Reminder: scientists’ attitudes affect what they investigate

You may have seen the headline that a new species of praying mantis was discovered, and named after Ruth Bader Ginsburg. Here’s what I consider the really interesting part:

Typically, researchers study mantis specimens’ male genitalia to delineate their species. But Sydney Brannoch, the Ph.D. candidate at Case Western Reserve University who led the ginsburgae study, decided to study female mantis’ genitalia instead—and, thanks to her innovation, was able to distinguish Ilomantis ginsburgae as a new species. (The specimen she studied had actually been sitting around since 1967; you can learn more about Brannoch’s methodology here.)

One of the most important ways that scientists’ goals, attitudes, and beliefs can influence how science is done is in what question is asked. An anecdote (from here) about industry funding of scientific studies put it this way: “Industry funding doesn’t bias the results, but it does buy the question.” (Of course, given positive publication bias, the money/persistence to ask a certain question over and over can affect what we think we know about the answer to a question.) But it’s not just industry funding that influences what questions get asked. In a society where weight is seen as the obvious cause of any health issue a fat person might have, the idea of looking at causes that are correlated with weight instead of assuming it’s the weight itself might seem ridiculous and not worth investigating.

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A response to Emma Lindsey’s “Why do fat people even care about dating skinny people?”

I thought that this Emma Lindsey piece did have some good points, but she also misses some stuff that seems obvious to me, as someone who’s actually fat and involved in fat acceptance, and she definitely comes off as condescending at times. But she’s also wrong in an interesting way instead of the same-old-same-old anti-fat-acceptance arguments.

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A bad relationship waiting to happen? Will the fat mouse’s constant body criticism sap the thin mouse’s self-esteem? Is the fat mouse setting up the thin mouse as the arbiter of attractiveness?

Emma Lindsey conflates wanting to date skinny people and wanting to be seen as equally valuable as skinny people (say, wanting to see more fat/skinny pairings in magazine ads). Romantically valuable, in this case, but it’s part of the overall project of wanting to be equally valuable.If fat people are only ever with other fat people, that implies there’s some reason for fat and skinny people not to date each other, and in this culture the implied reason is that a fat person is always too unattractive for a skinny person to date, that it would be inconceivable for a skinny person to find a fat person attractive–which Lindsey, as a not-fat person, knows from experience is not true, in addition to the fact that it reinforces all the bad memes about fat people being disgusting, etc. Perhaps it’s unavoidable that this will subconsciously “reinforc[e] the notion of “attractive” people as judges”, but I don’t think it’s better to never show fat/skinny couples, as if they are never a thing that happens and a skinny person would never be seen with a gross fat person. Continue reading

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Calories In-Calories Out: Not Even Wrong

I recently read an overall-pretty-good article in The Atlantic called “What Does a Calorie Measure?” about how calorie counting is being criticized by some people, often in favor of focusing on satiety. This helped me to hit on what I’ve decided is the perfect way of describing the calories in-calories out, ELMM philosophy: not even wrong.

Sometimes a good idea will get oversimplified in more casual speech–a blog post about how intent is not fucking magic becomes “intent doesn’t matter”, or “calories in-calories out uses two numbers that are harder than people think to calculate and most people aren’t that good at ignoring hunger anyway” becomes “calories in-calories out is wrong”. But it’s not wrong. It’s not even wrong.

The more strict meaning of not even wrong is that something is bad science because it’s unfalsifiable. Calories in-calories out fits this sense in a way–the average dieter isn’t going to have access to the kind of precision measuring equipment (measuring temperature or carbon dioxide) to calculate precisely how many calories they’re burning, and they’re probably going to rely on food packaging or measuring cups–or even more imprecisely, estimating “a fist-sized portion”, etc. to give them a rough count of calories. So if they gain or lose more weight than predicted, then they have to assume that their estimates of how many calories they burned or how many calories they took in were wrong. If scientists only had the tools available to the average person, calories in-calories out would be unfalsifiable.

But what I’m primarily getting at uses the phrase “not even wrong” in a looser sense. Calories in-calories out is not useful information. Most people most of the time will not be able to follow a food plan that relies on ignoring internal cues–even leaving aside all the problems with correctly estimating calories in/out. Satiety will be a more relevant cue to most people than the calories on a nutrition label.

Also, some thoughts about that Atlantic article not related to the main thrust of this post:

-If the salad is only 300 calories, no, I’m not going to feel an absence of hunger for several hours after a chicken salad, trust me. I’ll probably feel full longer than with 300 calories of cheesecake, but still.

