Against metabolism

the pound mouse, a leptin-insensitive mouse used to study obesity in the lab

the pound mouse, a leptin-insensitive mouse used to study obesity in the lab

Note: My internal definition of metabolism, in the context of “I have a slow metabolism”, translates to “basal metabolic rate”, scientifically speaking. This is also how I’ve been perceiving most people to mean it, when speaking colloquially. “Metabolic rate” is broader and includes total daily energy expenditure–in addition to basal metabolic rate, it includes energy burned by movement and in digesting food. When I was talking with my husband about this blog post after it was mostly finished, he expressed surprise that “how hungry you are” isn’t part of metabolism, so in some cases the reason people are attributing so much importance to metabolism may be that their understanding of the meaning of “metabolism” is different than mine.

I think that metabolism is overemphasized in online fat activism.

People like to point out that individual fat people don’t necessarily eat more than the average thin person–and the converse, that individual thin people sometimes eat much more than the average fat person. (This is especially likely to be true if you compare a fat person who is short, female, and older to a thin person who is tall, male, and a teenager.) People also like to point out that for any given weight (even if fat-free mass is well-preserved), a person who is at that weight after a diet will have a slower metabolism than a person who’s at that weight who hasn’t dieted. This is known in the scientific literature as adaptive thermogenesis*. (Conversely, metabolism disproportionately increases for people who are above their normal weight.) (When it comes to long-term weight-loss maintainers, the research is mixed, but it seems to be quite well established that those with relatively-recent weight loss burn fewer calories–20-25% fewer–than would be predicted by their new body weight.)

And this is true as far as it goes. But it seems to me that metabolism is one of the least important factors in why people weigh what they do (which is not to say that’s it’s completely unimportant), and it is increasingly unimportant the more people that people let their hunger and fullness signals guide what they eat, rather than eating mindlessly or eating what they believe they’re “supposed to” eat, whether “supposed to”  means “what Mark Bittman says” or “what Weight Watchers says” or “manly men are supposed to order big steaks” or “this is the amount of food the restaurant served me/my spouse served me/what’s in the package, so I guess that’s what I’m supposed to eat”.

The more important metabolism is in affecting people’s BMI, the more we would expect to see that short people have higher BMIs than tall people. And in fact, we do see that to some degree–though apparently the relationship has been getting weaker, and tall people’s BMIs have been catching up to short people’s. (How this may compare to people who are genetically predisposed to become fat in the current food environment is left as an exercise to the reader.) Additionally, some argue that one of the flaws of the BMI system is that while it works well for people of about average height, it gives short people a lower BMI than they “should” have, and vice versa for tall people. Still, it’s not as though there are no thin short people and no fat tall people. Anecdotally, I remember a short, thin friend talking about how a normal-looking-to-me pastry was SO BIG and made her so full, she couldn’t eat it all.

The folk explanation of hunger seems to go something like this: everyone (sometimes even regardless of age, height, activity level, and sex) is equally hungry. Fat people don’t actually require more food to sate their hunger, they just overeat all the time. (See JK Rowling’s description of how Dudley Dursley eats. She seems to be thinking, “Well, this is how I would feel if I ate that much–overstuffed and uncomfortable–so if other people eat that much, that must also be how they feel.”) If lifting weights allows you to eat more food and not gain fat, then that’s great, and we won’t even bother to ask whether you’ll have an increase in hunger that matches or even exceeds the greater amount of food you’ll “be allowed” to eat. Thin people (often teenagers) who eat a lot aren’t eating a lot because they’re that much more hungry than the other thin people; they just can “get away with it”, so they do. If you look at hunger and fullness hormones like ghrelin and leptin, this, like many folk understandings of natural phenomena, does not seem to be how it actually works.

In Traci Mann’s recent Washington Post interview, she talks about, among other things, the Cliff’s Notes version of why people usually regain weight after dieting. The change in metabolism is one of three factors that she lists; the other two are neurological (“Basically your brain becomes overly responsive to food, and especially to tasty looking food. But you don’t just notice it — it actually begins to look more appetizing and tempting.”) and hormonal (“As you lose body fat, the amount of different hormones in your body changes. And the hormones that help you feel full, or the level of those rather, decreases. The hormones that make you feel hungry, meanwhile, increases. So you become more likely to feel hungry, and less likely to feel full given the same amount of food.”).

