Category Archives: obesity

Fatness Is Strongly Influenced By Genetics, But How?

An image from twin studies featured in the talk by Jeffrey Friedman posted after the jump, or click on the image for the YouTube link

A reader e-mailed me a good question about weight loss that’s outside my area of academic expertise but within the realm of stuff I’ve read enough about that I can offer some speculations and references. I am continually amazed at how complicated nutrition is and how much disagreement there is even among people who study it for a living. The only thing I can say with complete confidence is that anyone who tells you weight loss is simple and anyone can do it is (A) lying, (B) misinformed, (C) trying to sell you something, or (D) all of the above.

Here’s the e-mail I got:

If you have the time to answer a question…

I recently came across these articles claiming, more or less, that metabolism does not account for why some people are fatter or thinner than others. 

Article 1 [BBC Health]

Article 2 [Mayo Clinic]

I remember your posts on Sour Salty Bitter Sweet about dieting not being an effective solution to weight loss [here], and it sounded like you thought someone’s weight had more to do with genetic factors than lifestyle factors. Do I have that right? Would you disagree with the articles? Or point to non-metabolic genetic factors?

-Anna Macdonald

simple! right? that's why everyone is precisely the weight they want to be! Image Credit: CDC.govBoth articles essentially argue that it’s a myth that fatter people have “slow metabolisms” and burn fewer calories than thinner people. Basal metabolic rates vary based on age, gender, and body composition (or maybe just body composition, but that tends to vary based on age and gender), but as far as researchers can tell, fat people have at least roughly the same metabolic rate as thin people. They just eat more.

I think they neglect or dismiss a few complications too easily—in both diet studies and over-feeding studies, subjects lose/gain less weight than they should based on caloric arithmetic, usually by a significant margin. That’s usually attributed to shifts in thermogenesis, or how much heat you generate, and unconscious motions like fidgeting. If you eat more than you’re used to, your body may respond by getting slightly warmer and engaging in more restless activity. Eat less, and your body may respond by getting cooler and engaging in less activity. There’s some evidence that even for the very rare individuals who lose weight and keep it off long-term, basal metabolic rate remains depressed compared to people with the same relevant characteristics (weight, age, gender, and body composition) who were not previously fat (see NYTimes “The Fat Trap”). Incidentally, there’s research from as early as 1980 suggesting that people who maintain weight loss long-term are frequently monomaniacal about food and exercise, engaging in behaviors that might be seen as evidence of an eating disorder in thinner people.

But in general, the articles seem pretty accurate up to the point where they claim that people can lose weight if they eat fewer calories and exercise. The BBC article even claims that “people not only manage to lose weight but are able to keep control of it in the long term,” which is technically true—a small percentage of the people who lose weight by dieting do—but certainly isn’t the norm. Both articles make an unsubstantiated leap from the idea that basal metabolic rate is at least relatively stable and consistent to the idea that therefore, anyone can be thin if they only eat as many calories as a thin person burns. The key question they fail to address is why fat people eat more calories than thin people in the first place.

I suspect that’s because most people think they know the answer: they assume fat people have less willpower, knowledge, or motivation than thin people and therefore make bad choices about what and how much they eat. There’s a widespread assumption that if fat people knew better or tried harder, they could be thin. Many people, whatever their weight, believe that they themselves would be probably thinner if they ate better and exercised more and would be fatter if they ate whatever they wanted all the time and exercised less (which is actually probably true, but only within a small range). A lot of people even have personal experiences with weight loss or gain that they may be able to attribute to conscious choices or lifestyle changes. However, for most people, those changes prove to be temporary and I think they overestimate how much control they actually have.

Fat people are not fat because they’re weak or lazy or unmotivated or unaware of the supposedly-dire medical consequences and actually-dire social consequences of being fat. Body size is strongly genetically determined and biologically-regulated. It may be sensitive to some environmental conditions, but that doesn’t mean it’s within individuals’ conscious control. If the tendency towards weight homeostasis doesn’t work by regulating how many calories people tend to burn, which I agree that it probably doesn’t, it must work by influencing how much people eat.

How Heritable Is Fatness? 

Also from the Friedman lecture below.Very. Perhaps less than eye color, but more than other conditions widely seen as having a significant genetic component, like schizophrenia or alcoholism. Based on twin studies, one of the classic ways of evaluating the genetic component of all kinds of conditions, weight consistently appears to be approximately as heritable as height—most studies conclude that just under 80% of variation in weight and height is attributable to genetics. Furthermore, genetic influence consistently trumps environmental effects by a wide margin. In adoption studies, another way of evaluating genetic influence, children’s weights are strongly correlated with their biological parents’ and not at all with their adoptive parents. 

In Stunkard et al 1986, which compared approximately 4000 sets of male twins, the “concordance rates for different degrees of overweight were twice as high for monozygotic twins as for dizygotic twins.” In other words, the “identical” twins who share nearly 100% of their genetic material were twice as likely to have similar body types than “fraternal” twins who share only 50% of the same genes. At age 20, comparisons of height, weight, and BMI for both sets of twins yielded heritability estimates of .80, .78, and .77, respectively (1.0 would be perfectly heritable, .00 would be not heritable at all). At a 25-year follow-up, the heritability estimates for the same traits were .80, .81, and .84.

In another Stunkard et al 1986, which divided a sample of 540 adult Danish adoptees into four weight classes: thin, median, overweight and obese, there were strong correlations between the weight class of the adoptees and their biological parents (p<.0001 for mothers, p<.02 for fathers). There was no correlation between the weight class of the adoptees and their adoptive parents.

In Stunkard et al 1990, the researchers used a Swedish database of twins separated early in life versus those reared together collected between 1886 and 1958. They ended up with 93 pairs of identical twins reared apart, 154 pairs of identical twins reared together, 218 pairs of fraternal twins reared apart, and 208 pairs of fraternal twins reared together. The mean age of comparison was 58.6 years old. The heritability estimates (shown in the chart below) are similar to those in the 1986 study. Notably, twins reared together were no more similar than twins reared apart.

"The fourth estimate of heritability, the intrapair correlation for the monozygotic twins reared apart, was the most direct and perhaps the best estimate of the heritability of the body-mass index. It was 0.70 for men and 0.66 for women."

A review study done in 1997 by Maes et al looked at the data from 25,000 twin pairs and 50,000 biological and adoptive family members, finding BMI correlations of .74 for monozygotic twins, .32 for dizygotic twins, .25 for siblings, .19 for parent-offspring pairs, .06 for adoptive relatives, and .12 for spouses.

Researchers have also been curious to see if the “obesity epidemic” has changed anything. Have environmental changes in the last few decades trumped genetic factors? Not really. In Wardle et al 2008, they evaluated 5092 sets of twins between the ages of 8 and 11 whose body measurements were taken in 2005. The heritability estimate for BMI was .77. In comparison, the shared-environment effect in the same study was estimated at .10.

As a 2008 review study of research on the heritability of fatness by Stephen O’Rahilly and I. Sadaf Farooqi concluded:

Hereditary influences on adiposity [fatness] are profound and continuing…. There is little serious doubt that the single most powerful determinant of inter-individual differences in adiposity is heredity.

Okay, But How Does It Work? Part I: Epigenetics

Genetics isn’t the whole story. We have known for a long time that children without access to adequate nutrition may have their growth "stunted," meaning they may never achieve the same height or weight as adults as they would have if they had been able to eat more as children. Dietary composition also seems to have an effect: populations with access to more protein (or calcium?) may grow taller or fatter than genetically-similar populations who consume less protein. The availability of highly-palatable, calorie dense, high-sugar and high-fat food in countries like the U.S. may create the conditions for some people (though clearly not all) to become fatter than they would in another environment. However, how fat they get in that environment  is still determined largely by genetics, just like how tall people get in the presence of ample protein is still largely determined by genetics.

There’s a lot of research being done right now on what are sometimes called "epigenetic" effects, which are factors that influence whether or not (and how) genes get expressed, without any changes happening in the genome itself. This is the idea that genes can get turned “on” or “off.”  Some epigenetic effects are trans-generational, meaning something that affects a particular individual or population may only show up in their offspring. So, for example, population that experienced a famine may have offspring who are more inclined to store fat when it’s available than a genetically similar population that didn’t live through a famine.

See: This Nature article or Herrera et al 2011

Okay, But How Does It Work? Part II: Leptin

Leptin-deficient child before and after leptin therapyThe expression of genes that affect body size probably involves changes in the endocrine system, and particularly the release or suppression of the hormones leptin and gherlin, which control appetite and satiety. Leptin in particular seems to be crucial to the regulation of body fat. It was only discovered in the mid-1990s, so scientists are still trying to understand how it works and what the implications are.

Some extremely fat children, like the kid pictured on the right, have been found to be deficient in leptin. They have seemingly insatiable appetites—when presented with meals in excess of 2,000 calories, they’ll eat the whole thing and still be hungry. After receiving leptin injections, they eat age-appropriate portion sizes and lose weight rapidly without dieting or engaging in any formal exercise program.

One of the major differences between people who’ve lost weight through dieting and people who weigh the same without having dieted is in their leptin levels. Most of what I know about leptin (and most of images in this post) are taken by the following talk by the biologist who discovered the hormone, Dr. Jeffrey Friedman:

In the very beginning of the talk, he makes some causal claims about high BMI/adiposity and mortality that I disagree with, because I’m not sure the correlations are actually caused by fatness, rather than social stigma, racism, poverty, lack of health insurance, etc. (all of which are also correlated with BMI). If fatness caused mortality, why would “overweight” people live longer on average than “normal” weight and “underweight” people and “obese” people who are active live longer than “normal” people who are sedentary? He also says that even modest weight loss is associated with significant health improvements, and I wonder if that claim isn’t based on studies where participants begin eating more vegetables and exercising, lose something like 5 pounds, and get healthier overall and researchers conclude that weight loss improves health when really the weight loss is totally meaningless. But once you get past that bit, he makes a pretty strong case for the genetic basis of body size and the role of leptin in the regulation of body fat.

Okay, But How Does it Work? Part III: Endocrine Disruptors

Just to complicate things even further, it turns out that a lot of the chemicals we’re exposed to can affect the endocrine system. Bisphenol A, the now-vilified chemical used primarily in plastics and also in the lining of aluminum cans, turns out to be an endocrine disruptor. Fluoride is also an endocrine disruptor. So are brominated fire retardants and many pesticides (even organic-certified ones, like copper sulfate).

Some of these may only affect people if they’re exposed at a particular point in their development—in utero, pre-adolescence, etc.—or at a particular dosage. So if your mom ate a lot of highly-acidic canned foods while she was pregnant with you, that might affect your thyroid function from birth. Or if you spent a lot of time on a rug treated with flame retardant chemicals as an infant, that might affect you, but maybe if you’d been 5 or 6 years old, it wouldn’t. Those are just hypothetical scenarios, the actual effects and doses of endocrine disruptors are not yet well understood or documented. So I’m not saying you should stop getting fluoride treatments. I suspect (and hope) that in another decade or so, we’ll have a better sense of how chemical exposure affects weight gain.

For more on endocrine disruptors and obesity, see Julie Guthman, Weighing In especially Chapter 5.

When Metabolism Matters: The Evidence From Overfeeding

If body weight is genetic, it should probably be nearly as difficult to gain weight as it is to lose it. Although it does seem to be possible to gain weight deliberately—some athletes and actors do this—it takes a lot of work. The results of overfeeding studies suggest that people who deliberately eat more than they would normally have to suppress their desire to stop eating and lose any weight they gain very easily as soon as they stop “overeating.”

BBC made an hour-long documentary about one of these studies, called “Why Are Thin People Not Fat,” which I first saw posted on Tom Naughton’s blog FatHead:

If you don’t want to watch it (spoiler if you do): ten thin people were told to eat twice as much as they normally do (the target caloric intake for men was approximately 5000 kcal/day) and refrain from exercise for four weeks. There was a lot of variation in the results—some gained more weight than others, some gained more fat than others. One of the participants gained muscle. None of them gain as much weight as they “should” based on caloric arithmetic, meaning there must have been changes in their metabolism. Additionally, the subjects report feeling pretty miserable: the amount of food they have to eat makes them feel sick. At least one of them mentions throwing up some of what he ate. They all get tired of milkshakes and chocolate and pork pies. And month after the experiment was over, the participants had all lost most or all of the weight they gained during the experiment without engaging in any deliberate weight-loss strategies.

