Over at the New York Times Magazine, Tara Parker-Pope writes about post-diet weight gain:
Briefly: For a given weight, people who gain and then lose fat tend to have slower resting metabolisms than people who didn’t get fat in the first place. Furthermore, they also tend to have the same metabolic set point as they did at the higher rate — which is to say, they crave food, and in general their bodies behave as if they’re starving:
A full year after significant weight loss, these men and women remained in what could be described as a biologically altered state. Their still-plump bodies were acting as if they were starving and were working overtime to regain the pounds they lost. For instance, a gastric hormone called ghrelin, often dubbed the “hunger hormone,” was about 20 percent higher than at the start of the study. Another hormone associated with suppressing hunger, peptide YY, was also abnormally low. Levels of leptin, a hormone that suppresses hunger and increases metabolism, also remained lower than expected. A cocktail of other hormones associated with hunger and metabolism all remained significantly changed compared to pre-dieting levels. It was almost as if weight loss had put their bodies into a unique metabolic state, a sort of post-dieting syndrome that set them apart from people who hadn’t tried to lose weight in the first place.
The men and women in question were part of an Australian study on weight loss, which had 34 participants survive a ten-week diet on 500-550kcal per day, losing roughly 30lbs each. Read that again: 500 kcal per day. No wonder their bodies adapted as if they were starving—they were. Returning to a sub-ante caloric intake was apparently insufficient to persuade their endocrine systems that the famine was over and metabolic normalcy could return.
Gary Taubes is unimpressed:
As you’ll already have guessed if you know who he is, Taubes is annoyed that Parker-Pope neglected to mention insulin.
Despite all the discussion in Ms. Parker-Pope’s article of hormonal changes in obese and weight-reduced obese individuals – of esoteric hormones like peptide YY, and ghrelin that influence hunger and satiety – not once in over 5,000 words does she mention the hormone that directly governs the storage and oxidation of fat in our bodies — insulin. This hormone is the “principle regulator of fat metabolism,” as the Nobel Laureate Rosalyn Yalow and her colleague Solomon Berson described it almost fifty years ago.
It’s now well accepted that chronically elevated levels of insulin and a condition known as insulin resistance are the common precursors to heart disease and type-2 diabetes. Some 75 million Americans suffer from insulin resistance, according to the Centers of Disease Control; they have what’s officially called “metabolic syndrome.” That obesity, too, is considered a disorder of insulin resistance – the first symptom physicians are told to look for to diagnose metabolic syndrome is an expanding waistline – begins to explain why it is so intimately associated with both heart disease and diabetes.
It’s a fair point: Insulin is pretty clearly the elephant in the room, and a discussion of obesity that doesn’t include insulin is clearly lacking. But there’s more going on than just this one omission. Taubes argues that insulin resistance is a major — perhaps the major — factor in this failure of the post-diet endocrine system to reset, and hammers on his favourite insulinogenic hobby-horses of refined grains and sugars.
Again, that’s a fair point. Parker-Pope doesn’t mention diet all that much, except to mention when it doesn’t matter whether someone lost weight on, say, Atkins or Weight Watchers. I wouldn’t be too surprised if most of the post-weight loss dieters kept to the common wisdom of low-fat, high-carb. But Taubes neglects the fact that adipose tissue itself induces insulin resistance — one would expect that dieters who drop a bunch of fat would also drop a bunch of insulin resistance.
See what I did there?
Go back to that original study. I suppose it’s possible for an extraordinary individual to lose thirty pounds in ten weeks on a starvation diet and not also lose a lot of muscle mass, but I will be dipped in shit if thirty-four of them managed to do so. Furthermore, Parker-Pope notes that part of the body’s response to dieting (it’s not clear from the article, but it’s implied that this comes from a Columbia University study involving 800kcal/day semi-starvation diets) is to change muscle composition:
Muscle biopsies taken before, during and after weight loss show that once a person drops weight, their muscle fibers undergo a transformation, making them more like highly efficient “slow twitch” muscle fibers. A result is that after losing weight, your muscles burn 20 to 25 percent fewer calories during everyday activity and moderate aerobic exercise than those of a person who is naturally at the same weight. That means a dieter who thinks she is burning 200 calories during a brisk half-hour walk is probably using closer to 150 to 160 calories.
This is a perfectly reasonable response from a body that thinks it’s starving to death: Turn energy-hungry fast-twitch muscle fibres into stingy slow-twitch fibres. Unfortunately, it leads to a muscular structure that burns far fewer calories — and one that’s substantially less massive. Muscle mass is important to metabolism, not only because the resting metabolic contribution of a pound of muscle is much higher than that of a pound of damn near anything else, but also because — and this is where you can imagine me shooting a stern glare at Gary Taubes, who didn’t bring this up — muscle also has a strong insulin response. This study seems to indicate that muscular insulin resistance increases the risk of metabolic syndrome, and fast-twitch fibres are more sensitive than slow-twitch.
Looking at the weight-loss stories in Parker-Pope’s article, we discover that every time exercise is mentioned in connection to weight loss, successful or otherwise, it’s always endurance exercise: Cycling, jogging, biking, water aerobics, and so on. (Parker-Pope herself runs marathons.) Unfortunately, this sort of training not only doesn’t lend itself to muscle-building, it also selects for slow-twitch muscle fibres and leads to adaptations in fast-twitch fibres that make them more closely resemble slow-twitch fibres. Strength training, on the other hand, has the obverse effect: It leads to greater development of fast-twitch fibres, with their higher insulin sensitivity (as well as greater potential for hypertrophy). High-intensity cardio (sprints, Tabata, &c.) will do the same.
The problem with developing fast-twitch muscle is that it tends to lead to muscle gain. If your mind works like mine you might have trouble with the idea that this could be a problem, but consider that every evaluation of fat loss made in Parker-Pope’s article depends on weight loss, and muscle is heavier (well, more dense) than fat. I can imagine that people looking to lose weight would see building muscle as counterproductive, especially since even critical-minded folks like Taubes aren’t talking about it, but then again I’m talking out of my ass even more than usual here.
By no means am I claiming that I’ve found the holy grail for fat loss. I’m just claiming that treating all weight as if it’s the same, and all exercise as if it’s the same, is thoroughly counterproductive. Also, this is further evidence that the answer to every question is “squat more“.