The address is near and dear to our way of thinking, because Taubes raises a difficult and correct truth: In order to pursue new knowledge of the world, we must be confident that our ideas are correct, but because we are very susceptible to fooling ourselves, this tendency will lead us to believe lots of untruth as well. He calls it a tightrope walk: The thin line between being confident in an unpopular or yet unknown piece of knowledge and being a fool who buys into his cherished untruths.
The idea is we’re always going to try to fool ourselves – that’s how our brains are wired — but here’s a way of thinking that will help us minimize the tendency. Another great philosopher of Science, Robert Merton, in the 1960s, put it this way: he said that Aristotle was right when he said “all men by nature desire to know” but then he added, what makes scientists different is they “desire to know that what they know is really so.”
Now here’s the catch: In science, as in life, you have to have faith in yourself and your ideas. You have to make decisions about what you’ll pursue, what you’ll continue pursuing despite times getting very tough, who you’ll do it with, who you’ll stay doing it with even after times get tough, where you’ll do it; why other people should do it with you and keep doing it with you through the tough times. You’ll make these decisions based on the assumption that what you believe is true really is. Without this belief we don’t do anything; it’s what drives us forward and allows us to act decisively. But if we fool ourselves, and we’re the easiest person to fool, we’ll make the wrong decisions – as individuals, as a society.
From this perspective, life becomes a tightrope walk in which you never actually see the rope. But it’s there. And, in all honesty, there’s almost invariably a net, too, so our missteps are rarely as damaging as we fear they’ll be while they’re happening. On this rope, we have to find the balance, time and again, between this need to think critically and skeptically about what we believe, and the need to have faith that what we’re doing and what we believe is right. Faith moves us forward; skeptical critical thinking keeps us balanced.
We’ve been told for decades that dietary fat makes us gain weight, yet research suggests refined carbohydrates are to blame. It’s time to turn the food pyramid upside down. Let’s examine the truth about what causes weight gain – and what we can learn about biases from the field of nutritional science.
Nutrition, as a scientific field, is reminiscent of psychology in its infancy — before Skinner’s or Pavlov’s ideas had made a dent, before there was Piaget, Kahneman, Tversky, Munger; before we had a field called “evolutionary psychology.” Heck, before biology itself had really come to grips with Darwin’s ideas about evolution through natural selection. (That didn’t happen until the modern synthesis in the 1940s.)
There were theories of mind, theories of self, theories of everything, but nearly all of them were incomplete and contradictory explanations of human behavior. Most were unscientific, in the Popperian sense. They couldn’t be falsified, and they claimed to explain too much, even patently opposite behaviors. It would be a long time before we started to pull the threads together and come up with coherent explanations of why we do what we do.
A similar pattern emerges as we survey the field of nutrition today. The ground is not steady. The most widely accepted and promulgated advice of the last fifty years is under attack: Maybe a calorie is not a calorie. Maybe the simple advice of “Eat less, move more,” nice as it sounds, is too simple, and frankly, wrong. (Reminding one of the second half of Einstein’s dictum: As simple as possible, but not simpler.) Maybe saturated fat is actually good for us. Maybe *gasp* salt is actually good for us.
These aren’t slight modifications of a prior theory but a 180-degree turn. (The visual metaphor is more literal than it seems: It’s not hard to argue, with the new evidence, that the old FDA food pyramid we’re familiar with should literally be turned upside down.)
He and his intellectual partner, Peter Attia, call it the Alternative Hypothesis. It goes roughly as follows: We don’t gain weight and get modern diseases like heart disease, obesity, and hypertension because we eat too many calories or consume too much dietary fat, but because we are consuming carbohydrates, especially sugar and easily digestible starches, at a pace that nature never intended. The resulting insulin resistance is the main culprit.
Fifty years ago, one in every eight or nine Americans would have been officially considered obese, and today it’s one in every three. Two in three are now considered overweight, which means they’re carrying around more weight than the public-health authorities deem to be healthy.
This, in the face of a rise in recreational exercise, gym-going, health-consciousness, and food pyramids. (Not to mention fast food, increasingly sedentary lifestyles, and so on — all the things you’ve heard before. Taubes thinks those are red herrings, by the way.)
The Causality Problem
The premise of the book is relatively simple: Trying to explain the explosion of obesity, hypertension, and heart disease by focusing on overeating or under-exercising (consuming more calories than we’re using) is missing the boat. It’s explaining something causally by simply describing it. Of course, we’re storing more energy than expended. Why?