-Is the idea of satiety useful from a HAES perspective? I think it can be. If you focus on it not as a way to weigh less but as a way for your body’s hunger and fullness signals to work the way they’re meant to with foods that are not too far from traditional human diets, and don’t interpret as an all-or-nothing, only-eat-foods-with-high-satiety-values, I think it makes sense.

 

 

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Genes and BMI Part 2: Evidence for a genetic influence on weight in a post-‘obesity epidemic’ world

My previous post talked about how it is possible for differences between groups to have one cause, and differences within those groups to have a different cause–that disproving changing genes as a cause of the ‘obesity epidemic’ does not prove that who gets fat and who doesn’t in our environment is due to, say, what your parents fed you as a child more than your genes. (There’s also a pretty good explanation of heritability and BMI here.) But is there positive evidence that it is not only possible, but that is indeed what’s happening–that genes play a fairly large role in who gets fat and who doesn’t in an “obesity epidemic”? Yes.

There’s a reason I’m being very careful to say “caused by changing genes” and not “caused by genes” as a great deal of popular writing does: whether and how much we gain weight given a change in environment is influenced by our genes, at both an individual and macro level. Just as the increase in height in response to more/better nutrition was part of our genetic potential, the population-wide increase in weight was possible because of our genetic potential. Both a general human tendency towards “thrifty genes”–genes that were influenced by a history of food shortages to store lots of fat in case of future food shortages–and differential “thriftiness” in individuals can lead to people putting on weight in good times in anticipation of bad times. And a tendency to put on more weight than before in good times after experiencing lean times–or a diet, since the intellectual part of our brains isn’t really talking to the homeostasis-keep-us-from-starving part of our brains–is also part of our genetic potential.

We can probably rule out “what your parents fed you as a child” as a reason why some people get fat and some don’t: adopted children’s BMIs are influenced a great deal by their biological parents’, with no significant influence from their adoptive parents’ BMIs. A study by Dr. Albert Stunkard of adult twins, some of whom had been adopted, found that the twins’ BMIs were very similar, and just as close together whether they were raised together or apart.

A deliberately-engineered change in environment can also show just how strong the genetic influence on weight is. A study by Dr. Claude Bouchard of 12 pairs of identical male twins found that within each pair, the two twins were highly similar to each other in amount and location of weight gain when Bouchard deliberately overfed the men by an extra 1000 calories a day–but there was a great deal of variation between different twin pairs. The pair gaining the most added about 29 lbs, while the pair gaining the least added about 9.5 lbs. (Most of the twin pairs returned to their original weight when taken out of the artificial-overfeeding environment.)

If it were just these three studies, then maybe things wouldn’t be so clear-cut. These were three of the ones that I remembered reading about in the past and/or that Traci Mann refers to in Secrets From The Eating Lab. But the title of this editorial from 2008 perhaps sums it up best: Obesity–still highly heritable after all these years.

(None of these measures of genetic effects on BMI are based on finding specific genes that influence BMI. Adoptee and twin studies are based on how much related or genetically identical individuals resemble each other, not on finding particular genes.)

Do any of these studies mean that significantly changing one’s BMI is completely impossible for everyone? No, but they do mean that for most people, the reason they weigh less or more than the average person in their environment is not because of some great effort or virtue on their part (or lack thereof), or because their parents gave them the exact right foods in the exact right ways, but because of their genes. And, sure, because of some of the new trendy research topics like gut bacteria, too. Some people will, through extraordinary effort, life circumstances, etc. be able to defeat their gene/environment combo, but most people who think they are thin through hard work would probably only be slightly fatter without their efforts. In other words, most thin people bragging about how they are thin through their own effort are the proverbial “born on third, think they hit a triple”. There was an editorial that I’ve never been able to find again, but it had a metaphor that really struck me: people would ask the writer, Isn’t it obvious that if you took two people and gave one free access to a constantly stocked fridge and gave the other carefully rationed meals, one would be fatter? The writer’s response: sure, but the difference in environment between people’s homes in obesity-epidemic countries is typically more like giving one person one constantly-stocked fridge and the other two constantly-stocked fridges.

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Genes and BMI Part 1: Between-group variation and within-group variation are different things!

The Atlantic recently published a piece that is overall worth reading (and which I hopefully will write a separate blog post about soon), Rethinking the Calorie. It’s a relatively comprehensive look at the reasons why measuring “calories in” is not straightforward at all; it spends a lot of time on gut microbes in particular. One thing that they get wrong, though they are hardly alone in getting it wrong, is this:

Until recently, the idea that genetics plays a significant role in obesity had some traction: Researchers hypothesized that evolutionary pressures may have favored genes that predisposed some people to hold on to more calories in the form of added fat. Today, however, most scientists believe we can’t blame DNA for making us overweight. “The prevalence of obesity started to rise quite sharply in the 1980s,” says Nestle. “Genetics did not change in that 10- or 20-year period. So genetics can only account for part of it.”

