things that won't kill you

HFCS Follow-up: What the Rats at Princeton Can and Can’t Tell Us

Mar 29 2010

Ed called my attention to last week’s press release about the study at Princeton currently getting some mass media attention. The press release claims:

Rats with access to high-fructose corn syrup gained significantly more weight than those with access to table sugar, even when their overall caloric intake was the same. 

i know it's a squirrel, not a rat. apparently no one's gotten a rat to do this and then circulated it with the right keywords to match my google search. this image likely not original to: http://ybfat101.com/notyourfault.shtmlThat’s pretty surprising, given that other studies have suggested that there is no difference between HFCS and sucrose. The Princeton study doesn’t offer a definitive explanation for the difference they found, but they suggest that it may have something to do with the slightly greater proportion of fructose in the HFCS.

As I noted in the first post on high-fructose corn syrup, HFCS-55, which is the kind used in soft drinks and the Princeton study, has roughly the same proportions of fructose and glucose as table sugar. Table sugar, or sucrose, is composed of fructose bonded to glucose so it’s a perfect 50-50 split. HFCS-55 contains 55% fructose, 42% glucose, and 3% larger sugar molecules. There’s a lot of evidence that fructose is metabolized differently than glucose, and may promote the accumulation of fat, especially in the liver and abdomen. Indeed, that’s why I believe that agave nectar is probably nutritionally worse than table sugar. Still, I’d be pretty shocked if a 5% increase in fructose could produce a statistically significant difference in weight gain, unless the rats were eating nothing but sugar-water. And they weren’t—in both of the experiments reported in the original study, the rats had access to unlimited “standard rat chow,”

Experiment 1: Rats Who Binge?

In the first experiment, 40 male rats were divided into four groups of ten. All of them had 24-hour access to rat chow and water. Group 1 was the control, so they just had chow and water. Group 2 had 24-access to an 8% solution of HFCS (.24 kcal/mL), which the press release claims is “half as concentrated as most sodas”. Group 3 had 12-hr access to the same HFCS solution. And Group 4 had 12-hr access to a 10% solution of sugar dissolved in water (.4 kcal/mL), which the press release claims is “the same as is found in some commercial soft drinks.” The two things of note so far are that none of the rats had 24-hr access to sucrose-sweetened water, and that the concentration of the sucrose was nearly 2x that of the HFCS syrup.*

Why the 24 hr vs 12 hr groups? According to the study:

We selected these schedules to allow comparison of intermittent and continuous access, as our previous publications show limited (12 h) access to sucrose precipitates binge-eating behavior (Avena et al., 2006).

In other words, they fed the sucrose group on a schedule that they already knew would cause binging. And they didn’t include a 24-hr sucrose group to control for that.

That helps to explain the results: the rats that had 24-hr access to HFCS-water gained less weight than either the rats who had 12-hr access to sucrose-water or the rats that had 12-hr access to HFCS-water. So according to the experiment, it’s better to consume some HFCS than it is to binge on sugar (not, obviously, how they chose to frame it in either the formal write-up or the press release).

Princeton rats

The only difference between the four groups in the first experiment that was statistically significant at a p<0.05 was between the rats who got chow only and the rats who got 12-hr HFCS. There was no statistically significant difference between the rats who had 12-hr access to sucrose-water and the rats who had 12-hr access to HFCS-water. There wasn’t even a significant difference between the rats who had 24-hr access to HFCS-water and the chow-only rats. So the only basis for the claim in the press release that HFCS is worse than sucrose is the fact that the rats with 12-hr HFCS got a “significant” amount fatter while the 12-hr sucrose rats didn’t. Even though the 24-hr HFCS rats didn’t either.

