Monday, March 22, 2010

New study on high-fructose corn syrup

A Princeton University research team is reporting that HFCS increases obesity in rats more than sucrose does. The research appeared in February in the Pharmacology, Biochemistry, and Behavior.

As always, no one study settles the argument on this type of debate. This study moves the needle five degrees toward showing that HFCS is metabolically different from equivalent amounts of table sugar.

The study appears in a refereed journal. It includes a strong research design, randomly assigning rats to a treatment (HFCS) group and two control groups.

[Update 3/23: part of the study includes two control groups, which received either plain sucrose or an ordinary rat food diet, so one can distinguish HFCS from sucrose; a comment says that another part of the study included only one control group, which received the rat food diet, so it is not possible to distinguish HFCS from sucrose].

On the other hand, studies in rats are just one element in an array of evidence. Other elements include human studies and describing a plausible biological mechanism. One mystery is how HFCS (55% fructose) could be much different from sucrose (50% fructuse). The conclusion section of the new article spends most of its time talking about the metabolism of fructose, mentioning but then somewhat breezing over the similarity in fructose content between HFCS and sucrose.
Given that sucrose is a disaccharide, which is metabolized to one fructose and one glucose molecule (Caspary, 1992), it has been argued that there is little difference between fructose and sucrose, since both provide about 50% fructose and 50% glucose in the blood stream; and until recently, there was no evidence that HFCS contributes to long-term weight gain beyond what sucrose contributes (Forshee et al., 2007). However, the present study suggests that HFCS and sucrose can have different effects on body weight and obesigenic measures.

HFCS is different than sucrose in many ways. First, HFCS-55 has proportionately slightly more fructose than sucrose (White, 2008). Second, fructose is absorbed further down the intestine than glucose, with much of the metabolism occurring in the liver, where it is converted to fructose-1-phsophate [sic], a precursor to the backbone of the triglyceride molecule (Havel, 2005). Third, fructose is metabolically broken down before it reaches the rate-limiting enzyme (phosphofructokinase), thereby supplying the body with an unregulated source of three-carbon molecules. These molecules are transformed into glycerol and fatty acids, which are eventually taken up by adipose tissue, leading to additional adiposity (Hallfrisch, 1990). And fourth, HFCS causes aberrant insulin functioning, in that it bypasses the insulin-driven satiety system (Curry, 1989). Whereas circulating glucose increases insulin release from the pancreas,... fructose does this less efficiently, because cells in the pancreas lack the fructose transporter.... Typically, insulin released by dietary sucrose inhibits eating and increases leptin release (Saad et al., 1998), which in turn further inhibits food intake. As previously discussed, meals of HFCS have been shown to reduce circulating insulin and leptin levels (Teff et al., 2004). Thus, fructose intake might not result in the degree of satiety that would normally ensue with a meal of glucose or sucrose, and this could contribute to increased body weight.
In each passage above where it seems the authors plan to talk about a mechanism that is specific to HFCS, the subsequent detail turns out to be all about fructose.

I enjoyed hearing a talk earlier this month by Barry Popkin (author of The World is Fat). Though he has also speculated about a possible distinct effect of HFCS, he now emphasizes just the sweetness and food energy content.

And this brings me to the final point that I wish news coverage of this topic emphasized more heavily. HFCS is a large part of our food supply, perhaps 40% or more of all caloric sweeteners. In these quantities, a special metabolic effect for HFCS is really beside the point for policy purposes. It could well be true that HFCS is making Americans obese in any case, just because we consume so much of it.

7 comments:

Audrae Erickson said...

Translating the study’s reported rat intakes to human proportions, the calories gained from high fructose corn syrup would be equivalent to about 3000 kcal/day all from that single source. In comparison, adult humans consume about 2,000 calories per day from all dietary sources. Such intake levels would be the equivalent of humans drinking a total of 20 cans of 12 ounce sodas per day - a highly unrealistic amount. Moreover, the researchers concluded that the rats gained more weight from high fructose corn syrup than they would have from sugar, yet they failed to provide sucrose controls for part of the study’s short-term experiments and no sucrose controls whatsoever were present in any of the long-term experiments.

No metabolic effects have been found in studies that compare sugar and high fructose corn syrup consumption in humans.

U.S. Department of Agriculture (USDA) data show that per capita consumption of sugar has always exceeded the per capita consumption of high fructose corn syrup. According to USDA estimates, annual per capita consumption of high fructose corn syrup for 2008 was 37.8 pounds. The 2008 sugar consumption estimate was over 9 pounds greater at 47.2 pounds per person.

For more information, please visit www.SweetSurprise.com.

Yoni Freedhoff said...

Parke, if only the nutritionism folks out there could read and take the time to digest your concluding paragraph.

Let's spend less time worrying about whether HCFS has a special contribution to obesity and start figuring out ways to reduce the world's caloric intake.

Aliza R. Wasserman said...

You know you're movin up in the world when your blog posts capture the attention of the HCFS lobby...

rui said...
This comment has been removed by a blog administrator.
Mark VII said...

This is so silly, trying to blame obesity on some magic or conspiratorial single cause. If in fact HFCS has any tendency to increase obesity, it's no more than 1 percent of the problem. Why focus on this?

Another point: If you get scientists focusing on something enough, they will find "proof" -- until the proof evaporates. Witness the early studies on vitamin C and colds, vitamin E and sex, and MSG. Ooops! They all turned out to be wrong. HFCS and trans fat and so on will eventually go the same way as other bogeymen, and the boring (and unfundable for research) causes will remain: huge servings, sedentary jobs, breakdown of regular meals, increasingly fat parents, and so on.

Anonymous said...

Audrae, Thank you so much for presenting an unbiased scientific analysis. Your point as well as the original authors' are very well made and appreciated.

Liz Pearsall said...

To Audrae Erickson,
Honestly, how much HFCS do you consume? How many soft drinks (by oz.) do you drink in a day? You are familiar with HFCS because you are with the CRA. Have you ever just given it up? Just give up anything that has HFCS, and experience how you feel? The children in schools get plenty of doses. What about you as a person--a fellow human being living on this earth? Honestly, let us know how much you consume and feed to your children. Thanks for the honest info.