Tag: weight loss

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My new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Also check out my new book, THE EXPLORER'S GENE: Why We Seek Big Challenges, New Flavors, and the Blank Spots on the Map, published in March 2025.

- Alex Hutchinson (@sweatscience)

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After an interesting e-mail conversation with Dr. Yoni Freedhoff of the pull-no-punches Weighty Matters blog, I ended up writing a guest post about some of the factors you need to think about if you ever look at the calorie number that your treadmill (or elliptical or exercise bike or whatever) spits out. Without giving away too much, I’ll say this: if you’re not considering the difference between gross and net calorie burn, you’re kidding yourself! READ THE FULL POST HERE.

THANK YOU FOR VISITING SWEATSCIENCE.COM!

My new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Also check out my new book, THE EXPLORER'S GENE: Why We Seek Big Challenges, New Flavors, and the Blank Spots on the Map, published in March 2025.

- Alex Hutchinson (@sweatscience)

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For those interested in the cause of obesity, a lengthy post by blogger and neurobiologist Stephan Guyenet is rocketing around the Internet. After a rather testy exchange with Gary Taubes at the Ancestral Health Symposium (which culminated with Taubes offering Guyenet this no-so-friendly advice: “I would just recommend in the future you should pay attention to populations that might refute your hypothesis rather than just presenting populations that support.  That’s always key in science.“), Guyenet decided to write a detailed dissection of Taubes’s carbohydrate theory of obesity, explaining why it’s “not only incorrect on a number of levels, but may even be backward.”

Here’s Taubes’s own statement of the theory in question, as quoted by Guyenet from Good Calories, Bad Calories:

This alternative hypothesis of obesity constitutes three distinct propositions.  First, as I’ve said, is the basic proposition that obesity is caused by a regulatory defect in fat metabolism, and so a defect in the distribution of energy rather than an imbalance of energy intake and expenditure.  The second is that insulin plays a primary role in this fattening process, and the compensatory behaviors of hunger and lethargy.  The third is that carbohydrates, and particularly refined carbohydrates– and perhaps the fructose content as well, and thus perhaps the amount of sugars consumed– are the prime suspects in the chronic elevation of insulin; hence, they are the ultimate cause of common obesity.

Guyenet’s post is an interesting read, and it certainly raises some questions about Taubes’s reductionist approach to obesity (which I’ve criticized in previous posts). It should be noted that Guyenet himself has a Grand Theory of Obesity, which he dubs the “food reward” theory. It basically argues that modern foods trigger reward behaviour in our brains without the accompanying satiety signals that traditional foods would offer. To his credit, he’s more circumspect about trumpeting the powers of his theory: the post I linked to is titled “Food Reward: a Dominant Factor in Obesity.” No doubt that Taubes would have said “the Dominant Factor…” 🙂

Still, my overriding sense is that scientists (and journalists, for that matter) with Grand Theories rapidly become unable to critically evaluate data that conflicts with their theory. Personally, I think it’s highly unlikely that we’ll find a single dominant factor that explains the dramatic rise in obesity over the last few decades, and the endless search for that one magic bullet distracts us from the obvious contributing factors that we already know about.

THANK YOU FOR VISITING SWEATSCIENCE.COM!

My new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Also check out my new book, THE EXPLORER'S GENE: Why We Seek Big Challenges, New Flavors, and the Blank Spots on the Map, published in March 2025.

- Alex Hutchinson (@sweatscience)

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Is it good to be a little bit overweight as you get older? That’s the message from a series of large, reputable studies (including one that made lots of news two years ago). The theory is that having a few extra pounds is good as you get old and frail, so that you don’t waste away to nothing if you get sick or break a hip. And the data seems to back up this theory.

But wait a sec. A new study in the Journal of the American Geriatrics Society from researchers at Loma Linda University in California (abstract here, press release here) shows the opposite:

[M]en over 75 with a body mass index (BMI) greater than 22.3 had a 3.7-year shorter life expectancy, and women over 75 with a BMI greater than 27.4 had a 2.1-year shorter life expectancy.