The documentary mentions another overfeeding study known as the Vermont Prison Experiment. Researchers at the University of Vermont led by Ethan Sims initially tried to use students as subjects. They were told to eat 2-3x their normal caloric intake, but even after 5 months, most had increased their weight by only 10-12%. Sims’ goal was 25%, so he turned to inmates at the Vermont State Prison, who he describes as “equally dedicated volunteers.” After 200 days of eating up to 9-10,000 kcal/day, some of the participants were still not able to gain 25% of their starting weight. For the few who were able to gain 25% or more, in order to maintain the goal weight for any length of time, they had to continue eating on average ten times the number of calories that should have been necessary based on simple caloric arithmetic. This is also explained by metabolic changes—whether through thermogenesis or unconscious activity, the men were burning vastly more calories than before despite being prevented from exercising. Again, after the study was over, the prisoners easily lost most or all of the weight they had gained.

In Conclusion

The genetic influence on weight seems to work primarily by affecting how much people eat, not how many calories they burn. Fat people burn more calories than thin people, but they also eat more than thin people. That doesn’t mean that fat people “overeat.” Most people, fat or thin, maintain a relatively stable weight over long periods of time. If fat people were eating more calories than they typically burn, presumably they would be constantly gaining weight. Appetite and satiety are governed by biology, not willpower. Most people seem to be capable of consciously and deliberately reducing or increasing their caloric intake temporarily, but that’s difficult and unpleasant and virtually impossible to maintain long-term.

Diet Soda Follow-up: Are Diet Sodas Better For You Than Regular Soda?

Artificial sweeteners definitely pre-dated the "obesity epidemic." Saccharin was being used commercially in the early 20th C. and diet sodas were widely available by the 1960s For more on the history of artificial sweeteners, see Carolyn de la Pena's brilliant book _Empty Pleasures_

Soda cans from the 1970s from Found in Mom’s Basement

In response to the recent entry about the association between diet soda and fatness, Jim asked:

Has anyone proved that drinking Diet Soda is better for you than drinking Regular Soda? Does Diet Soda have the same impact on the body as drinking say a glass of water? I haven’t done any research on it and I don’t know if any is out there. I’d really like to see a study of what happens to obese people who stop drinking diet soda and switch to regular.

There’s a ton of research on artificial sweeteners, but I can’t find any studies in which obese people who habitually consume artificially sweetened-drinks were made to switch to sugar-sweetened drinks. That might partially due to ethical/IRB concerns—it’s possible that asking people to consume more sugar than they were previously would be considered a significant health risk. On the other hand, there are studies in which subjects are randomly assigned to consume either artificial or caloric sweeteners, so maybe consuming regular soda falls into the realm of acceptable risk with informed consent.

In those kinds of studies, both “overweight” and “healthy”* individuals who consume regular sweeteners (usually sucrose or high-fructose corn syrup, which are nutritionally equivalent as far as we know) end up eating more calories overall than people who consume “diet,” artificially sweetened foods and drinks. The sugar/hfcs groups also gain weight and fat mass and have negative health indicators like increased blood pressure. I don’t think fatness is bad or that being thin is better, but based on the current available evidence, regular soda appears to be both more likely to make you fat and also worse for your health than diet soda.

*Stupid current labels for BMI categories that don’t correspond at all to actual health outcomes.(1)

A Closer Look at the Studies

This is apparently what Diet Coke looks like in Denmark. Or did in 2009. Pretty! In a 2002 study from Denmark, 41 “overweight” men and women between 21 and 50 years old were assigned to two groups, matched for sex, age, weight, height, BMI, fat mass, fat-free mass and usual amount of physical activity. One group was given sucrose-sweetened dietary supplements (2 g/kg of body weight daily; 70% from drinks and 30% from solid foods) and the other was given artificially-sweetened dietary supplements (an equivalent amount of food and drink by weight sweetened with a combination of aspartame, acesulfame, cyclamate, and saccharin, collectively and individually far below intake levels generally regarded as safe). All the supplements were commercially-available foods and included soft drinks, flavored fruit juices, yogurt, marmalade, and stewed fruits. The researchers note that “great efforts were made before the intervention to find the most palatable artificially sweetened food products on the market for which a matching sucrose-containing product existed.” As some of the artificially-sweetened foods were also fat-reduced, subjects in the sweetener group were given additional butter or corn oil every week.

The study lasted 10 weeks. In addition to the supplements, subjects were free to consume whatever they wanted and as much as they wanted. The subjects visited the lab weekly to pick up the supplements and have urine samples taken (which were used to validate their dietary records). Their height, weight, and fat mass were measured every two weeks. They also kept food diaries that included ratings of their  hunger, fullness, the palatability of the food they ate, and their sense of well-being over the course of each day in the week before the study began, the fifth week, and the tenth week.

Results: The sucrose group ate more calories overall than the sweetener group and got more of their calories from carbohydrates (58% compared to 44%). Both groups decreased how many carbohydrates they were eating in addition to the supplements, but the sugar in the supplements more than made up for the decrease in the sucrose group. The sucrose group gained an average of 3.5 pounds—which was, interestingly, only about half the weight gain that would have been predicted based on how many more calories they were eating. Their activity levels didn’t increase, so the most likely explanation is thermogenesis—i.e. their metabolism changed in response to the increased caloric intake. The group eating artificial sweeteners lost an average of two pounds. In the sucrose group, systolic and diastolic blood pressure increased; in the sweetener group, it decreased. There were no differences in appetite sensations, hunger, or satiety.

Similarly, in a 1990 study done at the Monnell Chemical Sense Center, a group of 30 subjects gained weight during a three-week period when they were given regular soda (sweetened with HFCS) and lost or maintained their weight during the two three-week periods when they were given diet soda (aspartame-sweetened) or no soda. In the regular and diet soda periods of the experiment, they were given 40 oz. of soda to drink every day. In the no soda period, they were told they could consume any beverages as they normally would. They also kept detailed dietary records for the duration of the experiment. The order of the 3-week periods was counterbalanced so some of them got regular soda first, some of them got the artificial stuff first, some of them had no soda for the first three weeks, etc. Here’s what the aggregate changes in their body weight looked like: 

Tordoff and Alleva 1990 in the American Journal of Clinical Nutrition 51: 963-9 (graph appears on 965)

During both the regular and diet soda weeks, they decreased their dietary sugar consumption by an average of 33% (i.e. aside from the sugar in the soda).

Studies like these also point to what I suspect is the more likely explanation why there’s never been a study like the one Jim describes: there’s just not much debate about whether consuming calorically-sweetened drinks leads to weight gain and possible health risks (which shouldn’t be conflated—weight gain is primarily an aesthetic issue, and high levels of sugar consumption may lead to negative health outcomes whether or not they make you fat). What is up for debate is whether artificial sweeteners are a good substitute and likely to promote weight loss or also bad and contributing somehow to weight gain. And if they’re contributing to weight gain, how and how much?

There appear to be three types of theories about why artificial sweeteners might cause weight gain and/or other undesirable outcomes.

Theory #1: Artificial sweeteners might have direct metabolic effects

I don't know what this has to do with anything, I just thought the entry needed more picturesIt’s possible that although they have no caloric value, artificial sweeteners could affect blood sugar or insulin in ways that cause the body to store fat. This is the theory being tested in the study described in the previous entry in which mice consuming aspartame in amounts comparable to an average-sized woman drinking 20 oz of aspartame-sweetened soda per day had higher fasting glucose levels than mice on the same diet minus the aspartame. The effect could be chemical, but seems more likely to be an effect of the sweet taste—i.e. the perception of sweetness might affect the hormones that govern appetite and metabolic rate.

Evidence for this is still extremely scant. Not only is it unclear whether or not the effect is reliable, biologically significant, or occurs in humans; it’s also unclear if it’s specific to aspartame or an effect of all artificial sweeteners, if it scales such that a small amount of aspartame causes a smaller increase in fasting glucose or only occurs at a certain critical level of aspartame consumption, if it only occurs after regular daily consumption over a long period of time or after a single dose, if it affects all people in the same way or only “overweight” people, if it interacts with other dietary conditions (i.e. does it only happen in conjunction with diets high in corn oil, like the ones the mice in the study were fed?), etc.

There are studies involving rats that suggest some kind of metabolic effect of artificial sweeteners might promote weight gain. Rats fed artificially-sweetened yogurt consume more calories than those fed sugar-sweetened yogurt.

However, it seems like it might not work the same in people—or at least that the effect might be smaller. Note that in both of the studies described above, subjects given artificial sweeteners decreased both their overall carbohydrate and dietary sugar intake. Additionally, in a 2001 study done at the Pennington Biomedical Research Center in Baton Rouge, 31 subjects (19 lean, 12 obese) were given sucrose (493 kcal), aspartame (290 kcal), or stevia-sweetened (290 kcal) "preloads" before lunch and dinner on three separate days. Their food intake, satiety (how full they felt), and postprandial (after-meal) glucose and insulin levels were measured. When they had the lower-calorie, artificially-sweetened preloads, they did not compensate by eating more at either the subsequent meals and reported similar levels of satiety as they did on the day they consumed the higher-calorie, sucrose preload.

Theory #2: Artificial sweeteners might have a psychological effect.

Another possibility is that drinking “diet” soda might make people believe that they can afford to eat more or nutritionally worse foods. This is similar to the “health halo” research being done by Brian Wansink and others, which has shown that people are more likely to underestimate the caloric content of foods they perceive as “healthy,” like a turkey sandwich from Subway, than they are with foods they perceive as unhealthy, like a Big Mac. They’re also more likely to order sides with the “healthy” choice that ultimately push the calorie content of the meals higher. Organic and “trans-fat free” labels or even just having calorie counts posted on a menu can have similar effects—triggering people’s dietary conscientiousness seems to cause many people to “treat” themselves to something extra.

However, it’s not clear that the “halo” affect actually influences total or long-term consumption. Thinking they’re getting the “healthier” sandwich may make people more likely to eat a bag of chips at that meal than they would have if they’d eaten a burger, but if that means they’re less likely to have an afternoon snack or they eat less at dinner, it might not affect their weight. I can’t find any studies that measure that.

Theory #3: Artificial sweeteners might change people’s palates

Artificial sweeteners might make people more accustomed to sweetness, which might cause them to eat more sweet things or sweeter things than they would otherwise. Since sweet things and the taste for them are seen as a kind of indulgence and not liking or eating sweet things is often constructed as proof of maturity, masculinity, or self-control, this is often described in morally judgmental terms like “infantilizing our taste sense” or “corrupting the palate.” But it’s not a theory entirely confined to blowhards. In an opinion piece in JAMA published in 2009, David S. Ludwig writes:

Individuals who habitually consume artificial sweeteners may find more satiating but less intensely sweet foods (eg, fruit) less appealing and unsweet foods (eg, vegetables, legumes) less palatable, reducing overall diet quality in ways that might contribute to excessive weight gain.

However, he admits that there’s no research showing this to be true. On the contrary, at least one study has found that people who consume artificial sweeteners regularly are more likely to eat foods generally considered to be healthy and less likely to consume foods generally considered to be fattening. According to a 2006 study done by the American Cancer Society as part of a larger project involving 1-2 million men and women who weigh 40% or more above average for their age and height, those who reported using artificial sweeteners also ate chicken, fish and vegetables significantly more often than non-users and consumed beef, butter, white bread, potatoes, ice cream and chocolate significantly less often. That study also found that artificial sweeteners were associated with weight gain. Given that their diets were apparently “healthier,” the authors conclude: “our weight change results are not explicable by differences in food consumption patterns,” perhaps implying that artificial sweetener might indeed be the culprit.

I think their data suggest something different entirely: people who drink diet soda are more likely to be dieters. They’re eating more of the stuff everyone tells them they ought to be eating to lose weight, and less of the stuff they’re supposed to avoid. It’s not working, and they’re getting fatter anyway, but that doesn’t mean diet soda makes you fat, it could simply mean that dieting doesn’t work.

Not Implausible, Just Not Supported By the Evidence

My suspicion is that if diet soda has any affect on weight, it’s a small one. I think it might be possible that in large amounts (probably 16 oz or more of diet soda per day), some artificial sweeteners might affect the metabolism slightly and lead to people being slightly fatter than they would be if they consumed less or no artificial sweeteners at all. However, I don’t think you’d see the results you see in studies like the ones from Denmark or the Monnell Chemical Sense Center if artificial sweeteners really have a dramatic, immediate effect on weight gain or fat storage.

Of course, that doesn’t mean artificial sweeteners are healthy, just that they probably don’t make you fat. Jury’s still out on the relationships between aspartame and cancer, sucralose (Splenda) and intestinal bacteria, saccharine and neurological function (especially in children), and stevia & its derivatives and DNA mutation. But for what it’s worth, most of the review articles I came across and Ludwig’s JAMA article claimed that concerns about cancer have basically been put to rest.

