Previously in this series: Intro, Part I, and Part II.

 Oprah 2005/2009

To test whether turning [fat people] into thin people actually improves their health, or is instead the equivalent of giving bald men hair implants, it would be necessary to take a statistically significant group of fat people, make them thin, and then keep them thin for long enough to see whether or not their overall health then mirrored that of people who were physiologically inclined to be thin. No one has ever successfully conducted such a study, for a very simple reason: No one knows how to turn fat people into thin people.
—Paul Campos, The Obesity Myth (2004)

Diets do cause weight loss…in the short term

People who think calorie restriction dieting “works” haven’t necessarily been duped by the diet industry or seduced by the prevailing nutritional “common sense” that weight loss and gain are a simple matter of calories in vs. calories out. Many of them believe it because their personal experience seems to confirm it, often repeatedly. Of course, “repeatedly” is part of the problem. Weight cycling—losing and re-gaining 5% or more of one’s total body weight—isn’t what dieters or public health policy makers are shooting for. Even people dieting with a specific occasion in mind, like a wedding or a high school reunion, would generally prefer to achieve permanent weight-loss.

But almost a century of research has shown that dieting—which usually involves calorie restriction—is not the way to do that. Studies repeatedly find that while eating less causes weight-loss in the short term, a majority of participants in weight-loss interventions focused on diet gain most of the weight back within 1 year and the vast majority (90-95%) gain all of it back within 3-5 years. Approximately 30% gain back more than they initially lost, and there’s some evidence that people who’ve lost and regained weight have more health problems than people who weigh the same, but have never lost and regained a significant amount of weight.

This is not controversial. Virtually every study of weight-loss dieting that has followed participants for longer than 6 months has found that the majority of dieters regain all the weight they lose initially, if not more. In other words, Oprah’s high-profile weight fluctuations are not the unfortunate exception to most dieters’ experience, they are the rule. A gallery of pictures of Oprah through the years illustrates the most frequent and reliable outcome of dieting:

             1985                           1988                             1992                             1996

              2001                            2005                          2008                            2010        

I am not concerned (in this entry) with why calorie restriction diets fail—there are competing theories and perhaps I’ll try to tackle them some other time. However, when it comes to evaluating public health policies aimed at the general population, like posting calorie counts on menus, it doesn’t really matter why the kind of behavior it’s designed to encourage fails, especially when it fails so spectacularly. Whether the problem is that 90-95% of people don’t have the willpower to stick to calorie-restricted diets or that most peoples’ metabolic rates eventually adjust or both or something else entirely, continuing to prescribe calorie restriction to individuals seeking to lose weight is futile at best. Given the health problems associated with weight cycling and psychological distress caused by diet “failure,” it’s probably also dangerous and cruel. More on that another day, too.

The goal of this entry is to provide a condensed-but-comprehensive overview of the evidence that convinced me that weight-loss dieting—and particularly calorie-restriction dieting or eating less—does not “work” for most people. By “work” I mean lead to significant weight loss—at least 10% of starting body weight—that lasts for more than 3 years (in keeping with the clinical definition of “weight loss success” proposed by the 1998 National Heart, Lung, and Blood Institute [NHLBI] Obesity Education Initiative Expert Panel proposed). I honestly tried to keep this as short as possible and bolded the “highlights” if you want to skim. However, if brevity is what you’re looking for, see this 2007 Slate article. Read more

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. 

That’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).

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

Although many states already tax soda (usually a fraction of a penny per ounce), a recent article in the New England Journal of Medicine on the potential benefits of a $0.01 per ounce tax on "soft drinks, energy drinks, sports beverages, and many juices and ice teas" has re-ignited the debate about whether or not we need a national soda tax. Back in July, Obama said a sin tax on soda was "an idea we should be exploring" in an interview with Men's Health although in the recent panic about industry profits and personal liberties, the White House has been quick to note that they haven't yet and have no plans to propose anything like it. 

Most people probably already know how the two sides shake out: promoters argue that soda makes people fat (which allegedly makes people sick and thus incurs social costs) so the tax would have the dual benefit of reducing the costs associated with obesity and generating money that would help cover health care costs (or balance state budgets). Opponents argue that soda isn't morally distinct from many other elective behaviors that sometimes (but not always) contribute to disease and health care costs, and as soda consumption is inversely correlated with income, taxing it would disproportionately burden those least able to pay.

All of those are actually pretty complicated claims, some of which I'll try to unpack below the jump but here's the short version: even promoters admit that the tax isn't likely to meaningfully reduce obesity or the diseases associated with it (note: not caused by it, as there's still no reliable evidence that fatness causes any disease besides osteoarthritis, and anyone who wants to hear more about that should consult Paul Campos' The Obesity Myth, J. Eric Oliver's Fat Politics, Glen Gaesser's Big Fat Lies, and/or Michael Gard and Jan Wright's The Obesity Epidemic). That means the only real argument in favor of the tax is that it would raise money. But everyone agrees that it would be a regressive tax. So unless you think that collective costs like state budget deficits and health care reform should be disproportionately shouldered by the poorest citizens, there is no good reason to support the soda tax (and this goes double for ill-considered suggestions that we just axe corn subsidies instead—also after the jump). Read more