fat

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 I

Dec 14 2009

I know this is misleading because lard is mostly unsaturated, but it's been one of the major icons of "bad" fat and also, how graet is this image? from http://www.npnworldwide.com/lard

This is probably going to be an even harder sell than MSG, but I swear I'm not just trying to be contrary. It's true that all the major sources of public health and nutrition advice, including the Harvard School of Public Health, Mayo Clinic, CDC, and American Heart Association continue to refer to saturated fats as "bad fats" and suggest that people avoid them as much as possible, limit them to <7-8% of their total caloric intake, and replace them with "good," i.e. unsaturated fats, whenever possible. It's also true that there are a few studies that suggest that increased saturated fat consumption is correlated (albeit weakly) with cardiovascular disease (CVD).

However, many other studies have found no increase in CVD associated with saturated fat consumption. And several recent review articles have concluded that the evidence for a connection between saturated fat consumption and CVD is inconsistent, insufficient or nonexistent.

There are basically three things that have convinced me that saturated fat isn't independently responsible for heart disease or death:

1) groups of people who eat vastly more saturated fat than most Americans frequently have lower rates of CVD—or no apparent CVD at all

2) the study that first inspired many people to think saturated fat was a bad thing had a lot of obvious flaws and has been thoroughly discredited

3) there's no good evidence that the proposed mechanism actually works—briefly: saturated fat supposedly causes heart disease by raising serum cholesterol levels because cholesterol is what clogs arteries and causes heart attacks and strokes, but serum cholesterol turns out to be a really poor predictor of CVD 

1) The French (and Polynesian and Melanesian and Masai and Fulani and Sri Lankan) Paradox 

photo by Arun Ganesh http://en.wikipedia.org/wiki/User:PlaneMadThe most confounding phenomenon for the theory that saturated fat consumption causes heart disease (sometimes called the lipid hypothesis or lipid-heart hypothesis or diet-heart hypothesis) is the virtual non-existence of CVD in multiple populations that eat way more saturated fat than most Americans. This has primarily been documented in the Pacific islands where coconuts, which are very high in saturated fat, are a staple food. For example, before the 1970s, the inhabitants of the island Tokelau got an estimated 55% of their calories from saturated fat, but heart disease was virtually unknown (according to Gary Taubes and Stephen Guyenet; notably, since their diet has shifted to include less saturated fat but more sugars and refined carbohydrates, many health indicators have worsened). Read more