Of course, there’s still the problem of how they all taste

(1) Broken record footnote: Weight is a poor indicator of health. People in the BMI categories labeled “overweight” and “obese” people are often as healthy or healthier than people in the “healthy” or “normal” BMI category. People in the “overweight” category live longer on average than people in the “normal” or “healthy” category. People who are “overweight” or “obese” who engage in regular physical activity are healthier on basically every measure than sedentary “normal” or “healthy” weight people. The people who are really (statistically) screwed are the “underweight.”

Diet Soda…Probably Not the Cause of the “Obesity Epidemic”

IN SHOCKING REVERSAL, NATION’S SCIENTISTS DECLARE THAT CORRELATION DOES, IN FACT, PROVE CAUSATION!

A couple of studies on artificial sweeteners presented at the American Diabetic Association’s Scientific Sessions in San Diego last week are being hailed as new evidence that diet soda can make you fat. For example, under the headline “2 New Studies: Diet Soda Leads to Weight Gain,” the blog Fooducate declares:

Not only will diet soda NOT help you lose weight, it may actually cause weight gain and diabetes!

image

Study #1 tracked the waist circumference and diet soda consumption of 474 people between the ages of 65 and 74 over an average of 3.5 years. In general, everyone got fatter between their baseline and follow-up appointments, but diet soft drink “users” got 70% fatter than “non-users.” Frequent users (those who consume more than 2 diet sodas per day) got significantly fatter: their waists grew, on average, 500 percent more than non-users.

It appears from this chart that only the difference between the heavy users and non-users was significant at the p<.001 level. The study hasn't been published, so I have no idea how big each of the groups is or whether the other differences are significant at the p<.05 level.

What’s that? A correlation, you say? Why, the only possible explanation is that the variable randomly assigned to the x axis must have caused the differences in the variable plotted on the y-axis! It’s SCIENCE!

CBS News:

Sorry, soda lovers – even diet drinks can make you fat. That’s the word from authors of two new studies, presented Sunday at a meeting of the American Diabetes Association in San Diego.

Business Insider:

Bad News, Your "Diet" Soda Is Making You Fat Too

Time Magazine:

More bad news, diet soda drinkers: data presented recently at the American Diabetes Association’s (ADA) Scientific Sessions suggest that diet drinks may actually contribute to weight gain and that the artificial sweeteners in them could potentially contribute Type 2 diabetes.

Because there’s no chance there’s some confounding factor, or that the causal arrow points in the other direction. After all, people who are getting fatter wouldn’t have any reason to be more likely to drink diet soda, would they?

The study’s authors are somewhat more modest about what their research shows:

“These results suggest that, amidst the national drive to reduce consumption of sugar-sweetened drinks, policies that would promote the consumption of diet soft drinks may have unintended deleterious effects.”

However, it still seems irresponsible to me that they claim their research shows that diet soft drinks have “effects,” deleterious or otherwise. Correlations are not effects. All they’ve shown is that, in general, people over 65 are more likely to consume “diet” drinks if they are also gaining more weight. Which is not especially surprising, if you think about it.

I wish people who write headlines and story leads like the ones quoted above would have “Correlation =/= causation” tattooed across their foreheads, backwards, so they’d be reminded of it every time they look in the mirror.

Study #2 and more incredulous owls below the jump:

20 MICE WHO ATE ASPARTAME SHOWED SOME POTENTIAL EARLY SIGNS OF DIABETES (MAYBE). ALSO, SIGNS OF DEATH.

Study #2 involved 40 mice, half of whom were fed chow + corn oil and half of whom were fed chow + corn oil + aspartame (6 mg/kg/day, which seems to be approximately equivalent to a 132 lb person drinking 20 oz of aspartame-sweetened soda per day). After three months on the diets, the mice on the aspartame diet had fasting glucose levels 37% higher than the mice only getting chow + oil. The fasting insulin levels in the aspartame-fed mice were also 27% lower, but that wasn’t statistically significant.

I’m not sure how biologically significant 37% higher average fasting glucose is, or what the range for each group was, or whether the aspartame-fed mice went on to develop diabetes. The latter is especially hard to answer because apparently, by 6 months after starting the diet, at 18 months of age, only 50% of the aspartame-fed mice and 65% of the control group mice were still alive—which, the researchers note, was not a statistically significant difference and is apparently about par for the course with mice, whose average lifespan seems to be between 1-2 years.

This study is intriguing, and does offer one possible mechanism by which aspartame could independently cause weight gain—if aspartame consumed in sufficient quantities has a biologically meaningful effect on blood sugar levels, then diet sodas could indeed be causing people to store more fat than they would if they consumed another calorie-free beverage. But this is far from a smoking gun. It’s not clear if all artificial sweeteners have the same effect. Or if it would also occur in mice not eating a high-fat diet. Or if the blood sugar effects only happen above a certain level of aspartame consumption. Or if it works the same in humans. Or if it does lead to diabetes or negative health outcomes or just produces some biological markers of pre-diabetes. And what this study also showed was that rats who eat aspartame are not significantly more likely to die early than rats who don’t eat aspartame.

BUT WAIT I HAVE MORE CORRELATIONS FOR YOU

Fooducate has one more piece of evidence to submit—the clincher, it seems, if you’re still not convinced by those two studies that diet sodas make you fat:

Still sipping away at your Diet Sprite?

Need more evidence that drinking diet soft drinks is bad for you?

Consider this – ever since diet soft drinks were introduced into the market, obesity and diabetes rates in this country have skyrocketed.

image

Consider this—ever since aerobics became a nationwide trend, obesity and diabetes rates in this country have skyrocketed! Consider this—ever since sushi became popular in America, obesity and diabetes rates have skyrocketed! STOP DOING AEROBICS AND EATING SUSHI. FOR THE LOVE OF GOD, THINK OF THE CHILDREN.

Why Posting Calorie Counts Will Fail, Part III: Calorie-restriction dieting doesn’t work long-term for most people

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

The article on "Making Weight Loss Stick" is by Bob Greene, the personal trainer and "fitness guru" Oprah first started consulting with in 1996. Sadly, I don't think that's *meant* to be ironic. 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:

Oprah in The Color Purple Screen shot of the infamous "fat wagon" episode first aired in the fall of 1988, when Oprah strode on set in what she proudly declared were size 10 Calvin Klein jeans after an Optifast diet, wheeling a Red Flyer wagon full of lard representing how much weight she'd lost  At the Emmy Awards, holding her third for "Outstanding Talk/Service Show Host"  Holding yet another Emmy at the end of that impressively-muscled arm, shaped with the help of trainer Bob Greene

             1985                           1988                             1992                             1996

 At the party celebrating the first anniversary of O Magazine  At the Academy Awards, wearing Vera Wang Presenting at the Emmy Awards presenting at the 2010 Oscars, possibly on the way back down again?

              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.


A Meta-Review of the Literature

Of course, I’m not the first person to try to figure out what kind of picture decades of weight-loss research was painting. I found 14 reviews of weight-loss research in peer-reviewed journals (Mann et al 2007, Jeffrey et al 2000, Perri & Fuller 1995, Garner & Wooley 1991, Jeffrey 1987, Bennett 1986, Brownell & Wadden 1986, Brownell 1982, Foreyt et al 1981, Wilson & Brownell 1980, Stunkard & Penick 1979, Wooley et al 1979, Foreyt 1977, Stunkard & Mahoney 1976). And they all say basically the same thing: calorie-restriction diets don’t work long-term. Here’s how three of the most recent ones came to that conclusion, and one meta-analysis that claims to challenge the consensus, although it turns out that all they’ve really done is redefine “success.” 

Diets Don’t Work—Mann et al 2007 (free full text): This review of 31 weight-loss studies by a team of UCLA researchers was aimed at developing recommendations for Medicare regarding obesity prevention and treatment. They were only able to find 7 studies of weight-loss dieting that randomly assigned participants to diet or control groups and followed them for at least two years (the “gold standard” required to make causal claims about the effects of dieting). And the “gold standard” studies did not support the claim that dieting promotes significant or long-term weight loss:

Across these studies, there is not strong evidence for the efficacy of diets in leading to long-term weight loss. In two of the studies, there was not a significant difference between the amount of weight loss maintained by participants assigned to the diet conditions and those assigned to the control conditions. In the three studies that did find significant differences, the differences were quite small. The amount of weight loss maintained in the diet conditions of these studies averaged 1.1 kg (2.4 lb), ranging from a 4.7-kg (10.4-lb) loss to a 1.6-kg (3.5-lb) gain. (223)

They also examined 14 studies with long-term follow-ups that didn’t involve control groups. The average initial weight loss in those studies was 14 kg (30.8 lb), but in the long-term follow-ups, participants typically gained back all but 3 kg (6.6 lb). Of the eight studies that tracked how many participants weighed more at the follow-up than before they went on the diet, the average was 41% with a range of 29%-64%, and in every case was higher than the percentage of participants who maintained weight loss. In other words, participants were more likely to regain more weight than they initially lost than they were to maintain their initial weight loss. Although Mann et al note several problems with these studies, like low participation rates in the long-term follow-ups, heavy reliance on self-reporting as the primary or only measure of weight, and failure to control for the likelihood that some of participants were already dieting again at the follow-up, those factors should have biased the results in the direction of showing greater weight-loss and better long-term maintenance, not less.

Finally, they looked at 10 long-term studies that didn’t assign participants to “diet” or “non diet” conditions randomly. In general, these were observational studies that assessed dieting behavior and weight at a baseline time and then followed up with participants to measure changes in behavior and weight over time. Of those studies, only 1 found that that dieting at the baseline led to weight loss over time, 2 showed no relationship between dieting at the baseline and weight gain, and 7 showed that dieting at the baseline led to weight gain.

Their recommendation to Medicare:

In the studies reviewed here, dieters were not able to maintain their weight losses in the long term, and there was not consistent evidence that the diets resulted in significant improvements in their health. In the few cases in which health benefits were shown, it could not be demonstrated that they resulted from dieting, rather than exercise, medication use, or other lifestyle changes. It appears that dieters who manage to sustain a weight loss are the rare exception, rather than the rule. Dieters who gain back more weight than they lost may very well be the norm, rather than an unlucky minority. If Medicare is to fund an obesity treatment, it must lead to sustained improvements in weight and health for the majority of individuals. It seems clear to us that dieting does not. (230)

Long-term Maintenance of Weight Loss: Current Status—Jeffrey et al 2000 (free abstract or full text with umich login): A review of 20 years of long-term weight loss studies that describes the weight loss and regain among patients who participate in behavioral treatments for obesity as “remarkably consistent” (7) which is visually represented by lots of graphs of different studies on the long-term results of weight loss studies that all pretty much look the same:

Very low calorie diets vs. Low calorie diets (Wadden et al 1993)  Fat restriction vs. calorie restriction (Jeffrey et al 1995)

Diet only vs. Diet + exercise (Sikand et al 1988) People who were paid $25/wk for successful weight loss vs. people who weren't paid (Jeffrey et al 1993)

Basically no matter what researchers do, most dieters achieve their maximum weight loss at 6 months and then gradually regain all or almost all of the initial weight lost within 3-5 years, if not faster. They conclude:

The experience of people trying to control their weight is a continuing source of fascination and frustration for behavioral researchers. Overweight people readily initiate weight control efforts and, with professional assistance, are quite
able to persist, and lose weight, for several months. They also experience positive outcomes in medical, psychological, and social domains (NHLBI Obesity Education Initiative Expert Panel, 1998). Nevertheless, they almost always fail to maintain the behavior changes that brought them these positive results. Moreover, as we hope we have shown, efforts to date to change this weight loss-regain scenario have not been very successful.

Confronting the Failure of Behavioral and Dietary Treatments for Obesity—Garner and Wooley 1991 (free abstract or full text with umich login): Like Mann et al, Garner and Wooley were seeking to translate the available evidence about weight-loss dieting into recommendations for treatment—in this case, best practices for mental health practitioners seeking to counsel and treat overweight and obese patients. They note that short-term behavioral studies consistently show that modifications in eating and exercise behaviors lead to weight-loss, but that as the duration of studies increases, “over and over again the initial encouraging findings are eroded with time” (734).