Step-by-step, detective-like, Taubes explores the current hypotheses and finds them wanting:
…(I will argue) that it is absurd to think about obesity as caused by overeating, because anything that makes people grow–whether in height or weight, in muscle or fat–will make them overeat. Children, for example, don’t grow taller because they eat voraciously and consume more calories than they expend. They eat so much-overeat–because they’re growing. They need to take in more calories than they expend.
We want to know what causes the overeating relative to energy expenditure. Why would any animal or human be driven to store more fat than they needed to function? Wild animals do not carry excess fat unless it has a useful physiological mechanism. (Whales keeping warm, squirrels preparing for winter, etc.)
Many have tried to explain this in psychological terms: Either we’re being manipulated into over-eating, or we’re too weak to resist the temptations of the modern age. Today’s food is just too damn yummy.
Taubes thinks this is the wrong way to approach the problem. What we really need to understand is the regulation of our fat tissue itself and why it would go awry. He calls it Adiposity 101:
The message of eighty years of research on obese animals is simple and unconditional and worth restating: obesity does not come about because gluttony and sloth make it so; only a change in the regulation of fat tissue make a lean animal obese.
The regulation of fat tissue is a bit different than we often imagine. Fat tissue is not like a savings account we add to and then pull from at an indeterminate time later. It’s more like the battery in a solar energy system: It stores excess energy when it is available, then releases it later when the energy isn’t available, at regular periodic intervals.
We’re constantly storing and releasing fat: During every meal, the body mobilizes its resources to store energy not immediately needed. Later, when we’re between meals or sleeping, the body breaks down the stored energy and uses it to fuel the cells. This is how a normally functioning body works. The principle of homeostasis tells us that the body wants to stay in balance: We should be storing only as much fat as needed to survive.
The problem comes when the body isn’t functioning normally, and the balance is lost. We tend to think this happens becausewe’re overeating. But what if that’s the effect, not the cause? It’s counter-intuitive, but so is the fact that the sun doesn’t revolve around the earth.
The culprit is resistance to insulin, a natural hormone which (amongother things) encourages fat storage and discourages the release of fat stores while it’s circulating.
Remember, we depend on fatty acids for fuel in the hours after a meal, as blood sugar levels are dropping to their pre-meal level. But insulin suppresses the flow of fatty acid from the fat cells; it tells the other cells in the body to burn carbohydrates. So, as blood sugar returns to a healthy level, we need a replacement fuel supply.
(But) if insulin remains elevated, the fat isn’t available…as a result, the cells find themselves starved for fuel, and we quite literally feel their hunger. Either we eat sooner than we otherwise would have or we eat more when we do eat, or both. As I said earlier, anything that makes us fatter will make us overeat in the process. That’s what insulin does.
Taubes thinks we’ve gotten the causality backwards: Overeating doesn’t make us fat any more than overeating makes young children get taller; getting fat causes us to overeat. Our cells are literally being starved for energy by the selfish fat tissue, growing on its own accord in a tumor-like fashion driven by an abundance of circulating insulin. A isn’t causing B…B is causing A. This error has been the source of bad dieting advice.
Resistance is Futile
How do we become insulin resistant in the first place? Simple: We over-consume easily digestible carbohydrates, which causes heavy and constant insulin response in our bloodstream. This level of carbohydrate consumption was not available to our ancestors year-round, making it a modern problem. (One objection that’s been raised here is that our ancestors simply didn’t live long enough to contract modern disease. I hypothesize that there’s an error being made: Many earlier humans lived perfectly long lives, certainly long enough to get obese and hypertensive, but one major reason average life expectancy waslow is because child mortality was so high.)
In any case, our cells eventually become resistant to insulin, and as more and more of the hormone is released in response–to keep our blood sugar down–our fat remains stored away tightly in the form of triglycerides (tri = 3 fatty acids, glycerol = a binding molecule; how our body stores fat for later).
The indicators for diseases we now associate with obesity, including hypertension, diabetes, and stroke, have now largely been lumped under the term Metabolic Syndrome. Because these indicators–high triglycerides, high blood pressure, low HDL cholesterol among them–are often associated with an expanding waistline, many have been led to believe that obesity causes the other associated diseases.
Not so, according to Taubes:
The simplest way to look at all these associations, between obesity, heart diseases, type 2 diabetes, metabolic syndrome, cancer, and Alzheimer’s (not to mention the other conditions that also associate with obesity and diabetes, such as gout, asthma, and fatty liver disease), is that what makes us fat–the quality and quantity of carbohydrates we consume–also makes us sick.
The insulin resistance is causing obesity and other problems. It isn’t that A causes B, it’s that C is causing A and B. Another important logical flaw.