I suspect that the hormonal changes are the ones that have the most powerful effect on weight regain, and that hormones have the most powerful effect on weight in general. (Do the neurological changes have something to do with the “eat impulses” that DebraSY describes?) While studies have found that things like how much food is presented does affect how much people eat (at least at that particular meal–I suspect that those bottomless soup bowls, different sized plates, etc are often balanced out by less food at a later meal, or a missed snack) my sense is that the strongest influence on how much people eat is how hungry they are, and that ultimately is mostly controlled by your homeostatic mechanisms, the stuff that tries to keep you in a given set point range, which is where the hormones come in.

(Complicating this, metabolism is affected by these hormones–or at least one of them. While looking up citations for this post, I came across a study that found that injecting leptin into people who’d recently lost 10% of their body weight nullified the slowdown of metabolism that caused them to need disproportionately (20-25%) fewer calories. So in a way it is misleading to talk about them as separate factors.)

There is a difference between “genes that affect weight” and “particular genes that we’ve identified that affect weight”, but with that caveat in mind: so far only one of the genes involved in body weight that’s been discovered, MRAP2, works by decreasing metabolism rather than other mechanisms such as increasing hunger.

I suspect that I am not one of those people with an abnormally-slow metabolism. My subjective assessment is that I eat about the same amount as an average man my age–I’m more active than a lot of people, but still, I think I do eat more than the average woman my age. But it’s because I am hungry.

My theory about why people put so much emphasis on metabolism: eating the same amount of food but weighing more feels a lot more concrete and objective as a defense of being fat than saying that you get hungry more easily. And people can easily assert that fat people probably aren’t really more hungry, they’re just deluded or not as tough in the face of hunger or whatever. And yet, we have the pound mouse, which gets so large because of the lack of a functioning leptin receptor, not because of how it extracts energy from food–and certainly not because of some genetically-encoded tendency for it to lie to itself about how hungry because it’s looking for a justification for being fat. And yet, if we lose 10% of our body weight, we have the same alterations to our leptin and ghrelin levels (and the same changes in energy expenditure relative to body weight) as a thin person who loses 10% of their body weight. And yet, plenty of anti-fat people will say “if you need to eat less than other people to be thin, just eat less”–but it’s not so simple to do that when you have neurological and hormonal changes trying to get you to do exactly the opposite. And yet, people will assume that fat people are deluded or lying when they say that they don’t eat more than other people. (They never seem to consider that they’re deluding themselves with the idea that they’re thinner because they work harder at being thin.) But we shouldn’t have to justify ourselves to these people in the first place. We’ve been chided all our lives to second-guess whether we’re really hungry, and we don’t need their help.

*How adaptive thermogenesis works, from “Metabolic adaptation to weight loss: implications for the athlete”:

Metabolic rate is dynamic in nature, and previous literature has shown that energy restriction and weight loss affect numerous components of energy expenditure. In weight loss, TDEE has been consistently shown to decrease [38,39]. Weight loss results in a loss of metabolically active tissue, and therefore decreases BMR [38,39]. Interestingly, the decline in TDEE often exceeds the magnitude predicted by the loss of body mass. Previous literature refers to this excessive drop in TDEE as adaptive thermogenesis, and suggests that it functions to promote the restoration of baseline body weight [1315]. Adaptive thermogenesis may help to partially explain the increasing difficulty experienced when weight loss plateaus despite low caloric intake, and the common propensity to regain weight after weight loss.

Exercise activity thermogenesis also drops in response to weight loss [4042]. In activity that involves locomotion, it is clear that reduced body mass will reduce the energy needed to complete a given amount of activity. Interestingly, when external weight is added to match the subject’s baseline weight, energy expenditure to complete a given workload remains below baseline [41]. It has been speculated that this increase in skeletal muscle efficiency may be related to the persistent hypothyroidism and hypoleptinemia that accompany weight loss, resulting in a lower respiratory quotient and greater reliance on lipid metabolism [43].

The TEF encompasses the energy expended in the process of ingesting, absorbing, metabolizing, and storing nutrients from food [8]. Roughly 10% of TDEE is attributed to TEF [44,45], with values varying based on the macronutrient composition of the diet. While the relative magnitude of TEF does not appear to change with energy restriction [46], such dietary restriction involves the consumption of fewer total calories, and therefore decreases the absolute magnitude of TEF [41,46]. NEAT, or energy expended during “non-exercise” movement such as fidgeting or normal daily activities, also decreases with an energy deficit [47]. There is evidence to suggest that spontaneous physical activity, a component of NEAT, is decreased in energy restricted subjects, and may remain suppressed for some time after subjects return to ad libitum feeding [29]. Persistent suppression of NEAT may contribute to weight regain in the post-diet period.