The authors are particularly perturbed that poor results are often presented by study authors as positive. For example, an 1981 study comparing standard behavioral therapy with a weight-loss drug, or the therapy and drug combined found that all of the treatment groups lost a significant amount of weight in the first 6 months, and then all of the treatment groups showed significant re-gain by the end of the 18 month follow-up.the consistency in the curves is really eerie after a while...the 6 month nadir, the gradual incline; also, it is completely baffling to me how someone could look at this graph and think the most notable part is the gap between the three treatments at 18 months

Instead of concluding that all of the treatments had failed to produce lasting weight loss, the authors conclude that these results provide hope for behavioral therapy, because that group showed the slowest rate of weight re-gain:

This most recent study provides grounds for optimism as to the future of behavioral treatment of obesity . over the long run, behavior therapy clearly outperformed the most potent alternative treatment with which it has yet been compared. (734 in Garner and Wooley, 135 in the original)

This pattern is nearly as consistent as the finding that weight is gradually regained and many individuals eventually weigh more than they did at the start of the treatment. After four years, nearly all participants in nearly all studies gain back nearly all the weight they initially lost: Adams, Grady, Lund, Mukaida, & Wolk, 1983; Dubbert & Wilson,1984; Kirschenbaum, Stalonas, Zastowny, & Tomarken, 1985; Murphy, Bruce, & Williamson, 1985; Rosenthal, Allen, & Winter, 1980, Bjorvell & Rossner, 1985; Graham, Taylor, Hovell, & Siegel, 1983; Jordan, Canavan, & Steer, 1985; Kramer, Jeffery, Forster, & Snell, 1989; Murphy et al. 1985; Stalonas, Perri, & Kerzner, 1984; Stunkard & Penick, 1979. And yet, the authors of those studies insist that the diet interventions are “effective,” sometimes claiming that if the subjects had not dieted they would weigh even more. They almost never admit that the treatments completely failed to do what they set out to do, which is produce a clinically significant weight loss that can be maintained long-term. When they do admit that the results are “disappointing,” they frequently call for more “aggressive” treatments like very low calorie diets (VLCD or <800 kcal/day) or supervised fasting (which is no longer approved because of the risk of mortality).

Garner and Wooley also evaluate studies that used VLCD, some of which involved Optifast, the protein shake that Oprah used to achieve her 67 lb weight loss in 1988. Just like with other calorie-restriction diets, people on VLCD generally lose weight initially, although drop-out rates are much higher than in other weight loss studies (50% or more). Participants who stick to the diet typically maintain the weight loss for about a year, but regain most if not all of the weight they lost within three years and many gain more than they initially lost (Swanson and Dinello, 1970, Sohar and Sneh, 1973, Stunkard and Penick, 1979, Johnson and Drenick 1977, Drenick SC Johnson, 1980, Wadden et al., 1983, Wadden, Stunkard, & Liebschutz 1988, Hovel et al., 1988). Based on all of those studies, they conclude:

Although the rate and magnitude of weight loss have been the basis for recommending the VLCD, its most remarkable feature is the speed of weight regain following treatment. (740)

Garner and Wooley found only two studies of weight-loss dieting that reported better long-term results, and both had extremely low rates of participation in the follow-up and relied on self-reported weights. For example, Grinker et al (1985) reported that 55% of the participants in a residential treatment program had maintained a 5-kg weight loss based on the responses of only 38% of the original participants. They suggest that it seems far more likely that the low participation in the follow-up biased the results than that those studies are right and all the other ones or wrong and conclude:

It is only the rate of weight regain, not the fact of weight regain, that appears open to debate. While this may be discouraging to the individual intent on weight loss, it should also provide some solace to the many individuals who have failed at dieting and have attributed the failure to a personal lack of will power. (740)

It is difficult to find any scientific justification for the continued use of dietary treatments of obesity. Regardless of the specific techniques used, most participants regain the weight lost. (767)

They make the following recommendation to mental health practitioners:

We suggest that at the least, if weight loss is offered, it should be done with full disclosure of the lack of long-term efficacy and of the possible health risks [which, as they explain, include physical and psychological risks correlated with weight fluctuation]. It is further recommended that alternative nondieting approaches aimed at improving the physical and psychological well-being of the obese individual be given priority over dietary treatments as a subject of research and that such treatments be offered on an experimental basis. (767)

Long-term weight-loss maintenance: a meta-analysis of US studies—Anderson et al 2001 (free full text): As the title suggests, this is a meta-analysis rather than a review article, meaning rather than summarizing and evaluating what other studies found, they lumped together the data from 29 different studies. 13 of the studies involved “very low energy diets” (VELDs), 14 involved “hypoenergetic balanced diets” (HBDs) and 2 involved both—in other words, they were all calorie-restriction diets, and about half of them required participants to eat less than 800 kcal/day. The authors claim that no long-term randomized, controlled studies were available, and it’s unclear why they didn’t think studies like Jeffrey and Wing 1995 (discussed below) should count.

They don’t provide details for any of the studies individually, but do disclose that the number of participants ranged from 6 to 504, the length of treatment ranged from 8 to 30 weeks, average initial weight loss ranged from 3.5 to 37.9 kg for women and 6.2 to 44.2 kg for men, and follow-up participation rates ranged from 50% to 100% with a median of 82%. In other words, these were very different studies. Here are the results of their aggregation of the data:

again, what they're focusing on is the relatively small loss maintained by year 5 rather than, say, the precipitous drop from year 1 to year 2

The average weight loss at 5 years for both VELDs and HBDs was 3.0 kg, or ~3.2% of the participants’ starting weight and 23.4% of their initial weight loss. Anderson et al conclude:

These average values are higher than those reported in earlier studies and indicate that most individuals who participate in structured weight-loss programs in the United States of the type reported in the literature do not regain all of the weight lost at 5 y. of follow-up.

Sure, not all of the weight, only 76.6% of it. It still seems to me like a perversion of the idea of “success” to claim that these results show that calorie-restriction diets are “effective.” The average initial weight loss was 14 kg. If you lost almost 31 lbs and then regained 25 lbs, would you consider your diet a long-term success? Mann et al wouldn’t. In the 14 long-term studies without control groups that Mann et al evaluated, they also note an average maintenance of ~3 kg. They just don’t think that’s very impressive:

It is hard to call these obesity treatments effective when participants maintain such a small weight loss. Clearly, these participants remain obese. (Mann et al 223)

Interpretation/equivocation aside, there’s still some discrepancies between their analysis and the consensus in the other reviews which I wish I could explain. It’s not like this was a study of a new treatment—they relied exclusively on existing studies, at least some of which were also included in the reviews of the literature discussed above. However, some of the studies they included must have reported (possibly significantly) better results to bring up the average. Since they didn’t evaluate the studies individually, it’s impossible to tell from their write-up whether those studies involved some sort of strategy that made calorie restriction dieting “work” (and somehow didn’t attract widespread attention) or whether the results in those studies were biased by low participation rates in follow-ups, self-reporting, or some other factor(s).

A Closer Look at the Studies Themselves

I have not read every single study referenced in the review articles, although I have at least glanced at many of them. The ones I chose to explore in further depth here either 1) meet the “gold standard” of randomized assignment to diet/non-diet conditions and at least 2 years of follow-up or 2) are too recent to be included in the review articles.

Long-term Effects of Interventions for Weight Loss—Jeffrey and Wing 1995 (free abstract or full text with umich login): This is one of the seven studies included in the first part of the Mann review. 202 participants between the ages of 25 and 45 who were between 14-32 kg above the MetLife standards for the “ideal weight” for their height were randomly assigned to one of five experimental groups:

  • a control group which received no intervention
  • a standard behavioral therapy group (SBT) that received instruction on diet (including advice on how to follow a 1000-1500 calorie/day diet), exercise (including the recommendation to walk or bike 5 days/wk with an initial goal of burning 250 kcal/wk and gradually increasing that to 1000 kcal/wk), and behavior modification (including keeping food and exercise diaries. This advice was given in weekly counseling sessions for the first 20 weeks and monthly sessions thereafter for a period of 18 months.
  • a SBT + food group, which received the same counseling along with premeasured and prepackaged breakfasts and dinners for 5 days/week for 18 months
  • a SBT + $ incentive group, which received the same counseling along with up to $25/week  for achieving and maintaining weight loss
  • a SBT + food + $ incentive group, which got the counseling, meals, and money

In addition to the 18 months of the study, the participants were contacted at 30 months (a full year after the study ended) for an additional follow-up, which was completed by 177 (88%) of the original participants. Here are the results:

 is this shape getting familiar? 

All the treatment groups lost weight during the intervention, achieving their maximum results at 6 months. However, by 12 months—even though they were all still receiving the treatment, they were beginning to regain weight. By 30 months, there was no significant difference between any of the treatment groups and the control group. The authors wheedle a bit, claiming the difference “approaches levels of statistical significance” (.08), but are honest enough to admit in the end:

The overall results of this evaluation reemphasize the important point that maintaining weight loss in obese patients is a difficult and persistent problem.

Preventing Weight Gain in Adults: The Pound of Prevention Study—Jeffrey & French 1999 (free full text): This more of a “failure of low-cost educational interventions designed to encourage weight loss” than a failure of weight loss dieting per se, but it’s still relevant because 1) the experimental group “got the message” communicated in the educational intervention but gained the same amount of weight over 3 years as the control group and 2) calorie labeling is essentially a large-scale, low-cost educational intervention. The idea that education will make people thinner relies on the assumption that people would not be (as) obese if they only knew they were gaining weight, that they should eat more fruits and vegetables, that they should reduce their consumption of high-fat foods, and/or that they should get more exercise.

But most people do know all those things. In this study, 228 men and 594 women employed by the University of Minnesota and 404 low-income women, all between the ages of 20-45, were recruited to participate in a 3-year study. Half of the participants were assigned randomly to a control group and the other half were assigned to the “intervention” group, which received a 2-4 pg monthly newsletter called Pound of Prevention. The newsletter emphasized five themes:

1) weighing yourself regularly (at least once a week)
2) eating at least 2 servings of fruit per day
3) eating at least 3 servings of vegetables per day
4) reducing the consumption of high-fat foods
5) increasing exercise, especially walking

In other words, “common sense” nutritional advice, although not explicitly calorie reduction. The newsletter included recipes, suggested particular areas/routes in the local areas for walking, and included a return-addressed, stamped postcard asking participants to report their current weight and also answer whether they had walked for 20 minutes or more, eaten 2 servings of fruit, eaten 3 servings of vegetables, or weighed themselves in the last 24 hours. Intervention participants were also invited to take part in a variety of activities during the three years, including 4-session weight control classes, aerobic dance classes, free 1-month memberships to community exercise facilities, walking groups, and a walking competition. Additionally, half of the “intervention” group was assigned randomly to an “incentive” group who were eligible for a monthly $100 lottery drawing for members who returned the postcards.

All participants were evaluated in annual physicals where they were weighed, their height was measured, their dietary intake evaluated using a standard 60-item Food Frequency Questionnaire, and they were asked about behaviors like exercising, eating fruits and vegetables, decreasing fat intake, using “unhealthy diet practices” like laxatives and diet pills or liquid diet supplements, weighing themselves, and smoking. At some point in the study, a questionnaire was administered to test “message recognition.”

Participation in the “intervention” group was high—68% of postcards were returned, 80% of the participants reported having read most or all of the newsletters at their annual visits, and 25% participated in one or more of the extra activities. The “message recognition” test was somewhat successful—the intervention group was significantly more likely to identify the 5 targeted treatment messages as being among the best ways to prevent weight gain; however, even 66% of the control group endorsed the treatment messages. The intervention groups were slightly-but-significantly more likely to weigh themselves and more likely to continue practicing “health weight loss practices” as measured by a 23-item questionnaire. However, changes in BMI, energy intake, percent of calories from fat, and rates of physical activity were not significantly different between the control and intervention groups. All participants gained an average of 3.5 lbs over the course of the 3 years.

In short, the intervention was a failure. The authors conclude:

It is easier to teach people what to do than to persuade them to actually do it…. The overall impact on weight itself…was very weak, indicating that stronger educational strategies are needed or, alternatively education alone is insufficient to deal effectively with this important problem.

Weight Maintenance, Behaviors and Barriers—Befort et al 2007 (free abstract or full text with umich login): Based on the abstract, this study sounds like a success, but under closer examination, not so much. The data was collected at a university weight loss clinic where participants were recruited to follow low-calorie or very low-calorie (500 kcal/day) weight-loss diets followed by a maintenance program. The “weight-loss” phase lasted for 3 months during which participants consumed prepackaged meals and/or shakes. The maintenance programs ranged from 6 to 21 months and consisted of weekly or bi-weekly meetings at the clinic during which participants were counseled to follow a structured diet plan with a daily calorie goal and exercise 150-300 minutes per week. In 3 out of 4 trials, the participants were also encouraged to continue consuming the shakes/prepackaged meals.

Out of 461 participants who started treatment, 44 dropped out during the 3-month weight loss phase and 211 dropped out during the maintenance phase. They sent follow-up surveys to everyone who completed the 3-month weight loss phase (n=417), and got 179 back (46.6.%). The more recently participants had been part of one of the studies, the more likely they were to respond to the follow-up survey. Responders had only been out of treatment for an average of 14 months.

Their claim that a “majority” of the participants maintained their initial weight loss is based on them lumping together respondents who had only been out of treatment for 6 months with people who had been out of treatment for 24 months or more, despite the fact that—just like in every other study of calorie-restriction weight loss—the results showed that most participants gradually regain weight. As they admit:

Compared to participants who were out from treatment for 24 months or longer, those who were out for less than 6 months (P<0.05) or for 6–12 months (P<0.01) had significantly greater weight loss maintenance, both in terms of kg and percent of baseline weight.