The implications are fairly obvious, from a diet perspective. We should cut our consumption of carbohydrates drastically, especially those that digest into the blood most easily and cause the most drastic insulin response.
Taubes smartly delimits himself from going beyond that advice, though:
It would be nice if we could improve on the foods to eat, foods to avoid, foods to eat in moderation. Unfortunately, this can’t be done without guessing. The kind of long-term clinical trials have not been undertaken that would tell us more about what constitutes the healthiest variation of a diet in which the fattening carbohydrates have already been removed.
Our conventional dietary wisdom, as I’ve described in my books, is based on science that was simply not adequate to the task of establishing reliable knowledge — poorly-controlled human experiments, observational studies incapable of establishing cause and effect, and animal studies that may or may not say anything meaningful about what happens in humans.
That’s why he and Peter Attia created the Nutritional Science Initiative, or NuSi, with the idea of pulling together a range of scientists and researchers to perform more precise experiments. The goal is understanding whether a calorie is really a calorie, whether carbohydrate-restrictive diets are more effective (and why) and a host of other pertinent questions. Only good data will convince the public (and the health officials it turns to for advice) that things need to change. Their work is underway as we write.
What makes Taubes an effective thinker, and writer is that he’s pulling from diverse fields in his quest to solve the obesity problem. While nutritionists typically silo themselves, to a certain extent, in their own field, with some influence from psychology to explain why obese people tend to overeat, Taubes instead pulls from anthropology, biochemistry, endocrinology, epidemiology, and the field of nutrition itself. By asking the right questions of the right people, he gets better answers. He isn’t afraid to step on toes. He also uses careful induction, sorting point by point the problems with competing hypotheses. This is something that reminds us of all great thinkers, from Newton to Darwin to Holmes to Munger.
Nutrition is a field changing in real-time: It needs precise thinkers with a strong penchant for self-criticism, truth-seeking, contrarianism, and boundary-crossing. Whether or not Taubes’ Alternative Hypothesis ends up being the correct one, the job needs to be done right. Observational studies, on which most nutritional recommendations are based, are not science: They are hypothesis-generators. Correlation generators. Figuring out causality is a tougher task.
The good news is that this core problem is solvable, and we suspect, like psychology, the field will come together in time.
There is no consensus on nutrition research.
Despite the rise in gym-going and healthy eating, one in three Americans is considered overweight.
The Alternative Hypothesis suggests that modern diseases aren’t because of too many calories but rather because of too many carbohydrates like sugar.
According to Taubes, a better understanding of the regulation of fat tissue is the key to unlocking the mysteries of our body.
We constantly store and release fat. When we become insulin resistant, the balance is gone and we gain weight.
Overeating doesn’t make us fat any more than overeating makes young children get taller; getting fat causes us to overeat.
Taubes recommends we cut our consumption of carbohydrates, especially those that digest into the blood most easily and cause the most drastic insulin response.
“The decision to reject one paradigm is always simultaneously the decision to accept another, and the judgment leading to that decision involves the comparison of both paradigms with nature and with each other.”
The progress of science is commonly perceived of as a continuous, incremental advance, where new discoveries add to the existing body of scientific knowledge. This view of scientific progress, however, is challenged by the physicist and philosopher of science Thomas Kuhn, in his book The Structure of Scientific Revolutions. Kuhn argues that the history of science tells a different story, one where science proceeds with a series of revolutions interrupting normal incremental progress.
“A prevailing theory or paradigm is not overthrown by the accumulation of contrary evidence,” Richard Zeckhauser wrote, “but rather by a new paradigm that, for whatever reasons, begins to be accepted by scientists.”
Between scientific revolutions, old ideas and beliefs persist. These form the barriers of resistance to alternative explanations.
Zeckhauser continues “In this view, scientific scholars are subject to status quo persistence. Far from being objective decoders of the empirical evidence, scientists have decided preferences about the scientific beliefs they hold. From a psychological perspective, this preference for beliefs can be seen as a reaction to the tensions caused by cognitive dissonance. ”
* * *
Gary Taubes posted an excellent blog post discussing how paradigm shifts come about in science. He wrote:
…as Kuhn explained in The Structure of Scientific Revolutions, his seminal thesis on paradigm shifts, the people who invariably do manage to shift scientific paradigms are “either very young or very new to the field whose paradigm they change… for obviously these are the men [or women, of course] who, being little committed by prior practice to the traditional rules of normal science, are particularly likely to see that those rules no longer define a playable game and to conceive another set that can replace them.”
