In
this study [paywall], rats with free access to high fructose corn syrup gained more weight, more fat, and had higher blood triglycerides than rats that had access to sugar instead.
That was true even when the hfcs + rat chow diet and the sugar + rat chow diet had the same number of calories. (The rats were allowed to eat as much as they want, and the researchers measured.)
Here is a press release (via @
tekniklr) explaining what they did.
It seems this definitively answers the question: HFCS is worse for you than sugar. (Wait, didn't we definitively answer that question
last year?)
What I like even better: it shows that how much weight you gain (assuming you, of course, are a
Sprague-Dawley rat) isn't a simple "calories in, calories out" equation - no matter how often people
say it is.
Just so we're all on the same page about "high fructose" - sucrose (table sugar) is 50% fructose, 50% glucose, bound together in pairs. HFCS comes in 55% fructose and 42% fructose versions. This study used the 55% version.
Similarly interesting, to me: "We have previously shown that rats are able to adjust for the excess calories obtained when consuming 10% sucrose by taking in fewer calories of chow and thereby maintaining a normal body weight" - remember that when you hear
"don't drink your calories" type advice. Your body adjusts. (at least, if you are a rat.)
So, why does HFCS make rats fat when sucrose doesn't? The researchers' guess is that fructose raises triglyceride levels in the blood, which in turn signals the body to store more fat. The elevated TG has also been associated with higher fat intake - so that eating fructose may make you want more fatty food.
Here's what they say about fructose, more generally:
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, 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 (Vilsboll et al., 2003), fructose does this less efficiently, because cells in the pancreas lack the fructose transporter (Curry, 1989; Sato et al., 1996). Typically, insulin released by dietary sucrose inhibits eating and increases leptin gain, and the insulin 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.
The Princeton press release says the researchers next want to study the effects of high fructose corn syrup alongside a fatty diet - "the equivalent of a typical fast-food meal containing a hamburger, fries and soda" ... I can't help thinking, didn't a guy
already do that?
Anyhow, check out
the press release. It's a good explanation of the study.
Ha! Wrong! (Sort of.)
About Beth
I am a freelance writer, based in Pittsburgh, PA, specializing in science and technical topics. Yes, I am available for new writing projects! 