What they don’t say is that the percentage of respondents who report maintaining their initial weight loss drops off precipitously after 24 months.

no graph; perhaps it would have been too damning?

Of the 31 respondents who’d been out of treatment for 24+ months, only 25.8% had maintained a weight loss of 10% of their body weight or more and 48.4% had maintained a weight loss of 5% or more. That means out of the original pool of 417 who completed the 3-month diet, only 8 had proven capable of maintaining weight loss equal to 10% of their body weight for more than 2 years and only 15 had proven capable of maintaining a weight loss equal to 5% of their body weight. Other participants might be able to maintain their initial weight loss—that data isn’t available, but the trajectory certainly doesn’t look good. And that’s based on the half of the participants who participated in the follow-up—as Garner and Wooley note, the higher the rate of participation and the longer the follow up, the less weight loss on average is maintained.

What About the National Weight Loss Control Registry?

Several of the studies and at least one person who commented on one of the earlier posts in this series mentioned the National Weight Loss Control Registry (NWCR) as evidence that people can indeed lose weight and keep it off. I’ve never disputed that. Even in the studies that show the least hope for long-term maintenance, there are exceptions to the general trend. But that’s what they are: exceptions.

According to the NWCR website, they have over 5,000 members, all of whom have lost at least 30 lbs and kept it off for at least 1 year; however, most of them have done far better—registry members have lost an average of 66 lbs and kept it off for an average of 5.5 years. As the research above suggests, that’s not remotely “representative” of people who attempt to lose weight. On the contrary, the entire raison d’être of the registry is to figure out what’s different about the 5-10% of dieters who lose significant amounts of weight and keep it off. The goal is to identify strategies that might help other dieters, but as the researchers who run the registry admitted in a 2005 article (free abstract):

Because this is not a random sample of those who attempt weight loss, the results have limited generalizability to the entire population of overweight and obese individuals.

Indeed, the kinds of things the registry members do are generally the same things the participants in most weight loss studies are counseled to do (or, in clinical settings, forced to do): most of them follow a low calorie, low fat diet, eat breakfast every day, weigh themselves at least once a week, watch less than 10 hrs of TV per week, and engage in very high levels of activity—420 minutes per week on average. The NWCR has yet to figure out what makes those things work for them and/or makes them capable of sustaining those behaviors when for most people, they don’t/can’t.

Collecting 5,000 success stories does not prove that dieting “works” for most people let alone that it’s the norm. Somewhere between 45 million and 90 million Americans diet to lose weight every year, most of them by attempting to reduce their caloric intake. According to a survey conducted in April 2010 by a private consumer research firm on behalf of Nutrisystem, 30% of Americans have dieted repeatedly—an average of 20 times. Unsurprisingly, weight loss attempts are more common among overweight and obese people. If calorie-restriction dieting “worked,” America would be a nation of thin people.

Conclusion: Putting the burden of proof back where it belongs

Traditionally, researchers assume that a treatment is not effective until they have evidence that proves otherwise. The reverse is true in regard to weight-loss dieting: most people assume dieting is effective for long-term weight loss and challenge anyone who believes otherwise to prove that it doesn’t—not that that’s difficult, given the consistent failure of most weight-loss interventions to produce lasting results. I have not been able to find one long-term, randomized, controlled study that shows that dieting works (i.e. a statistically significant group of people following a calorie-reduction diet losing a clinically significant amount of weight and keeping it off for more than 3 years). Instead, what all the research to date shows is that the most reliable outcome of calorie-restriction dieting is short-term weight loss followed by weight regain.

I suspect the stubborn persistence in prescribing calorie-restriction dieting as a weight loss strategy in spite of the available evidence probably has a lot to do with dominant and deeply-engrained attitudes about fatness, meritocracy, virtue, and effort. People exhibit remarkable cognitive dissonance when it comes to the research on weight loss—they hold up exceptions as the rule and claim that the 90-95% of people for whom calorie restriction dieting does not produce weight loss must simply not be trying hard enough. 

Imagine this scenario playing out with any other condition—imagine that instead of weight, we were talking about some kind of rash that was widely considered unattractive and thought to be correlated with a variety of other health problems. There’s a treatment that showed promise in short-term trials. In virtually every study, most of the people who get the treatment experience significant improvement in their symptoms, with peak results around six months. However, in longer-term studies, there’s a reversal. Just as consistently, the vast majority of sufferers—at least 75% and usually closer to 90 or 95%—experience a gradual return of their symptoms. For approximately 30-40% of participants, their symptoms actually get worse than before they started the treatment. Only 5-10% show lasting improvement. Of course you would want to do more research to figure out why the treatment works for that 5-10%, but in the meantime, would you keep prescribing it to everyone with the same skin condition?

Even if the problem is that only 5-10% of them fail to use the treatment as instructed—say, it’s a topical cream that only works if you apply it every hour on the hour and people get fatigued, especially by trying to wake up at night to put it on. If 90% of the affected population can’t use the treatment effectively, the results are the same as if the treatment never worked in the first place. Well, except for that part where 30-40% of them end up worse off than before they started the treatment…

So even if the calorie counts on menus were accurate, and people could accurately and reliably estimate how many calories they burn, and they did choose lower-calorie options at least some of the time, and they didn’t compensate by eating more on other occasions…in other words, even if the calorie counts worked the way they were intended to, the best you could hope for would be short-term weight loss. There’s no reason to believe the policy—even under ideal conditions—would have a lasting effect on most Americans’ weight or health.

When What I Want Isn’t What I Want: On Temptation and Disordered Thinking/Eating

Note: I try to avoid writing overly confessional, navel-gazing posts, but I’m making an exception today because I think personal narratives can be useful in attempting to understand the complexities and challenges of trying to eat “well.”  

I have never been diagnosed with an eating disorder, but I think it's hard for most people to reach this state--disordered or not. I thought I had reached it, but now I'm starting to think it's not a destination that I can "arrive" at but something that requires continuous work, like a balancing act or relationship.

All images in this entry from PostSecret 

When I work from home, I almost never eat out. That doesn’t mean I don’t eat prepared or processed foods—the freezer is almost always full of things from Trader Joes and the local Asian market (I know I could make tamales and pot stickers myself, and that that would probably be cheaper and perhaps better-tasting, but at least for now, other priorities win out over eating 100% cooked-from-scratch meals). But even if you don’t count TJ’s prepared foods and the occasional package of instant pho or ramen, I still eat mostly “homemade” food most of the time, even when I’m working under deadline pressure. A lot of that has to do with the fact that it’s usually quicker, easier, and cheaper to cook an egg, cut up some fruit or vegetables, or throw together a salad or sandwich than it is to go somewhere or get delivery.

Having to be at an office everyday, which I’ve been doing for the last six weeks due to a dissertation writing institute, has disrupted my eat-at-home habits. I’ve tried to pack lunches every night and keep “healthy” convenience foods like nuts and apples in my office to minimize the extent to which I end up eating out, but I haven’t been entirely successful. The availability of outside food has basically exposed me to a whole array of temptations that I don’t normally encounter, and I’ve found myself engaging in some of the patterns of impulsive or emotional eating, negative self-talk, and general anxiety about food that I thought I was mostly “over.”

"Disordered" eating (which may be a misnomer that implies there's such a thing as "ordered" eating) can manifest in many ways; starving and purging are only symptoms, the underlying "disorder" may exist or persist without those symptoms.

Bad Day Part 1: Pizza and Self-loathing

Here’s how last Friday went:

While getting ready in the morning in the bathroom, I weigh myself for the first time in about a week. I used to weigh myself multiple times a day, taking perverse pleasure in every decrease, no matter how small, even if it was clearly due to excretion or being dehydrated from drinking too much the night before. Now I’m not nearly as obsessive, but when I see that the number is over 110—the highest it’s been in at least two years—I feel disappointed and ashamed. I tell myself the number doesn’t matter, and even if it did matter, 110.4 is a perfectly acceptable number for my height and build. And even if it wasn’t a totally acceptable number, obsessing about it wouldn’t do any good. But the best I can do is repress the emotions. I can’t un-feel them. 

It's so hard to internalize the fact that restricting food actually represents a *lack* of control or self-restraint. Even when it takes the form of "restraint," it is unrestrained restraint. I mean, obviously, right, someone in control of their restraint doesn't let it kill them.  In the kitchen, I look at the last container of leftover nettle soup in the refrigerator and sigh. The factors in favor of taking it are many and obvious: it is tasty, relatively healthy, easy, and will prevent me from even having to think about leaving the office to get food. There was even a handful of oyster crackers left at my office from the day before, when I had made the “right” choice and taken the soup. But I tell myself I’m “sick” of it, since I had it yesterday. I briefly contemplate grabbing one of the packages of tamales from the freezer, but then I’d have to find something to transport salsa in. Also, I don’t really have the eating implements at the office for that, and it doesn’t even sound that good in the first place. I am conscious of and unhappy about the fact that I’m making excuses. I throw some cherries in a tupperware container to eat for breakfast, feeling like that’s a reasonably healthy “trade-off” for the potentially less-healthy lunch I’m setting myself up for.

It hasn’t been a good week for dissertation writing. I keep revising instead of adding new material—or, worse, writing blog entries and playing games online. I feel lazy and ashamed, and I know that what would make me feel better is to actually do the work. But I just keep not doing it—willpower failing on multiple fronts. However, this particular morning goes pretty well. I spend an hour or so on the egg post, but then I finish revising a section of the chapter that’s been frustrating me for a while. Around noon, when I start to get hungry and distracted, I decide that the best way to keep my momentum going is to take a break and go to lunch to try to circumvent the pit of despair that I seem to slip into around 1pm.

I wander outside contemplating my options and decide to get pizza. I know this is probably among the worst of the options available to me no matter what criteria you’re using—carbs, calories, fat, pizza has it all in abundance. My justification is that I have been vaguely wanting pizza for days, so perhaps if I just have it, I will stop thinking about it and possibly compensating for not having it by “splurging” on other foods.

It tastes good, but as with most foods I have ever craved or idealized, it’s not nearly good enough to warrant either “craving” or feeling guilty about. The idea that it’s a “bad” food only makes me want it more, it doesn’t make it taste better. I probably would have gotten more pleasure from the nettle soup. I make a note of this but endeavor not to mentally castigate myself. working to change my perceptions about what is pretty--on myself and other people--is a related challenge, and also one that takes continuous effort.

Perhaps because I can tell I’m on a sort of dangerous track, while I’m eating the pizza, I start thinking about a moment a few years ago that has become somewhat totemic for me as an example of my “disordered” past tendencies. I was looking at a friend’s stomach—she’s slender, but has a tiny rounded belly—and I thought something along the lines of: ugh, if my stomach ever looked like that, I’d start seriously starving myself. It was less…concrete than that because I didn’t put it into words, but it was something between that kind of thought and more general feeling of disgust and dread that seemed like it was directed outward (towards the friend) but was actually just a projected form of self-hatred. At the time, I took the comparative flatness of my stomach as evidence of my superior self-control. But I wasn’t in control—I was terrified of getting fat and ashamed of my hunger and hypercritical of my body. When I did feel beautiful back then, it was entirely dependent on feeling thin (not being thin, because it was entirely about perception, not reality) and it was a hollow, imperious sort of self-love that required other people to be fat and inferior. And most of the time, I didn’t feel beautiful at all.

Thinking about that moment and how completely insane I had to be to think this woman was fat seems to help. I say to myself: So I had pizza for lunch, so what? Eating two pieces of pizza is not some major “transgression.” It’s not going to make me fat or sick, it doesn’t make me morally weak, and it definitely does not make me less beautiful or deserving of love.

Bad Day Part 2: The Unscratchable Itch

After lunch, still feeling vaguely hungry but suspecting that I’m really just thirsty since I didn’t get a drink with my slices, I stop in a small market/deli and contemplate the bottled drinks. I know VitaminWater is basically just sugar-water—that the antioxidants and “superfruits” advertised on the label are classic appeals to what Michael Pollan calls “nutritionism,” that it is not going to make me healthier, that I won’t even like the taste that much. But for some reason, some part of me wants it—VitaminWater is now the thing I hope will scratch this itch I can’t seem to locate, which is probably the same itch I was trying to scratch with the pizza. Deciding not to agonize over it, I pick up a bottle of XXX vitaminwater ZERO (acai-blueberry-pomegranate flavored), without even checking to see what the “natural” zero-calorie sweetener is (it turns out to be stevia). I also grab an apple in case it turns out that I am actually still hungry or want a snack later that afternoon. And then, remembering that I have a 5 hr drive ahead of me that evening, and in anticipation of that or perhaps to offset the “virtue” of the apple and calorie-free vitamin water, I grab a bag of Werther’s Originals Chewy Caramels. Even though I clearly also have and succumb to cravings, I find myself being snarkily judgemental about people who talk about cravings, which I think results partially from popular representations of women as basically crave-beasts made utterly irrational by things like chocolate and low-fat/low-calorie yogurt.