So when a shift does happen, it’s almost invariably the case that an outsider or a newcomer, at least, is going to be the one who pulls it off. This is one thing that makes this endeavor of figuring out who’s right or what’s right such a tricky one. Insiders are highly unlikely to shift a paradigm and history tells us they won’t do it. And if outsiders or newcomers take on the task, they not only suffer from the charge that they lack credentials and so credibility, but their work de facto implies that they know something that the insiders don’t – hence, the idiocy implication.
…This leads to a second major problem with making these assessments – who’s right or what’s right. As Kuhn explained, shifting a paradigm includes not just providing a solution to the outstanding problems in the field, but a rethinking of the questions that are asked, the observations that are considered and how those observations are interpreted, and even the technologies that are used to answer the questions. In fact, often the problems that the new paradigm solves, the questions it answers, are not the problems and the questions that practitioners living in the old paradigm would have recognized as useful.
“Paradigms provide scientists not only with a map but also with some of the direction essential for map-making,” wrote Kuhn. “In learning a paradigm the scientist acquires theory, methods, and standards together, usually in an inextricable mixture. Therefore, when paradigms change, there are usually significant shifts in the criteria determining the legitimacy both of problems and of proposed solutions.”
As a result, Kuhn said, researchers on different sides of conflicting paradigms can barely discuss their differences in any meaningful way: “They will inevitably talk through each other when debating the relative merits of their respective paradigms. In the partially circular arguments that regularly result, each paradigm will be shown to satisfy more or less the criteria that it dictates for itself and to fall short of a few of those dictated by its opponent.”
But Taubes’ explanation wasn’t enough to satisfy my curiosity.
“The decision to reject one paradigm is always simultaneously the decision to accept another, and the judgment leading to that decision involves the comparison of both paradigms with nature and with each other.”
Anomalies are not all bad.
Yet any scientist who pauses to examine and refute every anomaly will seldom get any work done.
…during the sixty years after Newton’s original computation, the predicted motion of the moon’s perigee remained only half of that observed. As Europe’s best mathematical physicists continued to wrestle unsuccessfully with the well-known discrepancy, there were occasional proposals for a modification of Newton’s inverse square law. But no one took these proposals very seriously, and in practice this patience with a major anomaly proved justified. Clairaut in 1750 was able to show that only the mathematics of the application had been wrong and that Newtonian theory could stand as before. … persistent and recognized anomaly does not always induce crisis. … It follows that if an anomaly is to evoke crisis, it must usually be more than just an anomaly.
So what makes an anomaly worth the effort of investigation?
When the anomaly comes to be recognized as more than another puzzle of science the transition, or revolution, has begun.
The anomaly itself now comes to be more generally recognized as such by the profession. More and more attention is devoted to it by more and more of the field’s most eminent men. If it still continues to resist, as it usually does not, many of them may come to view its resolution as the subject matter of their discipline. …
Early attacks on the anomaly will have followed the paradigm rules closely. As time passes and scrutiny increases, more of the attacks will start to diverge from the existing paradigm. It is “through this proliferation of divergent articulations,” Kuhn argues, “the rules of normal science become increasing blurred.
Though there still is a paradigm, few practitioners prove to be entirely agreed about what it is. Even formally standard solutions of solved problems are called into question.”
Einstein explained this transition, which is the structure of scientific revolutions, best. He said: “It was as if the ground had been pulled out from under one, with no firm foundation to be seen anywhere, upon which one could have built.”
All scientific crises begin with the blurring of a paradigm.
In this respect research during crisis very much resembles research during the pre-paradigm period, except that in the former the locus of difference is both smaller and more clearly defined. And all crises close in one of three ways. Sometimes normal science ultimately proves able to handle the crisis—provoking problem despite the despair of those who have seen it as the end of an existing paradigm. On other occasions the problem resists even apparently radical new approaches. Then scientists may conclude that no solution will be forthcoming in the present state of their field. The problem is labelled and set aside for a future generation with more developed tools. Or, finally, the case that will most concern us here, a crisis may end up with the emergence of a new candidate for paradigm and with the ensuing battle over its acceptance.
But this isn’t easy.
The transition from a paradigm in crisis to a new one from which a new tradition of normal science can emerge is far from a cumulative process, one achieved by an articulation or extension of the old paradigm. Rather it is a reconstruction of the field from new fundamentals, a reconstruction that changes some of the field’s most elementary theoretical generalizations as well as many of its paradigm methods and applications.
Who solves these problems? Do the men and women who have invested a large portion of their lives in a field or theory suddenly confront evidence and change their mind? Sadly, no.
