Monday, March 19, 2007

Sweet Nothings from Fat Land

Warning: this will be a long post!

I’m currently reading Fat Land by Greg Critser, and while it’s a less-intriguing read than The Omnivore’s Dilemma, this weekend I came across one of the clearest explanations I’ve seen of the impact of the pervasive (since the 1980s, especially) presence of High Fructose Corn Syrup (HFCS) in American foods. Since farm subsidies for corn in the ‘70s made corn cheap and plentiful, and HFCS could be had much cheaper than real sugar, or sucrose, more and more manufacturers began using it.

Critser summarizes the effect:

“For years, food technologists and academics alike knew that, in addition to its properties of sweetness and stability (which made it so useful to convenience food makers) there was something else unique about fructose. Unlike its cousin sucrose, fructose is selectively ‘shunted’ toward the liver; it does not go through some of the critical intermediary breakdown steps that sucrose does. This was interesting, but for years no one knew exactly what it meant. Eventually, cell biologists figured out that fructose was being used in the liver as a building block of triglycerides. This it did by mimicking insulin’s ability to cause the liver to release fatty acids into the bloodstream (as demonstrated by Zammit in Scotland). Bombarded by fatty acids, muscle tissue develops insulin resistance. Whether humans consume enough high fructose corn syrup to activate the effect was something that eluded scientists until the year 2000, when researchers at the University of Toronto in Canada fed a high-fructose diet to Syrian golden hamsters, which have a fat metabolism remarkably similar to that of humans. In weeks, the hamsters developed high triglyceride levels and insulin resistance.”

“Preliminary human studies also indict concentrated fructose. Two years ago, the clinical nutritionist John Bantle at the University of Minnesota at Minneapolis fed two dozen healthy volunteers a diet that derived 17 percent of total calories from fructose—the percentage that Bantle believes about 27 million Americans eat regularly (particularly all of those fast-food “heavy users” and drinkers of 32-ounce Cokes). Bantle then measured the volunteers’ blood fats and sugars, and then switched them to a diet sweetened mainly with sucrose. The results were dramatic. The fructose diet produced significantly higher triglycerides in the blood—in men about 32 percent higher—than the sucrose-sweetened diet. The fructose diets also made triglyceride levels peak faster—just after the meal, when such fats can do the most conservative American Journal of Clinical Nutrition published one article that bluntly (and uncharacteristically) concluded that ‘these deleterious changes [by dietary fructose] occur in the absence of any beneficial effect…and these abnormalities…appear to be greater in those individuals already at an increased risk for coronary artery disease.’ ”

“The fructose trouble hardly ends there. Fructose consumption—it now constitutes 9 percent of the average individual’s daily energy intake (and up to 20 percent of the average child’s diet)—has lately prompted science to look at another, more controversial, theory—that fructose consumption itself may have led to increased rates of obesity, not merely through increased calories but through a variety of complex chemical reactions it stimulates in the human body.”

The book goes on to cite a number of studies conducted more recently that show a direct correlation between the rise in HFCS consumption and the rise in average BMI, however flawed that indicator of fitness might be. It also notes that public health workers and nutritionists have been “reluctant’ (understatement!) to single out HFCS since “most of their careers had been made in demonizing dietary fat.”

Now, all of a sudden, the cost of corn—and, as a result, HFCS—has increased dramatically leading Coca-Cola to consider returning to the use of real sugar in their soft drinks instead of HFCS. Could it be the beginning of a shift away from HFCS, and could a return to sucrose as the primary sweetener help tip the scales back in the other direction—figuratively if not literally? Only time will tell, but that’s probably wishful thinking on my part. I really don’t believe I’ll ever be able to actually “have my sugar-sweetened cake and eat it too.”

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