As I put them on the counter at the register, I feel like this is unlike me. I feel like I ought to be above these things: eating “junk food” for lunch, impulse-buying VitaminWater and candy. I’m not even entirely sure why I’m doing it. It certainly doesn’t make me happy.

Back at the office, I look at the nutritional information for the caramels, even though I don’t want to care. I used to count calories obsessively. I don’t anymore, and not just because caloric algebra is imprecise and restricting calories just prevents you from having enough energy and slows your metabolism. What concerns me more are the psychological effects: it causes me to moralize my hunger and food choices, making calorie-dense foods “bad,” and that causes me to crave them. Even when I resist the cravings, I feel ashamed for having them, and become more inclined to indulge in other self-destructive behaviors, either to “treat” myself for being good (resisting cravings) or to punish myself for my unruly appetite. Basically, it makes me want to eat more and enjoy the food I do eat less. Even people who lose weight the "healthy" way through diet and exercise almost always gain it all back, or more. 60% within a year, 97% within three years. 23% gain back more than they lost. Attaching moral significance to weight is a recipe for self-loathing.

Also, it’s unsustainable. My pattern for years was basically: for 2-6 months, I’d restrict myself to 1100-1700 calories/day (usually trying to alternate low and high days). I’d lose a few pounds, feel superior in a hollow way and make pejorative judgments about the moral character of everyone fatter than me (and given that my BMI was between 17.2-18.0, almost everyone I knew or met was fatter than me). But eventually, I’d run out of steam and I’d start “cheating” more, although most of the “cheating” seems pretty ludicrous now—I remember considering a small skim latte a big indulgence. Eventually, I’d stop weighing everything I ate and looking up nutritional values online and for maybe 6 months, I’d eat basically whatever I wanted (although I was always still following some form of restricted diet that usually had ethical/medical rationalizations, i.e. veganism, but was also at least partially motivated by the desire to stay thin). At some point, I’d notice that I had gained a few lbs, and that would inspire me to start counting/restricting again. Many dieters know this cycle well.  Of course, not all vegans are disordered eaters, but I think part of the gender imbalance in vegetarianism/veganism is related to the same factors that cause the gender imbalance in diagnosed eating disorders. More women than men use/abuse food as a form of self-control. Because I really don't think women are generally more "ethical" than men.

Even though calorie counting or “dieting” is often difficult and unpleasant and takes a lot of mental energy, it’s also incredibly difficult to resist because of the short-term weight loss and the illusion of control. The thing I still can’t seem to shake, no matter how much I try and want to, is the desire to be thin—or at least, to not be fat. Given that I know how to be (temporarily, unhappily) very thin by restricting how many calories I eat, it’s hard not to see calories, especially in sugary or starchy foods, as a measure of how bad the “bad’ things I eat are. The caramels turn out to be approximately 40 calories/caramel bad, which I immediately compare to the 20-calorie sugar-free popsicles in our freezer at home (another sin against the Church of Real Food, like the VitaminWater). Each one of these caramels = two popsicles. I eat three of them and ignore the apple, and then struggle to tell myself that that’s okay and that letting this become a matter of guilt/desire will only make me want more and feel worse, etc.

People also derive a lot of pleasure from monitoring their diet, weight, and body shape, too. But if it causes you more anxiety than pleasure, try stopping for a while. I know that's easier said than done, but deciding you don't want to worry or obsess anymore is the first step.

Saying “Enough!” and Giving Myself Permission to Eat What I Want

The rest of that day was better and this week has been fine. I really can’t emphasize this enough: last Friday was an exception, not the norm. However, that kind of lapse—and I’m referring to the thought patterns I indulged in, not the act of eating the pizza or caramels—has been happening way more frequently since the institute started. It’s been an unpleasant reminder that the balance I thought I had achieved—where I generally don’t make impulsive, emotional decisions about what to eat, don’t count calories, don’t feel bad about what I want, and just plain don’t worry so much about getting fat (and by the way, don’t gain weight: I was stable at ~105 lbs for almost 3 years after breaking the calorie-counting cycle)—is still really fragile.

I try to speak up when people make pejorative comments about fatness, I try not to make or think complimentary things about thinness or congratulate people on weight loss. But the idealization of thinness is pretty pervasive. It's difficult to resist. At first—hell, even when I started writing this entry—I thought the problem was the sudden exposure to all kinds of temptations I normally don’t have to deal with. But that’s not quite right. The kind of food that I want when I’m on campus is not the kind of food I actually find all that desirable. The reason it’s not tempting when I work from home is not just because it’s far away, but because there’s nothing inherently tempting about it. I made it into a temptation by constructing “food from home” as the virtuous alternative, which inevitably made it seem boring and oppressive and made me desire restaurant food as the “bad” other. And then, rather than choosing restaurant food that might have been nutritionally equivalent to something I’d eat at home, I was looking for a “treat” so I chose things that violated my beliefs about what is “healthy”…and still felt dissatisfied. Thus the itch I couldn’t scratch.

What I should have done from the start of the institute, and what I will do if I’m ever in this kind of situation again, is reject the impulse to moralize my lunch. I hereby give myself permission to eat as much restaurant food as I want, from whatever restaurants I want. I will eat pizza every day for a week if I want to. And the funny thing is that already, just by giving myself permission to do it, I find that I don’t want to. I only want it when I think I shouldn’t.

That’s basically the same strategy that a lot of proponents of “intuitive eating” recommend to people who want to break patterns of emotional or compulsive eating. It’s hard to listen to the cues your body supplies about hunger and satiety if the reasons you’re eating have more to do with being sad or angry or feeling deprived or wanting to be comforted or thinking you deserve a “treat” than they do with whether you physically need food. If you reject the idea that some foods are virtuous and others “bad” but therefore very desirable and rewarding, you rob food of the moral and emotional significance it has acquired due largely to contemporary anxieties about fat (which are not medically justified—see Paul Campos The Obesity Myth, J. Eric Oliver Fat Politics, Glen Gaesser Big Fat Lies or Michael Gard and Jan Wright The Obesity Epidemic: Science, Morality, and Ideology).

If you decide that you are going to eat what you want without judging yourself—without feeling shame or guilt or self-hatred or the culturally-constructed fear of fatness—a crazy thing happens: you will probably eat mostly “healthy” things in moderate amounts. I don't think most people do have to pick, but if I ever do, I hope I have the strength to choose fat and then try to learn to be happy.Here’s how another Margot, who writes the blog ReelGirl describes her experience of learning to “eat when you’re hungry, eat whatever you want, stop when you are full” (basically the intuitive eating mantra):

I was ready to stop dieting. I’d had enough. It bored me to tears. I was sick of it and bulimia too and thinking about calories or fat grams. I read a book called Overcoming Overeating and When Women Stop Hating Their Bodies (both by Jane Hirschmann), and I did exactly what the books said. I filled my house with an abundance of every food I wanted, and if I binged, I’d go out the next day and buy lots more. That action helped me like nothing else.

Keeping my house stocked with all the food I loved no matter what showed me that I was sticking with myself no matter what, even if I gained 300 pounds, I didn’t care, dieting was over for me. I didn’t gain much weight, by the way, maybe five pounds– going from extreme dieting, calorie counting, and throwing up to eating whatever I wanted hardly made a physical difference. (from an interview she did with A Weight Lifted)

The hardest part is really convincing yourself it’s okay to eat what you want. I’m actually not sure if she—or I—would stick with it if we did gain weight. Despite the fact that I believe that fatness is not a moral or medical concern, despite the fact that I think the idealization of thinness is destructive—especially to women, who are subject to far more scrutiny of their bodies and food choices and held to a much more restrictive standard—the desire to be thin is hard to shake. And as long as I care about being thin, I will probably still sometimes feel ashamed of my body or my desires or my food choices. I feel better and happier about my body and food choices than I did three years ago, in part because giving myself permission to eat what I want broke the negative thought patterns that used to really dominate how I thought about food. But it’s clearly still—and may always be—a work in progress. 

Most days, I am. All is probably too much to ask for.

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

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.

Experiment 2 (Males): Wait, Where’s the Sucrose?

In the first part of the second experiment, 24 male rats were divided into three groups of eight. Again, all three had unlimited chow and water. Group 1 had 24-hr access to the HFCS-solution, Group 2 had 12-hr access to the HFCS-solution, and Group 3 was the chow-only control. Sucrose, you’ll note, drops out entirely. According to the study:

Since we did not see effects of sucrose on body weight in Experiment 1 with males, we did not include sucrose groups in this long-term analysis in males.

But there were no effects of HFCS on body weight on the 24-hr schedule! The omission of sucrose from this experiment makes as much sense as the omission of a 24-hr sucrose group in the first one. The lead researcher’s reply to Marion Nestle’s criticisms offered no further clarification about this choice. 

We explain in the article that we purposefully did not compare HFCS to sucrose in Experiment 2 in males, because we did not see an effect of sucrose on body weight in males in Experiment 1.

This study went on for 6 months instead of 2 months and, as the table above shows, the groups with both 24-hr and 12-hr access to HFCS-water gained a significantly greater amount of weight than the chow-only rats. This time, the 24-hr HFCS rats gained more weight than the 12-hr HFCS rats.

Experiment 2 (Females): Sucrose is back (still only 12-hr)! But chow is limited.

In order to “determine if the findings applied to both sexes,” they also ran a slightly different version of the second experiment on some female rats (n unknown). The control group, as usual, got unlimited chow and food. Group 1 got 24-hr access to HFCS-water. The remaining two groups got 12-hr access to chow (“to determine if limited access to chow, in the presence of HFCS or sucrose, could affect body weight”) and either 12-hr access to HFCS-water or 12-hr access to sucrose-water. Yeesh. How about testing one thing at a time, guys?**

So this time, only the rats with 24-hr access to HFCS gained a significantly greater amount of weight than the chow-only rats, which flies in the face of the claim that rats with limited access to a palatable food eat more. And the 12-hr sucrose rats actually gained slightly more weight (though not a statistically significant amount) than the 12-hr HFCS rats.

In other words, the findings in the three studies were completely inconsistent. For male rats in the short term, 12-hr access to HFCS induces significant weight gain but 24-hr access to HFCS does not. For male rats in the long term, both 12-hr or 24-hr access to HFCS induces significant weight gain, but they didn’t test sucrose. For female rats in the long term, only 24-hr access to HFCS with unlimited chow induces significant weight gain and limited chow, HFCS, and sucrose do not. And yet, based on this, they claim:

In Experiment 2 (long-term study, 6–7 months), HFCS caused an increase in body weight greater than that of sucrose in both male and female rats. This increase in body weight was accompanied by an increase in fat accrual and circulating levels of TG, shows that this increase in body weight is reflective of obesity.

Despite the fact that Experiment 2 didn’t even test the long-term effects of sucrose consumption on male rats, and 12-hr HFCS (albeit with limited chow) didn’t cause significant weight gain in female rats.

As Usual: Needs More Research

Based on the results of all three experiments, they conclude:

Rats maintained on a diet rich in HFCS for 6 or 7 months show abnormal weight gain, increased circulating TG and augmented fat deposition. All of these factors indicate obesity. Thus, over-consumption of HFCS could very well be a major factor in the
“obesity epidemic,” which correlates with the upsurge in the use of HFCS.

Despite the fact that obesity has also increased in many countries where HFCS is virtually never used, like Australia. According to a 2008 USDA paper:

Australia and the United States have a high and rising prevalence of obesity. They have opposite sugar policies: virtually no distortions affect Australia’s use of sugar, whereas sugar policy in the United States taxes sugar use. Sugar consumption per capita in Australia has been flat from 1980 to 2001, after which it increased by 10%-15%. Sugar is the major sweetener consumed in Australia.

The fact that the experiment doesn’t seem to show that HFCS is necessarily worse than sucrose doesn’t mean the findings aren’t intriguing. I really do want to know, for example, why rats with 12-hr access to HFCS gain more weight in the short term than rats with 24-hr access to HFCS, but the 24-hr HFCS rats gain more in the long term. And if, as they claim, the rats in all the groups consumed the same number of calories—which Nestle doubts because, "measuring the caloric intake of lab rats is notoriously difficult to do (they are messy)”—why were there any differences at all at the end of the trials? If none of the rats are eating more (and indeed, it seems that in some cases the HFCS rats were eating slightly less), what is the mechanism causing them to gain more weight, at least on some feeding schedules?