I am not the only one who’s picked up on this—both Marion Nestle (a vocal critic of the food industry) and Karen Kaplan (not, as far as I can tell, a shill for the Corn Refiners Association) also dispute the claim that this research demonstrates anything conclusive about HFCS vs. sucrose. The lead researcher replied to Nestle’s post, and rather than addressing the discrepancy between the 12-hr and 24-hr HFCS groups, he merely corrects her assumption that the 24-hr rats should be fatter:

There have been several studies showing that when rats are offered a palatable food on a limited basis, they consume as much or more of it than rats offered the same diet ad libitum, and in some cases this can produce an increase in body weight. So, it is incorrect to expect that just because the rats have a food available ad libitum, they should gain more weight than rats with food available on a limited basis. –Bart Hoebel

Which just makes it all the more baffling why they didn’t include a 24-hr sucrose group. Additionally, according to their results, binging or “consuming more” doesn’t explain the results, because:

There was no overall difference in total caloric intake (sugar plus chow) among the sucrose group and two HFCS groups. Further, no difference was found in HFCS intake and total overall caloric intake in the groups given 12-h access versus 24-h access. Both groups consumed the same amount of HFCS on average (21.3±2.0 kcal HFCS in 12-h versus 20.1±1.6 kcal HFCS in 24 h), even though only the 12-h group showed a significant difference in body weight when compared with the control groups.

The only explanation they offer for these results is the slight difference in the amount of fructose the rats in the HFCS and sucrose groups consumed. But even that relies on the idea that the HFCS rats did not feel as satisfied by their sugar water and compensated by eating more:

…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.

Unless satisfaction itself makes rats thinner. Read more

Things That Won't Kill You Volume 4: Saturated Fat Part II: Cholesterol Myths

Feb 5 2010

image In retrospect, this probably could have been an entirely separate article in the "things that won't kill you" series, as many people still believe that dietary cholesterol (i.e. cholesterol in food) is a bad thing. For example, the article that image was taken from claims:

If you get too much dietary cholesterol (over 300mg a day) the extra cholesterol will accumulate in the walls of the blood vessels, making your LDL (bad) blood cholesterol levels rise. Over time, your arteries will become narrower, which can cut off the blood supply to your heart (causing a heart attack), or your brain (causing a stroke).

However, that's pretty easily dismissed—even Ancel Keys, "Monsieur Cholesterol" himself, never argued that dietary cholesterol was related to serum cholesterol or heart disease. In a 1952 article in Circulation, the journal of the American Heart Association, Keys noted that although rabbits and chickens that eat high-cholesterol diets will develop high cholesterol and atherosclerosis, or hardening of the arteries:

No animal species close to man in metabolic habitus has been shown to be susceptible to the induction of atherosclerosis by cholesterol feeding…. Moreover, even in the favorite species for such  experimentation, the herbivorous rabbit, the necessary concentration of cholesterol in the diet is fantastically high in comparison with actual human diets. Moreover, there is reason to believe that man has a greater power of cholesterol regulation than does the rabbit or the chicken. From the animal experiments alone the most reasonable conclusion would be that the cholesterol content of human diets is unimportant in human atherosclerosis.

Two "moreovers" in one paragraph, people! “Most reasonable conclusion”! Moreover, five decades of subsequent research haven't given anyone any reason to think differently. In 1997, Keys was even more direct:

There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter unless you happen to be a chicken or a rabbit.

Research done in the interim on the relationship between diet and heart disease in humans like the Framingham and Tecumseh studies showed no relationship between cholesterol consumption and blood cholesterol or heart disease. I'm not even going to modify this with "probably" or "as far as we know": There is no reason to believe that how much cholesterol you eat has any effect on your health.

But that doesn’t stop the AHA from recommending that “most people…limit cholesterol intake to less than 300 mg per day” and claiming that “an egg can fit within heart-healthy guidelines for those people only if cholesterol from other sources — such as meats, poultry and dairy products — is limited.” Despite repeated studies showing that egg consumption is not associated with higher serum cholesterol, myocardial infarction, cardiovascular disease, or all-cause mortality.Read more