Fat forms faster with fructose, study shows

TORONTO (Reuters) - High fructose corn syrup has been blamed for North America’s obesity crisis - unfairly, the Corn Refiners Association is charging in a new public relations campaign. But where does the science on the popular sweetener, and the fructose it contains, really stand?

The prevalence of high fructose corn syrup (HFCS) in processed foods is scorned by critics, who blame the sweetener and preservative for obesity rates that have been rising for about twenty years, and the poor health that can result. Now the Corn Refiners Association has jumped into the fray with commercial and print ads that compare the biochemical similarity of HFCS to sucrose and tout its all-natural status.

The truth about fructose and HFCS lies somewhere in the middle, said Dr. Elizabeth Parks, a physiologist and associate professor at the Center for Human Nutrition at the University of Texas’ Southwestern Medical Center in Dallas. Furthermore, there are still a lot of gaps in the science involving how our body uses fructose, Parks said.

High fructose corn syrup is produced by processing corn starch to change its sugars from glucose to fructose. The sweetener became a popular replacement for table sugar (sucrose) in the 1980s when pricing controls and quotas made it expensive to import sugar into the U.S.

Coca-Cola and Pepsi switched from sucrose to HFCS in 1984, and many other foods have since followed. Today, HFCS can be found in everything from cookies to salad dressing to breakfast cereal. By 2005, the average American was consuming 62.6 pounds of HFCS each year, compared to 58.8 pounds of sugar. Corn subsidies keep the price of HFCS low, and it’s easy to blend and ship because it’s a liquid.

There is some debate about how the body uses fructose and whether it differs from the way other sugars are processed. “I’m not confused,” Parks said about how fructose works in the body. “I just don’t know. The public is confused because scientists don’t know.” Science moves slowly, she pointed out, and nutritional science is still evolving. The breakdown of food and use of its components is a complicated process that is different in animals and humans, she said, and can also vary from person to person.

A new study from the University of Texas has filled in part of the puzzle, however. Parks and her researchers showed that our bodies turn fructose into fat more readily than glucose. The body will either burn glucose or store it as fat, and it has natural controls that regulate that process, she said.

“We do make some fat off glucose, but we can control the level that we do because we have that internal messenger system.”

Parks’ study involved 18 total tests performed on six participants, who were lean, healthy and in their late 20s. The study participants drank one of three sugary drinks in the morning: 100% glucose, 50% glucose and 50% fructose, or 25% glucose and 75% fructose. A few hours later, they ate a lunch, including a sandwich and chips.

Within four hours of consuming the drinks, the researchers found that fat formation (lipogenesis) had increased by about 40% in the participants who had either of the drinks with fructose compared to those who had the glucose drink. And when those who drank only glucose had a meal that contained fructose, among other sugars and food chemicals, their lipogenesis also went up.

But fat synthesis with fructose happens more quickly, Parks found, even in meals that also contain glucose. If the metabolic pathway gets flooded with fructose, the body’s messenger will slow the processing pathway down - but fructose enters that pathway later than glucose does, and therefore its movement into fat synthesis is uncontrolled.

“Fat synthesis was faster and greater when people ate fructose,” Parks explained, “and it’s because our biology doesn’t have a good way to slow processing of fructose away from fat synthesis.” There must be a reason for that, she said - something in our evolution that required that we be able to process a lot of fructose very quickly - but exactly what that is remains unclear.

Other research has implicated fructose and HFCS as one factor behind rising obesity rates in North America. A study done at the University of Florida in 2005 found that levels of uric acid, which blocks the action of insulin, the hormone that regulates blood sugar, in the bloodstream rose after fructose consumption.

But Parks points out that a problem as complex as obesity can’t be boiled down to the presence of one ingredient in our diets. “If we only focus on one food or one ingredient being bad for us,” she said, “we’re missing a huge aspect of the obesity epidemic.”

There are many other factors to consider and questions to answer, she said. Because fructose is sweeter than glucose, maybe we end up eating less sugar overall. Further research could indicate whether the metabolic response to fructose is the same or different in people who are overweight or obese. And a message like “stop drinking soda to lose weight” is often appealing simply because it’s easy to follow, she said, not because it’s the most effective way for all people to drop a few pounds.

Parks gives the example of swimming gold medalist Michael Phelps, whose enormous diet filled with pizza and other high-calorie foods garnered a lot of attention during the recent Summer Olympics in Beijing. Despite a diet that contains foods we would think of as unhealthy, she said, Phelps is in excellent physical condition, because the amount he exercises makes up for it. Not everyone spends hours a day in a pool doing intense physical training, but Parks’ message is that though we now have evidence that fructose may turn into fat more easily than other carbs, we can gain a bit of wiggle room in our diets by being physically active.

“If you’re active enough,” she said, “you can be much more flexible about what you eat.”

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