Does the concentration of the sugar have anything to do with it? In his reply to Nestle, Hoebel says:

Eating sucrose does not necessarily increase body weight in rats, although it has been shown to do so in some studies, usually employing high concentrations of sucrose, such as 32%. Our previously published work, has found no effect of 10% sucrose on mean body weight. At this concentration, rats seem to compensate for the sucrose calories by eating less chow.

I want to know if that’s true for HFCS as well. And did the difference in the concentrations of the HFCS and sucrose drinks have anything to do with the difference in the rats’ weight in this study?

Or does it maybe have something to do with sucrase, the enzyme that splits the fructose and glucose in table sugar? From what I’ve read, sucrase is present in the human digestive tract in sufficient amounts that it doesn’t rate-limit the absorption of those sugars in sucrose compared to the consumption of free fructose and glucose. But is it somehow involved in metabolism or appetite-regulation?

So rather than answering any questions about HFCS vs. table sugar, this really just raises a lot of new ones.

*It’s also not clear why they gave them different concentrations of sweetener. You’d think they would make them both soda-strength, or at least calorically equivalent.

**The failure to control for multiple variables does, in fact, complicate their ability to make any conclusions about gender difference:

In the present study, male rats maintained on 12-h access to HFCS also gained significantly more weight than chow-fed controls, while female rats maintained on 12-h access did not. It is possible that this can be accounted for by the fact that these males had ad libitum chow, while the females had 12-h access to chow. It is possible that the lack of chow for 12 h daily suppressed weight gain and TG levels
that might have otherwise been elevated in the female 12-h HFCS access group. This would indicate an effect of diet rather than a gender difference.

Things That Won’t Kill You Volume 3: MSG

From Flickr user "The Other Dan" taken in Corktown, Toronto 

Unlike juice, which has sort of a mixed reputation even among contemporary nutritionists and doctors, MSG has been consistently demonized. Most people can’t tell you why, they just know that it’s bad. If pressed, they might tell you that it’s "unnatural," that food manufacturers put it in processed foods to con people into eating "junk," that it’s basically salt (which I’ll address in a future post in this series), or that it gives some people headaches. Or they might just gesture to the fact that it’s common knowledge that MSG is basically some kind of poison—after all, why would Chinese restaurants be so eager to reassure you that they don’t use it if it were completely benign?

A recent commercial for Campbell’s New Select Harvest Light (which is the sort of self-satirizing product name I’d expect to find in David Foster Wallace’s fiction) suggests that even if people don’t know what MSG stands for, they know that it’s bad—potentially bad enough to deter people from buying a particular brand. Reading from a Progresso Light can, blonde #1 gets through "monosodium" but stumbles on "glutamate"—fortunately, the rainbow coalition includes an Asian woman who can translate that jargon into something we all understand: "That’s MSG."

Although people may still associate it primarily with Chinese restaurant cooking, the Campbell’s ad hints at its broader prevalence—MSG and other forms of glutamic acid are omnipresent in processed foods. They’re especially likely to be found in foods designed to taste like things that have a lot of naturally-occurring glutamate (or similar molecules like inosinate or guanylate). Stock, broth, and bouillon often contain MSG, as does anything cheese-flavored or ranch-flavored, like Doritos, which actually contain five different forms of glutamate. I taste it the most in instant ramen and Chex Mix, but even though I know what it tastes like on its own, I can’t always tell when something contains it or not. When used sparingly, it may not even be possible to discern because whether the glutamate in a dish comes from a mushroom or a salt, once it’s dissolved in liquid or on your tongue, it’s the exact same molecule:

from Wikipedia, showing up weirdly gray here

So even people who think it’s "bad" and expect to feel bad after eating it probably eat MSG, at least from time to time, without even knowing it, and without suffering any negative effects.

The Chinese Restaurant Syndrome Myth

The first person to suspect that MSG might be unhealthy was a Chinese-American doctor named Ho Man Kwok, who complained in a letter to the New England Journal of Medicine in 1968 that he experienced numbness radiating from the back of his neck down his arms, weakness, and heart palpitations after eating at Chinese restaurants. He had never experienced those symptoms after eating at restaurants in China, and hypothesized that they were due to either an excess of alcohol, sodium, or MSG in American Chinese cooking. The MSG explanation caught on, with one of the response letters estimating that as many as 30% of Americans regularly suffered bad reactions to MSG. The NEJM ran the letters with the title "Chinese Restaurant Syndrome," and by the next year, articles in Science and The New York Times were referring to the syndrome and its MSG etiology as verified facts:

"monosodium glutamate, which has been pinpointed as cause of ‘Chinese restaurant syndrome’ " (NYT May 10, 1969 Page 33, Column 1)

Last year, the New York Times ran an article that attempted to set the record straight. They quoted the daughter of Chinese restaurant owners in New York City in the 1970s, who remembered the publicity around "Chinese Restaurant Syndrome" as a "nightmare":

“Not because we used that much MSG — although of course we used some — but because it meant that Americans came into the restaurant with these suspicious, hostile feelings.”

From Flickr user Chinese restaurants were among the first in the U.S. to use MSG, which was mass-produced in Japan beginning in the early 20th Century after a scientist named Kikunae Ikeda isolated glutamate from seaweed-based soup stocks. In the 1940s, it had become increasingly common in a number of processed foods and cooking styles around the world, including in the U.S. American soldiers who’d tasted Japanese army rations generally agreed that they tasted better, and the difference was widely attributed to MSG. As the war industries were refitted for peacetime manufacturing, including the greatly-expanded industrial food system, there was a greater need for flavor enhancers that would make food taste good even if it was canned or wrapped in plastic and transported long distances. MSG was great at that. It was also sold for home cooks to use under the brand name Accent, which is still available in the spice aisle of many grocery stores, and as a major component of Maggi sauce, a Swiss brand, and Goya Sazon seasoning blends, popular in the U.S. primarily with Latino/a and Caribbean immigrants.

It’s not entirely clear why Chinese restaurants were singled out, aside from the random chance of Kwok having weird feelings after eating at them. MSG was then, and still is, everywhere in American food. I suspect that it has something to do with a latent or repressed xenophobia. However, the success of Chinese restauranteurs and the fact that MSG didn’t really cause any physical symptoms were probably just as important—Cuban restaurants, where pork shoulder is often rubbed with a mixture of spices including MSG, weren’t nearly as common as Chinese restaurants. And if it had been called "chicken stock, Doritos, bologna, and Stove Top stuffing syndrome," that would have been far more difficult to accept for all the people who ate those things regularly without experiencing strange numbness and heart palpitations.

Which, of course, they generally don’t.

That’s Exactly what Forty Years of Research Has Found

No study has ever been able to find statistically significant correlations between the consumption of MSG and any of the symptoms associated with what was eventually re-named "MSG symptom complex" in 1995. According to a review article published in Clinical and Experimental Allergy in April 2009:

Descriptions of MSG-induced asthma, urticaria, angio-oedema, and rhinitis have prompted some to suggest that MSG should be an aetiologic consideration in patients presenting with these conditions…. Despite concerns raised by early reports, decades of research have failed to demonstrate a clear and consistent relationship between MSG ingestion and the development of these conditions.

Even studies involving self-identified "MSG-sensitive" subjects failed to find a significant increase in the frequency of MSG-attributed symptoms. In one study, only 2 of 130 self-identified "MSG-sensitive" subjects responded to MSG in 4/4 treatments. Additionally, no one’s ever found any clues as to why MSG, which is just the isolated form of a naturally-occurring amino acid salt, would cause numbness or heart palpitations.

The Fat Rat Caveat

Peanut & Missy, from Flickr use "a soft world" 

A decade before Kwok’s letters on "Chinese Restaurant Syndrome" were published, some scientists began doing research on the effects of MSG on mouse brains. In 1968, a neuroscientist named John Olney, also known for his work on aspartame, attempted to replicate earlier studies where mice were fed massive amounts of MSG via feeding tube. The most dramatic result wasn’t in the brain, where he was looking, but their bodies: the mice fed MSG became "obese" (which had a different medical definition in 1968 than it does now, but still referred to unusual fatness). Given that glutamate registers as "deliciousness," one might assume that the difference was that the MSG-fed rats just liked their food a lot more and ate past satiety, but the MSG was administered by feeding tube, so taste shouldn’t have had anything to do with it. Based on his work, manufacturers voluntarily agreed to stop using MSG in baby food.

Subsequent studies have repeated the finding: mice and rats fed large amounts of MSG gain weight, and it’s not entirely clear why. As far as I can tell, the amount of food they consume is generally controlled, although if they have free access to water, perhaps they’re drinking like crazy to make up for amounts of MSG as high as 10 g per day, out of 100 g food total. However, the mice in most of the studies are fed amounts of MSG that far exceed what a human even surviving on instant ramen and Doritos alone would consume. There’s no evidence that the amounts typically consumed as a flavoring do any damage to people, no matter how young. People all over the world eat MSG all the time, both in processed foods and home-cooked foods, seemingly without suffering any negative effects. The growing consensus among people who’ve looked at the research is that

"toxicologists have concluded that MSG is a harmless ingredient for most people, even in large amounts" (Harold McGee On Food and Cooking 2004).

But it does seem like vast amounts of MSG can cause weight gain, sluggishness, and brain lesions in the retinal and hypothalamus regions. I’d advise against getting 10% of your daily intake of food from MSG.

 A Nutritional Yeast Connection?

from Flickr user A random suspicion I haven’t been able to confirm is that MSG might be similar in many ways to nutritional yeast, the worst-named ingredient in the world. Nutritional yeast, also known as "nootch," is primarily used by vegans and some vegetarians as a flavoring agent that adds a slightly cheesy, deeply savory flavor to things ranging from popcorn to sauces to seitan. It also makes a tasty breading for tofu.

According to Wikipedia, "Modern commercial MSG is produced by [bacterial] fermentation of starch, sugar beets, sugar cane, or molasses." Nutritional yeast, on the other hand, is "produced by culturing yeast with a mixture of sugarcane and beet molasses, then harvesting, washing, drying it." Obviously whatever bacteria they use to ferment MSG results in a different product, but I wonder if they aren’t just different iterations of the same process. Ferment some sugar and molasses; in one case, extract the salt composed of sodium cations and glutamate anions and ditch the bacteria that do the fermenting; in the other, keep the yeast. Perhaps? If anyone knows more about the similarities or differences between the two, let me know.

From Flickr user "Fenchurch!"It definitely seems like MSG doesn’t have any of the nutritional benefits of nutritional yeast, which is full of vitamins and minerals and protein, but it would still be a delightful irony to discover that the maligned substance behind a million Chinese restaurant disclaimers is related or comparable in any way to a crunchy, natural food bulk bin staple.

I don’t use MSG often, largely because I prefer the yeasty flavor and nutritional benefits of nootch, but I don’t think homemade chex mix is nearly as good without a teaspoon or so of MSG, and a little bit can perk up lackluster soups and sauces. Most grocery stores still sell Accent, and increasingly carry Maggi sauce and Goya Sazon as well. You can also buy giant bags of it at Asian markets. If you use too much, it will make food excessively salty and overpower subtler flavors, so use a light hand and taste as you go.

More tips on how to use MSG and recipes in future entries.

Against the Soda Tax

awesome depth of field courtesy of Stephane Pompougnac http://www.flickr.com/photos/vox_efx/3063389109/

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 CamposThe 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).

1. Even advocates claim the tax would only lower demand modestly. According to a study that hasn’t been published yet (referenced in the New England Journal of Medicine article) the price elasticity of soda is –0.8 to 1.0, meaning if the price of soda is increased by 10%, consumption should decrease by 8-10%. The $0.01 per ounce tax would actually increase the cost of a 20 oz soda about 20% (unless you’re buying it at a sporting event), so presumably it should decrease consumption by up to 20%. I’m a little skeptical about that, and am looking forward to seeing how they determined its price elasticity, but I sort of doubt that soda is "unit elastic" meaning the percent change in demand will always be approximately equal to the percent change in price. Unit elasticity usually relies on the assumption that a good is readily replaceable—perhaps they assumed that tap water serves all the same dietary, social, and psychological functions as soda? Or that regular soda drinkers will switch to diet if there’s a $0.15 to $0.20 incentive? Nonetheless, their simultaneous insistence that this tax would address state budget problems or fund health care in any meaningful way is predicated on the fact that it’s not likely to decrease demand significantly. Most soda consumers will be more than willing to pay another dime per can of soda.

