major appetite hormones. Three of them (insulin, leptin and CCK) tell us when we have had enough to eat and one of them (ghrelin) temporarily inhibits the effect of the other three and tells us that we need to eat. Every piece of food we consume will stimulate the release of one or more of the ‘enough to eat’ hormones once we have had enough to eat.

Fructose will not stimulate the release of any of the ‘enough to eat’ hormones. Fructose skips the fat-creation control mechanism in the liver (PFK-1) and is directly converted to fatty acids (and then body fat) without passing through either of our major appetite control gateways (insulin or CCK). Fructose is also invisible to our built-in calorie counter (the hypothalamus).

We can eat as much fructose as we can shove down our throats and never feel full for long. Every gram of the fructose we eat will be directly converted to fat. There is no mystery to the obesity epidemic when you know those simple facts. It is impossible not to get fat on a diet infused with fructose.

In 1870, the only way anyone could eat any significant amount of fructose was either to be the king of England (or a close relative), or to come into the small fortune required to buy sugar (50% fructose) or honey (40% fructose). Alternatively, you could buy a lot of fruit and juice it yourself. Whichever way you cut it, money was required.
There was no cheap or easy way to eat fructose in any kind of quantity. But 130 years later, the average American was eating 33kg of fructose every single year just from sugar, HFCS and fruit juices. And that was before you started counting consumption from honey and syrups (together a further kilo per annum).

Statistics on Australian fructose consumption are harder to come across. We don’t have an equivalent of the US Department of Agriculture fastidiously compiling ‘food disappearance data’. But from the data we do have, our consumption is significantly lower than in the US.

In 1999, every person in Australia ate just under 38kg of sugar. This lower amount seems mostly to be related to the fact that we drink only half as much carbonated soft drink as our American friends. But we are catching up fast. Soft-drink consumption increased by 30 per cent in the 90s alone.

Add the fructose from the sugar (19kg) to the 3.5kg we were getting from juices, and it means Australians were consuming about 22.5kg of fructose by the turn of the 21st century. It’s not as bad as the 33kg the Americans were guzzling, but it’s still an awful lot more than the less than zero kilos of added fructose we were eating 130 years before that.

Some diseases are directly related to increased body mass, such as osteoarthritis and fractures (due to increased pressure on joints and bones), hernia and sleep apnoea (the treatment for which is becoming a huge industry), but these are relatively insignificant when compared with the mass murderers of modern society.

The biggest killer in Australia today is cardiovascular disease (CVD). In Australia, 48,000 people will die from a CVD this year, over 30 times as many as will die in a car accident and over 300 times as many as will die from AIDS. MI was almost nonexistent as a cause of death in 1900 and caused no more than 3000 deaths per year by 1930 (in the US). Dr Paul Dudley White, who introduced the electrocardiograph machine to America, said during a 1956 American Heart Association televised fund-raiser: ‘I began my practice as a cardiologist in 1921 and I never saw an MI patient until 1928.’ By 1960, there were at least half a million MI deaths per year in the US.

The prevalence of type II diabetes is now increasing so rapidly that the Centers for Disease Control have characterised it as an epidemic. The International Diabetes Federation estimated that in 2003 about 194 million people worldwide, or 5.1 per cent of the adult population, had diabetes, and that this will almost double to 333 million by 2025.

The number of people with confirmed insulin resistance was estimated at 314 million in 2003 and is expected to increase to 472 million by 2025. In less than two decades, almost one billion people worldwide will be affected by a potentially life-threatening disease that was virtually unheard of less than 30 years ago. What’s worse is that these figures are likely to be underestimates (they have already been revised upwards by 11 per cent since the predictions were first made in 2001).

Pulling all of this together, we have a universal theory for what has been observed in a multitude of studies in the last three decades. Fructose increases circulating fatty acids, particularly LDL cholesterol. Increased fatty acids lead directly to heart disease and stroke. Increased fatty acid levels also reduce the effectiveness of insulin in clearing the blood of glucose. Increased blood glucose leads to type II diabetes and feeds cancer.

Fructose Intolerance

Some people are afflicted with an intolerance to fructose. There are two types of intolerance: Hereditary Fructose Intolerance and the much more common Fructose Malabsorption.

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