Why do we get fat

Chapter 16 The Laws of Obesity (1)
Few people envy the fate of guinea pigs, and few people aspire to be guinea pigs.It's no exception in my weight loss story.Still, like scientists, we can learn something from the guinea pigs in our experiments.

In the early 20s, a young scholar at the University of Massachusetts, George Wade, conducted such an experiment.He removed the ovaries of female mice, and observed the mice's weight and behavioral changes, and began to study the relationship between sex hormones, body weight and appetite.The consequences of ovariectomized mice were quite dramatic. The mice started eating voraciously and quickly gained weight.

Ovariectomized mice become "insatiable".A rat eats too much, and the extra calories go to its fat tissue, and the little ones get fat.This also confirmed our guess: overeating is also the cause of human obesity.

So Wade conducted a second, revealing experiment: After the mice had their ovaries removed, Wade put them on a strict postoperative diet.Even when the mice were hungry after surgery, even if they were so eager to eat, the doctors who kept them ignored it.In the jargon of experimental science, the second experiment was to control overeating.Only allow these postoperative mice to eat as much food as they did before surgery.

The result may be beyond your expectation: the mice still get fat, and get fat quickly.However, these mice are completely squatting now, and only move a few steps when they are needed to get food.

Even if we only know the results of the second experiment, we can understand it in the old fashioned way: it must be because the mouse became lazy after the ovariectomy, it expended too little energy, and that's why it got fat.This explanation can also make us more adhere to the belief that "calorie intake balance determines weight loss".

However, if both experiments are taken seriously, the conclusions will be very different.After a mouse was ovariectomized, its adipose tissue absorbed calories from the bloodstream, which were then converted into fat.If the animal could eat more to compensate for the calories it now stores as fat (as it did in the first experiment), it would.If it can't do that (as in the second experiment), it has less activity because there are fewer calories available to burn.

Wade and I explained it this way: animals don't get fat by eating more, they eat more when they get fat.Cause and effect are reversed.Gluttony and laziness are both consequences of obesity.Basically they are all caused by dysregulation of animal fat tissue.Ovariectomy caused the mice to store body fat; to compensate for energy, the animals either ate more, expended less energy, or both.

In order to explain why this happens, I'm going to have to say something academic for a moment.It turns out that removing the ovaries from the mice was equivalent to removing estrogen, which is normally secreted in the ovaries.Therefore, when the ovariectomized mice were artificially injected with estrogen, they were neither greedy, lazy, nor fat, and their actions were no different from ordinary mice.One of the things estrogen did in the mice was to affect an enzyme called lipoprotein lipase, or LPL for short.First of all, let me say that the effect of LPL on humans is similar to that on mice.

In short, the role of LPL is to "pull" the fat that happens to "pass by" near it in the blood circulation into the cells to which it belongs.If LPL is attached to a fat cell, then LPL will pull the fat in the blood circulation into the fat cell, and the animal (or person) where the fat cell is located will be a little fatter, of course, the amount is very small.If LPL attaches to a muscle cell, the fat is pulled into that muscle cell, and the muscle cell burns the fat as fuel.

Estrogen happens to inhibit, or "disable," the activity of LPL on fat cells.That is, the more estrogen around the cells, the less fat LPL pulled into the cells from circulation, and the less fat those cells accumulated.So, after estrogen removal (ovary removal), the fat cells thrive with LPL.

The LPL then does its "regular job" of pulling the fat into the fat cells.At this point you will find that the animal is much fatter than normal because the cells have more LPL performing the "fat pulling" task.

So, what does LPL have to do with increased appetite?Animals have the urge to binge eat because other tissues in their bodies need the energy in the blood circulation to maintain the operation of body functions.The more calories stolen by fat cells, the more the body must eat to compensate.In fact, fat cells are so desperate for calories that there aren't enough calories to get to other cells.A meal that used to satiate animals no longer satisfies them.As animals get fatter and heavier, their calorie needs increase further.Therefore, the animal will feel that it is already hungry and crazy. If it cannot satisfy its new hunger, it can only choose to settle down to reduce energy consumption.

Diets to lose weight had no effect on the mice, nor did attempts to force them to exercise.The only way (besides reoperation) to stop these animals from gaining weight was to give them back the estrogen.In doing so, they lost weight again, and their appetite and energy levels returned to normal.

Therefore, it is the removal of the ovaries that reduces the level of estrogen, which eventually causes the fat cells of the mice to malfunction, so they gain weight.This is likely why many women gain weight after hysterectomy or menopause.They secreted less estrogen, and their LPL pumped more happily during the "fat-pulling" task.

The stories of these lab rats help reverse our notion of cause and effect in obesity.It tells us that two behaviors—gluttony and laziness—are not the causes of obesity, as we think them to be, but in fact their consequences.It also tells us that if we pay attention to the hormones and enzymes that regulate the fat tissue itself, then we can more precisely understand why obesity occurs, not only in these mice, but in their subsequent behavior.

For nearly half a century, when it comes to the topic of obesity and weight loss, there will be such an obvious tendency-medical experts are not at all interested in the topic of fat tissue itself and how our body controls it.They simply ignored the regulation of adipose tissue because they had already concluded that the problem was behavior, the brain, not the body.Almost everyone does.

We've been talking about dysregulation of height growth—why some people grow over 2 meters tall, while others never grow to 1.4 meters—with focus only on the hormones and enzymes that regulate growth.However, when we talk about obesity and weight loss, the dysregulation of abnormal growth of fat tissue that is typically manifested, the hormones and enzymes that regulate growth are assumed to be irrelevant.

