Why We Get Fat

It is surprising how little we know about nutrition. We all need food to survive, however, we still haven’t comprehended its inner mechanics.

Nutrition has become a myth, cult, and dogma more than science. That’s precisely what makes it so difficult to even discuss it. Why We Get Fat is not a diet book, but a biological one and the science of what’s happening in our body that makes us fat.

Conventional wisdom

We are causal-seeking machines. We demand immediate, direct explanations of all events happening around us. The effortless the evidence and the more compelling the narrative, the better. The problem is that when media, lobbies, and governmental interests get in the way, these explanations can depart from reality.

We’ve grown being told that we remain lean because we’re virtuous and we get fat because we lack self-control. That we are the only ones to blame. That obesity is caused by overeating. That nutrition can be solely explained by the first law of thermodynamics — reducing an extremely complex process to a simple “calories-in, calories-out” story.

But all thermodynamics says is that if something gets more or less massive, then more or less energy has to enter than leave it. It says nothing about why. It says nothing about cause and effect.

While there are some bits of truth here and there, the oversimplification of the argument makes us draw the wrong conclusions.

Cause and effect, reversed

Conventional wisdom argues that fat accumulation is driven by a simple energy balance, what we call “calories-in, calories-out”. However, this narrative is flawed. Cause and effect are reversed.

We don’t get fat because we overeat, we overeat because we are getting fat.

Think about it in another way: picture a kid growing. She definitely consumed more calories than she expended. Yet you’d never tell that she gained weight because she ate too much or exercised too little, but because she was growing. Her body demanded those calories and it found a way to get them: either by increasing the appetite or reducing energy expenditure.

We can conclude that anything that makes us grow, also makes us overeat — because the body requires it.

The same goes for exercising. There has been a prevailing narrative that exercise will make us leaner. This belief is rooted in the observation that people who are lean tend to be more physically active than those of us who aren’t. This is true. However, again, it gets cause and effect backward. This observation tells us nothing about whether “runners” would be fatter if they didn’t run.

On top of that, calories burned from exercising not only represent an extremely small fraction of our daily expenditure but will also lead to more appetite. In other words: it takes a lot of running to burn an extra slice of cake.

We ended up buying into this “exercise more and eat less” narrative because it feels intuitive and reinforces our beliefs.

Estrogen, insulin, LPL, HSL, and CHOs

Obesity is nothing but a disorder of excess fat accumulation.

🧪 An experiment was made in the early 1970s. George Wade studied the relationship between sex hormones, weight, and appetite by removing the ovaries from rats — deregulating de activity of estrogen.

  • Rats eat too much, the excess calories find their way to the fat tissue, and the animal becomes obese. Which would fit the “calories-in calories-out” story. But…
  • After putting them on a strict diet, rats still got just as fat, just as quickly.
  • If rats were injected with estrogen, it resulted in normal behavior.

Estrogen inhibits an enzyme called LPL. Which is a key factor in partitioning fat among different body tissues. Wade’s rats overate because they were losing calories into fat cells that were needed in other places. The fatter the rats got, the more they had to eat to feed the non-fat cells. The body became unable to regulate its fat tissue, creating a cycle of getting fatter and fatter.

❓ A series of questions are worth asking:

  • What regulates fat accumulation? As it turns out, insulin does. In a nutshell, higher levels of insulin signal the body to store fat. Lower levels of insulin lead to its release.
  • If insulin happens to regulate fat, what triggers the secretion of such hormone? In part, CHOs do. Higher levels of CHOs in the bloodstream -> follow the release of insulin -> follow the accumulation of fat.
  • What regulates LPL on fat cells? The presence of insulin. The more insulin our body secretes, the more active the LPL becomes on the fat cells, and the more fat gets stored in fat cells.
  • What else? Insulin also suppresses an enzyme called HSL, which works to make fat cells “leaner”. It does so by breaking down triglycerides into their component fatty acids so that they can escape into circulation. The more active HSL is, the more fat we liberate and can burn from fuel.

Fat regulation

Fat is carefully regulated throughout the body. That’s the reason we don’t get fat in the back of our hands or in the forefront. It is also heavily determined by our genetics.

Moreover, a simplistic approach on the matter quickly reveals the silliness of the “calories-in, calories-out” framework.

1 kilogram of fat contains 7.500 calories. If we only overeat, on average, by 20 calories a day — which is an overly optimistic assumption — after 25 years, we’d add up to 20 kilograms. Now think of all the food decisions we make in a day and how unattainable it would be, without scientific instrumentation, to balance out food. If these assumptions were right, it’d be impossible for any human to remain lean.

First published on November 13, 2021