2. Although sugary drinks have probably contributed to the relatively small average weight gain over the past few decades, no one really thinks soda alone is what’s making people fat. Even for people who might reduce their soda consumption as the result of a sin tax, The New England Journal of Medicine estimates (conservatively by their own admission) that people would probably compensate for an average of 25% of the lost calories by eating or drinking more of something else. If people rely on soda as a source of a "sugar buzz" or have what might be called an "addiction" to sugar, it seems likely that they would compensate with other sugars. Some might substitute with diet soda, but it’s worth noting that longitudinal studies suggest that people who drink diet sodas actually have a greater chance of being obese than people who drink regular sodas. The causal arrow is almost certainly obesity—>drinking diet soda and not the other way around, but if drinkers of diet soda are more likely to become obese than drinkers of regular soda, that certainly challenges the notion that soda is a necessary cause of obesity. The relationship certainly isn’t as linear as the relationship between cigarettes and smoking, which it’s often compared to. And proposed "twinkie taxes" that would levy other calorie-dense, low-satiety and vitamin-poor foods haven’t gained any political traction because just like soda, it’s possible to consume things like frappucinos, Doritos, Wonderbread, instant ramen, or "fast food" remain non-obese. Plus, unlike soda, each of those does contain nutrients generally recognized as desirable. Despite all the cultural stigma and personal shame associated with some "sinful" foods, the healthfulness and morality of most things we eat and drink turns out to be a little too tricky to legislate.

3. The idea that this tax would be limited to "sugary" drinks is almost certainly not going to work in practice. Restaurants and gas stations aren’t going to start charging a different price for their diet soda and unsweetened iced tea than they do for their regular soda and sweetened iced tea, especially when they have self-service soda fountains. While there’s actually nothing more objectionable about taxing unsweetened iced tea or diet soda than regular soda (less, probably, if the former are more likely to be consumed by wealthier people), there’s a good reason the supporters of the tax aren’t calling for it: there’s no moral defense of a tax on soda water or unsweetened iced tea. No one thinks plain soda water makes people fat or causes disease (okay, I’m sure someone somewhere does, but they probably also think crystals heal people and agave nectar is "natural" and microwaves communicate your private personal information to the aliens who abducted Kennedy). 

Some people, even those who are opposed to the tax like Katherine Mangu-Ward of Reason.com, have suggested that we could just eliminate corn subsidies instead. Mangu-Ward notes that the projected annual revenues from the soda tax are, coincidentally, just about equal to the subsidies we pay to corn farmers. Joe Weisenthal makes a similar suggestion over at The Business Insider.

The first problem with this idea is that, as I’ve mentioned before, the farm cost of the corn in soda is only 1.6% of the price. Less than 2 pennies of a $1.20 bottle of soda go to the farmers who grow the corn that becomes high fructose corn syrup. Even if the elimination of the subsidies doubled the price of HFCS, the cost of soda would only go up a cent or two.

The second problem is that not all subsidized corn becomes HFCS. Less than 12%, according to the National Corn Growers Association. Most of it, as anyone who’s seen King Corn or read Michael Pollan knows, is used to feed livestock (how much exactly is a little unclear; I’ve seen a number of claims that eighty percent of all corn grown in the U.S. is consumed by domestic and overseas livestock, poultry, and fish production, but those may be outdated because of the rise of ethanol. Still, the most recent stats I could find on the NCGA website claim that 42 percent of U.S.-grown corn is fed to domestic livestock. The upshot: a substantially larger part of corn subsidies go towards feedlot beef than soda).

Rather than having a comparable effect as taxing soda, Mangu-Ward’s plan is far more akin to a tax on feedlot beef. And that, more even than the power of corn growers, is what would make it politically impossible. Weisenthal mysteriously suggests that it would be politically easier to eliminate "any subsidies that go towards high-fructose corn syrup," as if the industry behind the most-produced crop in the country and all the industries that rely on it have less clout than the "soda industry."

For the record, I’m not opposed to higher beef prices on any moral or economic  or even nutritional grounds. I’m not convinced that corn-fed beef is a necessary part of a healthy diet (although nor am I convinced that it’s necessarily unhealthy either, as the effects of dietary saturated fat and cholesterol seem highly dependent on what else you eat them with), and I suspect that the mass production of cheap meat might contribute to a number of environmental and social ills. I am all for reforming the seemingly-outdated system of agricultural subsidies that encourages certain kinds of farming and discourages other ones, but honestly, I don’t know exactly what that reformed system should look like. And I doubt Mangu-Ward or Weisenthal do either. I suspect that simply eliminating subsidies for the commodity grown in the largest quantities is not the best way. And in any case, it wouldn’t increase the cost of soda, fund health care, or fix state budget crises. As ever, not all simple answers are best.

Things that won’t kill you Vol. 2: Fruit juice

This may seem like a strange thing to argue about, because the popular consensus still seems to be that juice is healthy. Jamba Juice markets itself as "the category-defining leader in healthy blended beverages, juices, and good-for-you snacks." They even use Jamba as an adjective to mean the opposite of high fructose corn syrup and trans-fats (adding those things to juice ""just wouldn’t be Jamba"), which again, constructs the brand as healthy vs. the demon poisons that make people fat. Even if it’s foolish to go looking for truths in advertising, I don’t think Jamba Juice’s branding generally occurs to people as a massive irony or lie. Advocates of banning or restricting soda vending machines in schools often claim that the soda should be replaced with 100% fruit juice with no added sugars, and for many people, a glass of orange juice still represents "part of a nutritious breakfast" strongly with desirable nutrients like Vitamin C.

The Case Against Juice

But a number of health trends have begun cast suspicion on juice, especially the (impartial and incomplete) shift from primarily low-fat to primarily low-calorie and low-carb dieting in mainstream weight-loss culture, and the growing concern about the role sugars (especially fructose) play in personal and national obesity.

On the low-calorie front, people who believe that losing weight or maintaining a healthy weight is all about the basic algebra of calories-in vs. calories-out often end up axing all caloric beverages from their diets because they have a bad satiety-to-calorie ratio—I mean, obviously, right? Fruit juice is just fruit with some or all of the filling fiber removed. If the goal is maximum satiety on minimum calories, you’re better off eating whole fruit and drinking water or artificially sweetened beverages.

On the low-carb front, people who believe that what’s important is not how many calories you eat but what kind are also going to see juice (and sometimes most fruits and vegetables as well) as "unhealthy." It does seem to be true that diets high in carbohydrates drive up insulin levels, slowing metabolism and encouraging the body to store fat. And the overwhelming majority of the calories in most fruit juices are in the form of carbohydrates. Some green vegetable juices have protein content approaching 50% of the carbohydrate content, but that just makes it 75% bad rather than 100% bad, at least as true carbophobes are concerned.

And finally, there are some non-carbophobes who might avoid juice because they’re wary of sugar qua sugar, rather than sugar qua carbohydrate. The carbohydrates in fruit juice primarily take the form of fructose—wikipedia has a handy chart of the kinds of sugars in common plant foods. It doesn’t seem like there’s a true consensus yet about whether or not fructose is especially bad—despite recent studies linking fructose to obesity, even within the medical community, some people still advocate fructose as a "low glycemic" sugar that’s better for diabetics. It basically all comes down to whether you think the fact that fructose is digested in the liver and doesn’t trigger insulin production is a good thing or a bad thing. To link it to other sugar purveyors: pro-agave nectar people should also think that fruit juice is healthy and people who think hfcs is bad because they think it’s "high fructose" compared to other sugars are, well, a) wrong, but b) should also be advocating hfcs-sweetened sodas over fruit juices, which are even richer in sugar.

Personally, I think the evidence that fructose in large amounts causes equivalent blood sugar spikes to other sugar, increased "bad" cholesterol and triglycerides and signs of insulin resistance compared to glucose, and can cause non-alcoholic fatty liver disease consumed in vast quantities suggests that it is certainly no better and possibly much worse for human health than glucose or sucrose. But "worse for human health" is relative, not absolute, and depends a lot on amount, kind, and context. 

What is health?

I’m generally convinced by the argument made by people like Gary Taubes that a diet composed of almost-exclusively proteins and fats might better represent the pre-agricultural, hunter-gatherer diet (as would cyclical feast and famine) and prevent carbohydrate-induced insulin resistance and fat storage. Jared Diamond makes some of the same points in Guns, Germs, and Steel. But the benefits of agriculture ultimately outweighed the costs—both for the species as a whole and measured by individual health metrics. In the immediate aftermath of the transition to agriculture, lifespans and average height decreased, but after a few thousand years, people depending on rice, corn, and wheat began to get healthier again

Does that mean carbohydrates are a healthier basis for a diet than proteins and fats? No. But it does mean that people can (and do) live very long lives uninterrupted by diet-based disease during which they are strong and energetic enough to physically do anything they want to do while eating a diet consisting substantially of carbohydrates. And I think that’s not a bad working definition of "healthy."

It seems to me that the debate comes down to a difference between ideas about nutritional "health" based on what might be theoretically optimal (for a very limited set of criteria), ideas about health based on potential pathology, and ideas about health based on actual health outcomes

Fear of juice is based on the first two—the idea that either people should eat as few carbohydrates as possible in pursuit of some sort of optimal diet, or that the fructose in juice will cause fatness (an aesthetic problem, not a medical problem) or disease and eventually death. Based on actual health outcomes, I think it would be almost impossible to make a case for the claim that drinking fruit juice—occasionally or regularly—is categorically unhealthy or the direct cause of disease or death.

In fact, things like fruit juice and hamburgers and Doritos, which can each be constructed as "unhealthy" are hard to entirely rule out of a "healthy diet." Even proponents of a soda tax generally agree that the only reason soda is a reasonable target is because it has no identified nutrients (what would happen if they fortified them, I wonder?).

The nutrient-density of juice is the primary reason for the long tradition of juice being regarded as a health food. If your concern is about essential vitamins and minerals (like many older models of nutrition, which people like Marion Nestle stand by) or consuming carbohydrates for fuel, which many physically active people still do, it’s hard to argue with the healthfulness of juice. I agree with Michael Pollan’s claim that popular beliefs about health often fall prey to "nutritionism," or the attempt to reduce food and nutrition to scientifically-identified nutrients and vitamins. At the same time, I don’t think you have to be brainwashed by the continued prevalence of nutritionism to believe there’s good evidence that many of the nutrients that scientists have identified are actually valuable or promote health and well-being (even if they’re not the only valuable aspects of food).

All juices are not created equal

The person who requested this entry was concerned specifically about fresh juices being portrayed as unhealthy, because they seem to have been smeared by concerns about packaged juices being just other source of dietary sugar.

While not all fruits lend themselves as readily to the production of refined sugars as sugar beets, some like apples, pears, and grapes can be turned into a nutrient-poor sweetener without most of the fruits’ color, flavor, or minerals and many fruit juices marketed as 100% natural fruit juices, like Juicy Juice, are sweetened with fruit juice that’s basically been turned into a sugar syrup. The nutritional distinction between those drinks and hfcs-sweetened soda is probably negligible regardless of whether your primary concern is calories, carbohydrates, sugar, or vitamins.

But the reason packaged juices often combined with fruit-based sugar is that many fruit juices aren’t actually that sweet on their own, or their sweetness is offset by the intensity of the flavor, as anyone who’s ever tried 100% cranberry or concord grape or cherry or blueberry juice knows. The fresh juices you can get at juice bars or make at home are calorie-dense, but they’re also extraordinarily nutrient dense and not likely to be consumed in quantity or alongside meals. They’re more often enjoyed on their own, like a snack, particularly after a workout—basically just like fruit. When you leave in some of the pulp, it becomes even less nutritionally distinct from fruit, and when you include vegetable juices or the juices of things like wheatgrass and ginger which are difficult or unpleasant to eat raw, you may be enjoying something that could, by some criteria, be healthier than a piece of fresh fruit.

Some juices even have pretty well-established medicinal uses. Cranberry juice, for example, can help prevent and cure urinary tract infections (that study notes the existence of "diet" cranberry juice, which I’d never heard of, but now that I have I wonder why there aren’t more "diet" juices sweetened with artificial sweeteners rather than pear or grape juice-sugar. Not that those would necessarily be "healthy" by everyone’s standards, especially given the links between saccharin and cancer and suspicions about the healthfulness of aspartame and sucralose…)

Ultimately, while I don’t think even the occasional hfcs-sweetened Capri Sun is incompatible with a "healthy" diet and life, I think it’s unreasonable to conflate fresh juice without added sweeteners with juices sweetened with refined juice-sugar. I guess people trying to eat an "optimal" diet a la Gary Taubes should avoid all juices, fresh or no, but I don’t envy them their carbohydrate-less life, nor am I convinced that the total deprivation of many foods that have aesthetic, gustatory, social and/or cultural value is necessarily "healthy" or "optimal" either. For the vast majority of people who think fruit and vegetables are part of a healthy diet, fruit juice and especially fresh fruit juice should also pass muster as a "healthy" choice especially when consumed in moderation, which I suspect fresh fruit juices usually are.