Why on earth are we getting fat?
How on earth should we lose weight?

When we pay attention to the regulation of adipose tissue, we draw conclusions on the above issues that are quite different from the traditional view that "the focus is on the balance of energy intake and expenditure".As with Wade's experiments with rats, we are forced to conclude that people gain weight because their adipose tissue is dysregulated.One of the obvious consequences of this dysregulation is changes in eating behavior (bulimia) and lack of exercise (laziness).And we always talk about the consequences of those who are obese or who fail to lose weight.

We now refer to these laws as the Laws of Obesity in honor of the superseded laws of physics.

first law of obesity
Even though the human body is not as delicate as mechanical tissues, fat is also finely controlled by the body.

This law holds true even if some people are unimaginably prone to obesity.What I mean by "control" is that in health our bodies work tirelessly to maintain a certain amount of fat in adipose tissue - no more, no less - and that stored fat is used To ensure a steady supply of energy to other cells.The implication is that some people gain weight because this adjustment goes wrong and the body loses balance, not that this adjustment no longer exists.

The evidence that adipose tissue is finely regulated is indisputable, and fat isn't something we just throw away like unburned calories.After reading the first part and seeing various obesity stories, you will know that men and women gain weight differently.Like Wade's experiments and what we know about estrogen and LPL, we already know that hormones play an important role in regulating body fat.Certain parts of our body are relatively fat-free, such as the backs of the hands and forehead, while others are not.This shows that local factors play a certain role in the location of obesity.Just as local factors have a definite effect on where hair grows - some places grow and others don't.

In fact, if our parents were obese, we are more likely to be obese.Obesity within families and the localized distribution of the fat itself may be genetic in nature, as indicated by the natural excess gluteal fat in some African tribal women.Body fat is indeed regulated and controlled by the body, because how do genes passed from one generation to the next affect our fat and its distribution if not through hormones, enzymes and other molecules that can regulate it?
The amount and even the type of fat an animal has is also extremely finely regulated by the body.After all, we humans are just a species of animals, and some wild animals may be born "fat", such as hippos and whales.They distribute their fat according to the season, either as an insulation layer for winter preparation, or as fuel for annual migration or hibernation.Females put on weight when they are preparing to give birth, and males put on weight to gain a weight advantage when competing for a mate.But they never become obese, which means they don't suffer from many of the adverse health consequences of obesity that humans do.For example, a hippopotamus' obesity does not predispose it to diabetes.

No matter how plentiful their food supply, wild animals maintain a steady weight—neither too fat nor too thin.This means that their bodies ensure that the amount of fat in their adipose tissue is always beneficial and never becomes an obstacle to survival.When animals do accumulate significant amounts of body fat, it is always there for some legitimate reason.The animals were equally healthy whether they had more or less fat.

Ground squirrels, hibernating rodents, can double their usual body weight and body fat during the last few weeks of summer.One researcher described to me the results of his experiments. When the ground squirrels were at their peak body weight, they had so much body fat that it was like "opening a can of oil, and there were huge lumps of fat everywhere."

But like Wade's ovaryless mice, the ground squirrels accumulated the fat no matter how much they ate.If they were housed in a laboratory and fed a severely restricted diet from the spring when they woke up from hibernation until the end of summer, they got as much fat as ground squirrels who ate to their hearts content.Whether these ground squirrels are kept awake and fed in a warm laboratory during the winter, or they are allowed to go into complete hibernation without eating and consume only their own fat to survive - they end up burning fat during the winter, And the rate is the same.

The camel's hump is another example of nature's purposeful storage of large amounts of fat.The hump provides a huge fat store for the camel to survive in the desert.Without a hump, camels would have to store their fat under the skin like we do, so insulation would be a big problem in the desert heat.The same is true of the fat-ripped desert sheep and fat-tailed quolls, small desert animals that almost without exception store their fat in their rump or tail.

The truth is, there is very little we can do to change the habit of accumulating fat in these animals, and we can't make them "lose weight" at our will.Even if the researchers adjusted the food supply so little that they would almost starve to death, it would not help, and they would still get fat when they should.At certain times of the year, the amount of fat in these animals is controlled entirely by factors in the organism itself, independent of food availability or the energy expended to obtain it.This sounds perfectly plausible. If an animal that needs a lot of fat to survive the winter needs to collect excess food in advance to accumulate fat, then only one summer of food shortage is enough to wipe out the entire species.

Could it be that the theory of evolution singles out humans as the only species on this planet whose body cannot regulate fat mass to cope with binge eating or famine?Do you really believe that some people are so fat that they struggle to walk and have such low self-esteem, just because there is too much food on offer?No, evolution didn't turn us into a special species.

A final argument for body fat being finely regulated by the body is that the rest of our bodies are equally finely regulated.Why is fat the only exception?When the body fails to regulate, cancer, high blood pressure, and heart disease will occur, and the consequences are extremely serious.When people accumulate too much fat, it is also a sign that the regulation program of fat tissue is wrong.What we need to understand is: what is the defect and what to do about it.

The second law of obesity

Even if fat dysregulation is extremely small, it can still lead to obesity.

Remember that 20-calorie-a-day thing I discussed earlier?If we ate just 20 extra calories a day—just 1% or less of our basic daily calorie allowance—that would be enough to turn us from skinny at 20 to fat at 50.In the logical context of the calorie balance theory, this leads to an obvious problem: If we need to consciously balance calories in to calories out to within 1% in order to stay in shape, who? Can it be done?This seems impossible, and it is.

(End of this chapter)