There are at least four possible positions on the thermodynamics of weight gain:
1. Weight gain does not depend on calories in versus calories out, even in the loosest sense.
2. Weight gain is entirely a function of calories in versus calories out, but calories may move in unexpected ways not linked to the classic “eat” and “exercise” dichotomy. For example, some people may have “fast metabolisms” which burn calories even when they are not exercising. These people may stay very thin even if they eat and exercise as much as much more obese people.
3. Weight gain is entirely a function of calories in versus calories out, and therefore of how much you eat and exercise. However, these are in turn mostly dependent on the set points of a biologically-based drive. For example, some people may have overactive appetites, and feel starving unless they eat an amount of food that will make them fat. Other people will have very strong exercise drives and feel fidgety unless they get enough exercise to keep them very thin. These things can be altered in various ways which cause weight gain or loss, without the subject exerting willpower. For example, sleep may cause weight loss because people who get a good night sleep have decreased appetite and lower levels of appetite-related hormones.
4. Weight gain is entirely a function of calories in versus calories out, and therefore of how much you eat and exercise. That means diet is entirely a function of willpower and any claim that factors other than amount of food eaten and amount of exercise performed can affect weight gain is ipso facto ridiculous. For example, we can dismiss claims that getting a good night’s sleep helps weight loss, because that would violate the laws of thermodynamics.
1 and 4 are kind of dumb. 1 is dumb because…well, to steal an Eddington quote originally supposed apply to the second law of thermodynamics:
If someone points out to you that your pet theory of the universe is in disagreement with Maxwell’s equations — then so much the worse for Maxwell’s equations. If it is found to be contradicted by observation — well, these experimentalists do bungle things sometimes. But if your theory is found to be against…thermodynamics I can give you no hope; there is nothing for it but to collapse in deepest humiliation.
But 4 is also dumb. We have a long list of things that affect weight gain – for example, patients on the powerful psychiatric medication clozapine usually gain a lot of weight – fifteen pounds more on average than people on safer antipsychotics. Other medications are known to increase weight to a lesser degree, and some medications even decrease weight, though you wouldn’t like the side effects of most of them. Certain genetic diseases are also known to cause increased weight – Prader-Willi syndrome, for example.
One could try to rescue 4 by saying that people with rare genetic diseases or taking powerful prescription-only medications are a different story and in normal people it’s entirely controlled by willpower. But first, this is an area where possibility proofs are half the battle, and we have a possibility proof. And second, there are more than enough studies about genetics, microbiome, and, yes, sleep showing that all of these things can have effects in normal people.
So 1 and 4 are out. And although I do sometimes see people pushing them, they mostly seem to do a thriving business as straw men for people who want to accuse their opponents of saying something absurd.
The most interesting debate to be had is between 2 and 3. 3 says that all of the interventions that we know affect weight – certain pills, certain recreational drugs, changes in gut bacteria, whatever – do it by affecting appetite and exercise drive. 2 says that basal metabolism is also involved. 3 seems to at least leave open the possibility of just starving yourself even when your body is telling you really hard to eat. 2 says even that won’t work.
There’s room for a little bit of gradation between 2 and 3. A lot of people suggest that one way “fast metabolism” presents is by people fidgeting a lot, which is sort of the same as “your body increases its exercise drive”.
But in general, I think 2 is an important issue that does cause at least some interpersonal weight differences.
We’ll start with the “possibility proof” again. MRAP2. It’s a gene. Scientists can delete it in mice. These mice will eventually develop excessive appetites. But when they are young, they eat the same amount as any other mouse, but still get fatter.
Likewise, 2,4-dinitrophenol is a cellular uncoupling agent which increases metabolic rate and consistently produces weight loss of 2-3 pounds per week. It would be an excellent solution to all of our obesity-related problems if the papers on it didn’t keep having names like 2,4-Dinitrophenol: A Weight Loss Agent With Significant Acute Toxicity And Risk Of Death.
So what about everyday life?
A study of individual variation in basal metabolic rate found very significant interpersonal differences. A lot of that was just “some people are bigger than others”, but some of it wasn’t – they state that “twenty-six percent of the variance remained unexplained”. The Wikipedia article puts this in context: “One study reported an extreme case where two individuals with the same lean body mass of 43 kg had BMRs of 1075 kcal/day (4.5 MJ/day) and 1790 kcal/day (7.5 MJ/day). This difference of 715 kcal/day (67%) is equivalent to one of the individuals completing a 10 kilometer run every day”
Dr. Claude Bouchard and his team stuck 12 pairs of male identical twins in isolation chambers where their caloric intake and exercise could be carefully controlled, then fed them more calories than their bodies needed. All sets of twins gained weight, and in all twin groups both twins gained about the same amount of weight as each other, but the amount of weight gained varied between twin pairs by a factor of 3 (from 4 to 13 kg).
A lot of the sites that talk about this thing are careful to say that people “can’t blame” genes for their obesity, because obesity levels have been rising for decades and genes can’t change that quickly. I think this is wrong-headed. True, genes are not the source of the modern rise in obesity levels. But it’s entirely possible that a globally rising tide of obesity has disproportionately affected the people with the wrong genes. Just as Bouchard fed the same amount extra to all his study participants but some of them gained more weight than others, so if you put an entire civilization worth of people in an obesogenic environment, some of them might be genetically predisposed to do worse than the rest.
A more practical question – can individual people’s metabolism change?
I am personally predisposed to answer in the affirmative. In my early twenties, I ate a crazy amount every day – two bagels with breakfast, cookies with lunch, a big dinner followed by dessert – and I stayed pretty thin throughout. Now I’m thirty, I eat a very restrained diet, and my weight still hovers at just above the range where I am supposed to be. I know that people are famously bad at understanding how much they’re eating and exercising, but seriously if you try to convince me that I’m eating more now than I was then I’m going to start doubting my own sanity, or at least my autobiographical memory.
But there’s not much evidence to back me up. Metabolic rate is well-known to decline with age, but linearly and predictably. And it changes with muscle mass, but only minimally – and I don’t think I used to be any more muscular.
The sites that talk about drastic and unexpected ways to change metabolism seem mostly crackpottish. This isn’t to say their methods don’t work – green tea, for example, has a statistically significant effect – but it’s all so small as to be pretty meaningless in a real-world context.
So my own story seems to be on shaky ground. But as far as I can tell, the people arguing that they’re trying just as hard as anybody else but still unable to lose weight because of their metabolism are very possibly right.