The prevailing theory of why we get fat is that we just eat too much. But, as Nesse and Williams (Why We Get Sick) would say, that is only the proximate explanation; it may illuminate the underlying physiological mechanisms that result in obesity, but it does not explain why humans are inclined to eat more than they expend in energy. An evolutionary explanation requires that we discover the sources of the adaptive value of overeating to the human species. In other words, we need to separate the “how” we get fat from the “why” we get fat.
To untangle the “why” from the “how” we have to understand that the dynamics of weight change, the loss or addition to weight, underlie the eventual weight we may realize. The dynamics are not so simple as the calories-in, calories-out model make them out to be. Food is not just calories and activity is not just burning calories, they are signals that alter our metabolism which determines how the nutrients and energy are used.
The calories-in and calories-out model addresses weight change dynamics but does not address the rest point of those dynamics, which is where our weight settles, if it settles at all. I am not denying in what follows that excess intake of energy, in whatever form, may lead to an increase in weight. That is a truism that leads nowhere.
I believe there are simple reasons why we get fat and become fatter as we age.
- Humans are “fat” primates. The fat is “there” to protect our large brain against the energy variations of the foraging human adaptation.
- We are genetically programed to eat more energy than we spend.
- We move when hungry and rest when fed. This was essential to our survival and reproduction in the ancestral landscape.
- Fat accumulation was essential to reproduction. Beyond the age of reproduction, this adaptation works against us (antagonistic pleiotropy).
- When fat mass grows relative to lean mass, fat receptors begin to out compete lean tissue receptors in the competition for energy.
- Our immune system attacks fat cells as a foreign invader (the fat cells show invasion of macrophages and inflammatory cytokines) and the resulting inflammation tips our evolutionarily acquired mild insulin resistance into a pathological, inflammatory form of resistance.
- There was no evolutionary advantage in limiting our ability to gain fat, meaning, there is no fat set point because nobody could get fat enough long ago at an age young enough to jeopardize fertility.
If you put those together, it is easy to see why we get fatter as we age.
The simplest explanation consistent with evolution is that the tendency of modern humans to grow fatter with age is antagonistic pleiotropy, which means that genes that favor survival and reproduction in our youth become deleterious when we are beyond the age of reproduction. In other words, the ability readily to store fat supports survival and reproduction, but becomes deleterious beyond the age of reproduction when the demands of reproduction and sexual competition alter energy flux. In the Paleolithic, this would have been a young age, perhaps an age near 25, which is consistent with the time of the onset of weight gain for most of us. Our energy landscape has changed so that the energy demands of acquiring energy have fallen dramatically.
Once past the period of reproduction, the genetically programed fat storage continues to operate and people get fatter. A too-simple, but direct, way to put this is that evolution doesn’t care how fat we get, it only cares that we have enough energy to support reproduction. Females are programmed to store fat, males are programmed to eat more than they need to carry out their activities. They become fatter at different rates and ages, females a bit earlier once reproduction is over and males later. Neither would have an upper limit on body fat, but women would have a fatter body composition than men.
According to this view, children should be capable of rapidly and readily increasing their fat stores. The rise in childhood obesity fits this evolutionary program. There was scant selective pressure to turn down the ability to gain weight and fat stores after reproduction, so now it becomes a battle to remain slender and lean as we get older.
Energy intake must be uncoupled with energy expenditure if humans were to survive the stochastic variations of intake and expenditure during evolutionary times. Any other strategy was far too dangerous. Humans that lived according to the energy balance model are dead and left no genes to us. In Why We Get Fat paper (2001), I showed that our ancestors went hungry about one-third of the time and balanced energy over long time periods, not daily like so many try to do. Silly, really silly.
A further part of the puzzle is that obese individuals do not suffer diminished appetite. Paradoxically, they are often more driven by hunger than people who are closer to a “normal” body weight. This appears to reverse causality in the set point theory which implies the theory is wrong.