In order to manipulate an individual’s body mass, energy intake must be adjusted based on the individual’s energy expenditure. In the context of weight loss or maintaining a reduced body weight, this process is complicated by the dynamic nature of energy expenditure. In response to weight loss, reductions in TDEE, BMR, EAT, NEAT, and TEF are observed. Due to adaptive thermogenesis, TDEE is lowered to an extent that exceeds the magnitude predicted by losses in body mass. Further, research indicates that adaptive thermogenesis and decreased energy expenditure persist after the active weight loss period, even in subjects who have maintained a reduced body weight for over a year [14,48]. These changes serve to minimize the energy deficit, attenuate further loss of body mass, and promote weight regain in weight-reduced subjects.

TL:DR version: total energy expenditure includes the energy you burn just by existing, the energy you expend during exercise, the energy you expend by moving but not exercising, and the energy you use to digest food. When you lose weight, not only are all of these reduced because of your reduced body size, but all of them are also reduced because your body works more efficiently (beyond what would be expected just by your smaller size) in using energy for just existing and for exercising, because you move around and fidget less, and because all these other adaptations mean you need less food to maintain your weight and so you use less energy digesting food.

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There’s no such thing as an “anti-science” answer to a nonscientific question

From time to time I come across people saying that Health At Every Size and/or Fat Acceptance is “anti-science”.

People who say that tend to be making at least one of two mistakes. Continue reading

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The power of fat-shaming vs thin-shaming

There’s a reason why the tagline for my blog mentions size acceptance. While my primary focus is on fat acceptance and health at every size, I would generally recommend the same things for skinny people that I would for fat people. I believe that, even if they are “underweight”, in most cases the best thing that skinny people can do for their health is listen to their bodies: eat when they’re hungry, and do exercise that feels good (including in a “challenges are fun!” sort of way) rather than pushing through pain. And body-shaming of any kind is just plain mean.

But I agree with posts like this that skinny-shaming and fat-shaming are not the same thing. They are both bad, but they are not equally bad because they are not equally powerful. One has the weight of fashion, Hollywood, and the moral panic about obesity behind it, and the other does not.

If they were equally powerful, when people wanted to hurt someone thin (but not runway-model-thin) like Cassey Ho, they would mostly throw “you look anorexic” and “eat a sandwich” at her rather than telling her how fat she is. Tellingly, after she photoshopped a selfie to look thin, she got a “still too fat” comment. I don’t think I believe the person writing it really thought she still looked fat in the picture; I think they said it just to hurt her. But that is more proof of how much power fat-shaming has. That is why it is one of the first weapons people reach for.

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I’ve got some bad news for you…

In the USA, my home country, consumption of fruits and vegetables is plummeting. Consumption of red meat is soaring, as is sweetener consumption. Obesity rates keep going up. Americans are getting less and less exercise. Deaths from heart disease keep going up.

April Fool!

In actuality, compared to levels in 1985, fruit and vegetable consumption has gone up, red meat consumption has gone down, and consumption of sweeteners is about the same. The obesity rate hasn’t changed since the early 2000s. Americans have increased their exercise since 2000. Age-adjusted deaths from heart disease are down by more than half compared to 1950.

If you find any of that surprising, consider why that is. Remember that the media has a bias toward sensationalism and bad news. Don’t forget to take health news stories, and science journalism generally, with a grain of salt.

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Look AHEAD vs. DPP?

One of the articles I came across when researching my last post was called “Diet, Diabetes, and Doubt: Is Preventive Medicine Lost In Space?” by David Katz. I wanted to make a few quick points about it.

Dr. Katz writes:

The AHEAD methodology also helps account for the putatively disappointing results of the long-term study. Diabetes requires treatment—so all patients in AHEAD were treated. Those in the lifestyle intervention group reduced their reliance on medication, while those in the control group took more. But since failing to treat diabetes with state-of-the-art medication is unethical, everyone was provided that. The study was actually comparing feet and forks to pharmacotherapy. When both intervention and control groups are being treated, differences between them diminish, an occurrence known in research as “bias toward the null.” This exerted a profound effect in the AHEAD trial, making the positive findings more noteworthy still.