The change in obesity rates between population does not imply that there isn’t a significant role for genetics in who gets fat. The amount of within-population variation is an order of magnitude different than the change in weight of the population between the 1980s and now.

Americans have gained about 30 lbs, along with about an inch of height, since the 1960s. But you can also find Americans with a three hundred lb difference in weight–100 lb people and 400 lb people both exist, and neither are all *that* uncommon. Speaking of that one-inch increase in height (or the ~4-inch increase in height that many countries have experienced over the last hundred years), that also doesn’t disprove that genetics play a significant role in height, and no one would seriously argue that it did, because differences between populations and the differences within populations don’t necessarily have the same causes.

For that matter, the differences in gut microbes and their association with BMI is all very interesting (sincerely!), but since they’re looking at differences between individuals in the same population and not differences between the gut microbes of, say, 1960s Americans and now, they’ve done nothing to show that gut microbes have anything to do with the significant changes in BMI at the population level known as the “obesity epidemic”.

This isn’t the first time that the difference between within-group variation and between-group variation has come up in a political context. It’s also come up in the context of race and intelligence, or more accurately, IQ tests, since we can’t directly measure actual intelligence. Performance on IQ tests has a significant heritable component; some people have tried to argue that this means that if black people as a group have lower IQ scores, it must be for genetic reasons. Those people are making a similar error, but in reverse–they are assuming that the cause of between-group and within-group differences must be the same, but they are taking a big component of within-group differences and assuming it must apply to between-group differences; in the case of BMI, people are also assuming that between-group and within-group differences must have the same cause(s), but they’re assuming that the “real” cause is the between-group cause.

An analogy I’ve seen used in the context of race and IQ is also useful here. Imagine two gardens with many varieties of corn growing in them. Within each garden, environmental conditions are the same. Each part of the garden is getting equal amounts of light, water, fertilizer, etc. The only reason the plants vary within each garden is because of their genes. But one garden gets optimal light, water, fertilizer, etc. and the other does not get the right amount of those resources. The difference between the gardens is not because of the plants’ genes, it’s because of their environment.

The concept is a bit counterintuitive, but it’s something I would expect scientists and experts on nutrition and weight to understand. And yet I see a surprisingly large number who don’t, even among those who are a bit smarter than to go along with “everyone knows” in other cases–for example, Barbara Berkeley. But definitely plenty from a certain food & nutrition writer who seems to be a very popular source of quotes and commentary for journalists.

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Gut bacteria and blood sugar

There is an interesting new study out that looks at gut bacteria, a personalized-diet-creating algorithm, and blood sugar. Basically, they collected a bunch of data including biometrics (e.g. age, weight, hip circumference, A1c), family history, and, notably, gut bacteria (in a stool sample), then had participants use a continuous glucose monitor and keep track of their food, exercise, and sleep for week, then used that data to create an algorithm predicting blood sugar response, used that algorithm to create personalized “good” and “bad” diet plans that would either keep blood sugar levels down or spike them, respectively, pitted those diets against “good” and “bad” personalized diet plans created by a dietician with access to the same meal and glucose monitor data, and along the way looked at the way glucose response changes and is changed by gut bacteria.

I read a few articles and a blog post about this study before reading the full text of the study itself, and whether because I was reading quickly and missed a small but important word that went against the general emphasis of the article (I missed a “both” in this Atlantic article), information was omitted, the articles were just unclear, or actually misleading (it seemed like this ScienceDaily article’s repeated vague references to diets “working” were designed to encourage people to think of weight loss rather than blood sugar response), there were several ways that the study was not what it initially appeared. Continue reading

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Review: Secrets from the Eating Lab

I first became interested in this book after reading an interview with author Traci Mann from shortly before the book came out. If her name seems familiar, you may recognize it from a study that is often cited in fatosphere blogs, Medicare’s search for obesity treatments: diets are not the answer [article/press release about the study]. This is a relatively short, readable book, with occasional flashes of humor, which despite its brevity is a fairly comprehensive look at the science around weight loss and gain, set points, and the psychology behind eating. However, despite its strong critique of diets and the weight loss industry, and its skeptical stance towards the importance of BMI, it is not 100% weight neutral because it recommends staying at the low end of your set point range, so readers for whom any pro-weight-manipulation talk is problematic should proceed with caution.

Continue reading

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