An easy explanation is that the obese have far more fat cells with receptors that outcompete muscle and other lean tissue receptors for energy. The obese capture in their fat more of the energy they consume than someone with a leaner body composition. In other words, it is easier to gain fat mass if you are fat. A body composition that is far different from the ancient pattern alters the terms of competition between body tissues for energy.
A large fat mass, relative to evolutionary measures, exerts a “mass action” effect that favors fat relative to lean body tissues in the competition for energy. It is a simple matter of receptor counts; becoming “too fat” means there are far more fat receptors than there are for other tissues. This means that even matching energy intake to expenditures is not enough to stay in a narrow range of body weight after you become fat enough. Your fat will capture more of the energy that you take in even though lean body tissues may starve. The simple energy balance model blames their excess energy intake.
I think the causality is backward. As Taubes and I have suggested, people are not fat because they eat too much, they eat so much because they are fat. It is well-known that obese individuals eat more than lean individuals. It is also well-known that most diabetics suffer a sarcopenic form of diabetes. They have large fat mass with diminished muscle mass. This is the prevalent form of diabetes among the aged.
In the critical competition for energy, the brain’s energy flux is threatened. The brain’s defense is to reduce insulin sensitivity in the periphery (the rest of the body). Brain imaging show that obese individuals exhibit reduced brain mass. It is well-known that they are systemically inflamed and have the inflammatory form of diabetes. I summed this up as the “selfish brain, greedy fat” hypothesis in my book. The German group that proposed the selfish brain theory have traced the metabolic pathways that lead to brain malnourishment in the competition for energy among the tissues. A leading figure in selfish brain theory just published a book in Germany that makes the arguments in a readable form (if you can read German).
Life can be maintained over a wide range of body weights. A host of models, including mine, show that there may be a there may be a continuum, a limit cycle, a stable and an unstable equilibria of body weights consistent with energy balance. So, the theory is incomplete on both evolutionary and mathematical grounds. Others, including mine, show that fat accretion may increase without limit. It is easy to see why there may be no limit on fat accretion. First, there would be weak to no selective pressure against fat accretion during youth in the adapted evolutionary environment. Second, the positive feedforward dynamics wherein fat mass tips receptor counts from lean tissues and brain tissues toward fat tissues. Such a dynamic may lead to unlimited fat accretion, as a rising number of 500, 600 and more pound individuals show.
An elegant survey of models of body weight change support the views I am expressing. Their finding is “An imbalance between energy intake and energy expenditure will lead to a change in body weight (mass) and body composition (fat and lean masses). We show that the generic dynamic behavior of body composition for a clamped diet can be divided into two classes. In the first class, the body composition and mass are determined uniquely. In the second class, the body composition can exist at an infinite number of possible states. Surprisingly, perturbations of dietary energy intake or energy expenditure can give identical responses in both model classes, and existing data are insufficient to distinguish between these two possibilities.”
In the end, I think is really all comes down to the idea that fat accretion favors survival and reproduction in youth, but turns against us when we pass the reproductive age. All is not lost though because my argument does suggest things we can do.
References, I could give hundreds, but three suffice to make a case. Many more are contained in my book.
Manninen, A. (2004). Is a calorie really a calorie? Metabolic advantage of low-carbohydrate diets. Journal of the International Society of Sports Nutrition. Not much new here, but it does damage to the “kindling wood” theory that any source of food is just a source of energy as though it is kindling for a furnace. There is no model of metabolism in that theory.
Mathematical models of energy homeostasis, Ratchada Pattaranit and Hugo Antonius van den Berg, in J. R. Soc. Interface (2008) 5, 1119-1135. This review shows the reversed causality Taubes and I mention.
Chow, C. C., & Hall, K. D. (2008). The Dynamics of Human Body Weight Change. (P. E. Bourne, Ed.)PLoS Computational Biology, 4(3), e1000045. doi:10.1371/journal.pcbi.1000045.g003
There are many possible equilibria some stable and some not. The possibilities as shown in Chow and Hal appear in the graph at the head of this post when I can get Weebly to get with it.