Why the brain matters in obesity


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Those of you interested in nutrition may already be following the online debate between Gary Taubes and Stephan Guyenet — back in August, Guyenet critiqued Taubes’s carbohydrate-insulin hypothesis, and now Taubes is returning the favour by critiquing Guyenet’s food-reward hypothesis. I’m not going to get into the nitty-gritty of the debate here, except to say that I think it’s a mistake to frame this debate as an “either-or.” Despite Taubes’s insistence to the contrary, the two ideas can coexist — and even if they do, I suspect they still don’t add up to the “whole truth” about obesity. Here’s one reason why.

In one of his recent posts, Taubes makes the distinction between body-centred and brain-centred theories of obesity (or you can think of it as physiology vs. psychology, one of his commenters points out). Taubes believes obesity originates in the body:

In this paradigm, specific foods are fattening because they induce metabolic and hormonal responses in the body — in the periphery, as its known in the lingo — that in turn induce fat cells to accumulate fat. The brain has little say in the matter.

Leaving aside the precise mechanism, I largely agree with the idea that regulation of calories in and calories out isn’t under the conscious control of the brain. And I’m pretty sure Guyenet would agree too. But I’m not quite ready to conclude that the brain plays no role.

This is a figure from a study published in the Archives of Pediatrics & Adolescent Medicine in 2009, from researchers at Penn State (no wisecracks please). The text is freely available here. The study followed 1,061 children, who were tested at the age of 3 for self-control (the length of time they were able to refrain from playing with a fun toy after being asked not to) and then again at the age of 5 for delayed gratification (the classic Marshmallow Test, which I’ve written about before, except using M&Ms, animal crackers or pretzels: they could have a small amount anytime, or a larger amount if they waited 3.5 minutes). Then their BMI was tracked until their turned 12.

The results are pretty clear: doing well on either or both of the impulse-control tests predicts less weight gain nine years later. So the question is: how can a test that involves (not) playing with a toy when you’re 3 years old predict future weight gain, if the brain has no say in weight gain?

Let me be absolutely clear: I don’t think “better impulse control” will play any useful role in weight loss for the vast majority of people. Once you’re overweight, I suspect physiology totally swamps psychology in most cases. But if you’re looking for an overall understanding of the mechanisms of weight gain and loss — and if, like Taubes, you insist that the correctness of your theory means that all alternate ideas must be 100% incorrect — then I believe you can’t ignore the brain (and its interactions with the modern food/physical activity environment) completely.

9 Replies to “Why the brain matters in obesity”

  1. I’ve long been a fan of Guyenet, but sometimes his explanations get a little hard for me to follow. In the Taubes-Guyenet debate, I think that Taubes’ carb hypothesis better explains the way my body reacts to carbs. As far as Guyenet’s comments about food rewards, I get my rewards from the better feelings I get on a low-carb diet.

  2. Does this remind anyone else of Noakes Central Governor vs. traditional model argument? brain vs. body?

    Interesting. I’m inclined to that we ignore the brain at our own peril. Obviously, there’s a nice interplay and interaction going on. How important both sides are, who knows, but this isn’t a one or the other thing.

  3. I don’t have enough physiology background to really comment, but I’d imagine the brain probably regulates hormone release in a similar way that manages blood glucose levels or muscle activation. So it does seem similar to the Noakes central governor model – the cells themselves don’t control the release of insulin or other hormones, but signal the brain to do so. Therefore, it would make sense that both cell activity and brain function could affect metabolic function.

  4. @Steve: And the biggest similarity between the Central Governor debate and this one: the total polarization, with neither side seemingly able to imagine that any middle ground could exist!

  5. I’m not a scientist but I understand a fair bit about the nervous system and brain function. I can’t fathom that anything we do does not involve the brain. That’s like saying running doesn’t involve the arms or something. Look at what leading brain research guys like VS Ramachandran and Bach Y Rita say and they’ll tell you that we know very little about the brain. The majority of our brain function is subconscious. We very likely have no idea of all the intricate processes that go on around hunger and obesity.

    Further, how is it that we think the brain and the body are two separate entities? Did anyone ever remove their brain and then go for a run, lift weights or a swing a golf club? Aren’t all our brain and other bodily structures made up of atoms and molecules? And aren’t all these systems connected?

  6. I can’t resist doing a little hairsplitting on the graph:

    The study set out to ‘examine the extent to which self-regulatory capacities, measured behaviorally at ages 3 and 5 years, were linked to rapid weight gain in children from age 3 to 12 years’.

    First of all, the differences in weight-GAIN between the groups don’t seem too spectacular, since all ‘groups gained between 0.2 and 0.5 BMI and the ‘neither’ group had a 0.2-0.3 lower BMI to start with. Unless you are prepared to assume that self control had already created a difference in BMI at 3, the graph appears to show that having a high BMI at 3 predicts an even higher BMI at 12.

    Since the ‘neither group also gained BMI the graph also shows that there is at least some other factor than self control at work.

    Secondly, the graph shows a z-score, in other words the deviation of the different groups from a normal BMI, measured in SD’s. Though there is undoubtedly a BMI gain in all groups and there are equally certainly differences between the groups, how significant are these, now that they remain within 1 sd?

  7. @RH: Entirely fair points. The data is hardly overwhelming.

    “Since the ‘neither’ group also gained BMI the graph also shows that there is at least some other factor than self control at work.”

    Absolutely. I should clarify here that I don’t for a minute think that “impulse control” is the major (or even A major) factor in the obesity “epidemic.” But I think it’s a mistake to flip to the opposite extreme and say that obesity is like catching a cold — some bodily response that can’t in any way be influenced by the brain. I’m citing this study to refute that sort of absolutist thinking, not to start my own absolutist camp!

    As for the strength of the evidence, I’ll at least mention that, in the same issue of the same journal as this study, there was a very similar study that tested 800 kids at 4 years old and measured BMI at 11. “Using multiple logistic regression, children who failed the ATDG [ability to delay gratification] task were more likely to be overweight at 11 years (relative risk, 1.29; 95% confidence interval, 1.06-1.58)”.

    Once again, the results are fairly weak. That might mean that they’re simply a statistical fluke; or it might mean that impulse control makes a fairly small (but real) contribution to the overall risk of obesity. The fact that two different studies found the same type and size of effect strengthens the case for the latter interpretation — but certainly not beyond doubt.

  8. “I’m citing this study to refute that sort of absolutist thinking, not to start my own absolutist camp!”

    As a regular reader of your blog, I am very much aware of that and that is exactly what I appreciate in your blog! It always gets me thinking for myself on what the evidence means.

    As to the graph I hope you’ll excuse my hammering on the same nail:

    I think the study with the graph doesn’t prove what it set out to prove. The problem is that the authors chose a BMI Z score as a measure for weight gain. As said it reflects the deviation from the mean BMI of the whole population of the same age, measured in standard deviations.

    Aparently, the Z score is a common measure in pediatrics and for an single individual a Z score makes sense. If you have a positive Z score, there is no arguing that you are fatter than average, even if it is below 1. There is no null hypothesis that you’re actually average but scored above average by mere coincedence.

    If you have average or median Z scores of a group, this is different. Now you can argue that under the null hypothesis, you’d get the same results at least once if you take 20 completely random samples. Unless I am missing something, all the four groups in this particular study are like any random sample from the general population, since their median is way below 2 times the standard deviation.

    Feeding these standard deviations as input into a statistical test feels kind of odd, and can in my opinion only prove that the four groups really are four distinct, but still ramdom samples taken from the same population.

    Of course, that still leaves us the other study.

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