In other words, the difference between the groups would be greater if neither group had modern medical treatment–but why is that even a relevant question? Are we trying to find out what kinds of benefits people with diabetes would experience if they followed a program similar to those in the intervention group of Look AHEAD compared to normal treatment by their doctors–a practical question–or are we trying to prove that fat=bad? The goal of the study was not to find out how best to treat diabetes in areas with little or no access to medication, or how to treat diabetes in people with bad/no health insurance.

Still, the fact that the study looked at people who already had well-controlled diabetes even before the start of the study and who had access to appropriate medication is an important caveat for people who have poorly-controlled diabetes and/or do not have good access to appropriate diabetes drugs–or for people who are having trouble finding drugs with tolerable side effects. Even if, like me, you are aggressively skeptical about the magnitude of the contribution of BMI to health in order to correct for societal bias in the opposite direction, I think at least the exercise portion of the intervention would be helpful to people with poorly-controlled diabetes.

Also (as implied by Katz’s later words that “both intervention and control groups are being treated”) the study was not comparing “feet and forks to pharmacotherapy”, they were comparing feet and forks plus pharmacotherapy to pharmacotherapy alone. While the intervention group needed less medication, they still benefited from medication in this study.

“But to the extent that the negative results, with regard to cardiovascular event prevention, remain both surprising and disappointing, there is a fundamental explanation for them: too little, too late. What works for prevention may not always work nearly as well for treatment.”

This article’s overall point is not wrong–the Look AHEAD study doesn’t necessarily overturn the results of the DPP study, and an intervention may work for prevention but not treatment. (Remember when the protagonist’s mom in 50/50 wants to give him green tea? [relevant part starts at 1:50]) But there’s more to consider: how do the two studies compare in rigor? And what about the publishing bias towards positive findings? A study finding no effect of a lifestyle intervention on preventing diabetes isn’t going to be cited by “virtually every clinical and clinical research diabetes paper”. (See Ioannidis’ “Why Most Published Research Findings Are False”.)

In fact, although both the DPP and Look AHEAD were fairly rigorous studies involving thousands of participants, the DPP only lasted an average of three years of study per participant. A followup, DPPOS, looked at the longer-term benefits of the initial intervention; they were still present but attenuated. This suggests that, although DPP’s intervention is often described as “preventing” or as “preventing or delaying”, it would be more accurate to describe it as “delaying” diabetes. And delaying is great! But not only does “delaying” not fit into our black-and-white thinking that you’re either healthy or you’re not, nor into our moralizing “if you act right/repent of your wicked ways, you will be healthy forever until you peacefully die of old age at 100″, nor our related, just world theory-inspired “health is under your complete control and genetic factors are trivial”, it just doesn’t make as good a headline.

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The Look AHEAD study: a rare long-term weight loss study

I’ve blogged before about the Look AHEAD Type 2 diabetes study, but mostly focused on the effect of the weight loss on cardiovascular events, which is what the study was designed to measure, as well as comparing the amount of calorie restriction to some reference points. I was looking at it again recently and thought I would examine it as a study of weight loss itself, as it is by far the longest-running study of weight loss that I have seen. According to Dr. Thomas Wadden, the lead author of the study, “This is the largest and longest controlled evaluation of a behavioral weight-loss program to date.” It was also a fairly large study, with 5145 participants.

(The Fat Nutritionist has a good, more general overview of why diets tend to fail in the long term. David Spero has a post about Look AHEAD worth reading on Diabetes Self-Management.) Continue reading

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Historical Fat and Not-Thin People, Part 4: “Stagecoach” Mary Fields

Mary_Fields“Stagecoach” Mary Fields was not exactly fat: at 6′ tall and ~200 lbs, she had a BMI of about 27, the middle of the overweight range. Probably, based on accounts of her life, a lot of that was muscle. But I couldn’t resist featuring her because of her story. This post by Kristen Majewski is one of the best online biography I’ve found of her; this one at the Toledo Blade is also very good and contains some reflections from the archivist for Toledo’s Ursuline Convent (where Mary Fields worked for part of her life), Sister Kathleen Padden, as well as some of the nuns there before her. According to the Toledo Blade:

Miss Fields arrived by train in 1878. As Mother Amadeus helped her old friend get settled in her new quarters, she asked if there was anything she needed.

According to the book Working for the Ursulines, Miss Fields answered, “Yes, a good cigar and a drink.”

Continue reading

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