Why the contradiction? Actually, there are some very good reasons. The authors start by explaining some of the potential flaws with the earlier studies that seemed to show that being a bit chubby helped you live longer. The key problem is that the earlier studies measured weight just once, at the beginning of the study, and then waited to see how quickly the subjects died. But people who were skinny at the beginning of the study might have been skinny because they were already sick, possibly without having being diagnosed yet. If you’re skinny because you’re partway through a dramatic weight loss than ends with your death, that’s not quite the same as being thin with a long-term stable weight and healthy lifestyle.

The new Loma Linda study is able to address this problem, along with a few others. It relies on two large studies of Seventh-Day Adventists in California, one in 1960 and the second in 1976. Weight was measured on both occasions, and mortality was monitored until 1988. By looking only at the people whose weight stayed the same (within 5 kg) between 1960 and 1976, you get to study the effects of having extra weight, rather than the effects of gaining or losing it for whatever reason (both of which could have significant effects, but are separate questions).

Another quirk of the study is that Seventh-Day Adventists are forbidden to smoke. So to further eliminate confounders (e.g. people who were thin because they were puffing on cancer sticks), the analysis was able to completely exclude any past or present smokers, plus anyone with any history of coronary heart disease, stroke or cancer at baseline, and still have a total of 6,030 people aged 25-82. The point here is that we’re looking just at the effects of extra weight, stripped away of as many confounders as possible.

And sure enough, higher BMI corresponded to higher risk of death for 75- to 99-year-olds: above 22.3 was bad news for men, and above 27.4 was bad news for women. Obviously this study can’t tell us why there’s a difference between men and women, but the researchers suggest that women may benefit from having a bit more fat because that’s where estrogen is produced after menopause; too little estrogen may leave them susceptible to everything from hip fracture to insulin sensitivity problems. Here’s how the “hazards ratio” (basically your odds of dying relative to the healthiest group) looks as a function of BMI:

So what does this mean? Well, we’re not going to rewrite the medical textbooks based on a few Seventh-Day Adventists in California. It’s just one study, etc. etc. But given the methodological differences between this study and the previous ones, it certainly seems reasonable to wonder whether the apparent paradox of overweight people living longer is simply an artifact of the confounders this study managed to eliminate. I’m not saying you should panic if you’re overweight — I’m just saying you shouldn’t panic if you’re not.

THANK YOU FOR VISITING SWEATSCIENCE.COM!

My new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Also check out my new book, THE EXPLORER'S GENE: Why We Seek Big Challenges, New Flavors, and the Blank Spots on the Map, published in March 2025.

- Alex Hutchinson (@sweatscience)

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Interesting new study from Paul Williams’ National Runners’ Health Study — no, wait, this is a new one, not the one I wrote about a few days ago! This one looks at identical twins to find out the extent to which your body shape is dictated by your genes. Yes, the old nature vs. nurture debate…

Williams has an enormous data set of over 100,000 runners, including 926 identical twins. He explored the relationship between two quantities: the difference in how much a pair of twins ran, and the difference between how much they weighed. Various studies have found that genetic factors account for 40% to 70% of the variation in BMI. But Williams found that the more the active twin exercised, the less genetics seemed to matter. Here’s a graph:

The numbers on the right-hand side represent how much more the active twin runs than the less-active twin. Of course, for some people the results will seem absurdly obvious: the greater the difference in activity levels between two people, the greater the difference in their BMI. Still, it’s a good reminder that genetics isn’t destiny. Here’s what Williams concludes:

Extrapolating the coefficients of Table 3 shows that BMI inheritance might be eliminated completely by running 7.05 km/day (23 mi/wk) in women and 13.51 km/d (60 mi/wk) in men, a projection that is consistent with our previous finding of uncorrelated BMI values in 35 pairs of MZ twins whose running differed by an average of 8 km/d [31], but a projection that should nevertheless be considered with caution.