Almost always the men who achieve these fundamental inventions of a new paradigm have been either very young, or very new to the field whose paradigm they change. And perhaps that point need not have been made explicit, for obviously these are men who, being little committed by prior practice to the traditional rules of normal science, are particularly likely to see that those rules no longer define a playable game and to conceive another set that can replace them.
Therefore, when paradigms change, there are usually significant shifts in the criteria determining the legitimacy both of problems and of proposed solutions.
That observation returns us to the point from which this section began, for it provides our first explicit indication of why the choice between competing paradigms regularly raises questions that cannot be resolved by the criteria of normal science. To the extent, as significant as it is incomplete, that two scientific schools disagree about what is a problem and what is a solution, they will inevitably talk through each other when debating the relative merits of their respective paradigms. In the partially circular arguments that regularly result, each paradigm will be shown to satisfy more or less the criteria that it dictates for itself and to fall short of a few of those dictated by its opponent. There are other reasons, too, for the incompleteness of logical contact that consistently characterizes paradigm debates. For example, since no paradigm ever solves all the problems it defines and since no two paradigms leave all the same problems unsolved, paradigm debates always involve the question: Which problems is it more significant to have solved? Like the issue of competing standards, that questions of values can be answered only in terms of criteria that lie outside of normal science altogether.
Many years ago Max Planck offered this insight: “A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.”
One thing that has always baffled me is how we get fat.
Why We Get Fat by Gary Taubes unearths the biological truth around why we’re getting fat. In the process, Taubes dispels many accepted ideas on weight-loss and nutrition.
While it’s easy to believe that we remain lean because we’re virtuous and we get fat because we lack self-control or discipline, the evidence clearly says otherwise. Taubes methodically tackles conventional (and governmental) wisdom and why it is wrong.
This is a biology book, not a diet book. It’s about the science of what’s happening in our body that makes us fat. Let’s explore Taubes argument.
Is this a simple calories-in calories-out problem?
Do low-calorie diets work? In the short-term yes but overall, no.
“The two researchers who may have had the best track record in the world treating obesity in an academic setting are George Blackburn and Bruce Bistrian of Harvard Medical School. In the 1970s, they began treating obese patients with a six-hundred-calorie-a-day diet of only lean meat, fish, and fowl. They treated thousands of patients, said Bistrian. Half of them lost more than forty pounds.”
They concluded, “This is an extraordinarily effective and safe way to get large amounts of weight loss.” Yet, shortly after, Taubes says “Bistrian and Blackburn gave up on the therapy because they didn’t know what to tell their patients to do after the weight was lost. The patients couldn’t be expected to live on six hundred calories a day forever, and if they returned to eating normally, they’d gain all the weight back.”
So, even if you lose weight on a low-calorie diet, you’re stuck with the what now problem.
What if i just exercise more?
What happens when we increase our energy expenditure by upping our physical activity? Taubes says “Considering the ubiquity of the message, the hold it has on our lives, and the elegant simplicity of the notion-burn calories, lose weight, prevent disease-wouldn’t it be nice if it were true?”
Alas, believing doesn’t make it so. While there are many reasons to exercise regularly, losing weight isn’t one of them.
Taubes looks at the evidence and walks us through a chain of reasoning. The evidence says obesity associates with poverty. In most modern parts of the world, the poorer people are, the fatter they are likely to be. Yet, it’s the poor and disadvantaged who sweat out a living with physical labor. This is one of the reasons to doubt the assertion that expending a large amount of energy on a regular basis makes us fat.
Another reason to doubt the calorie-out hypothesis is the obesity epidemic itself. We’ve been getting fatter for the past few decades which suggests that we’re getting more sedentary. Until the 1970s, that is, before the obesity problem, Americans were not believers in the need to spend leisure time sweating.
In addition, it turns out there is very little hard evidence to support the belief that the number of calories we burn has any meaningful impact on how fat we become. The American Heart Association even calls the data supporting this claim “not particularly compelling.”
A study by Paul Williams and Peter Wood collected detailed information on almost 13k runners and then compared the weekly mileage with how much they weighed year-to-year. As you would expect, those who ran the most tended to weigh the least, but, perhaps unexpectedly, all these runners tended to get fatter with each passing year (even those running more than 40miles a week!)
According to Taubes, the belief in exercising more to weigh less is “based ultimately on one observation and one assumption. The observation is that people who are lean tend to be more physically active than those of us who aren’t. This is undisputed. … But this observation tells us nothing about whether runners would be fatter if they didn’t run or if the pursuit of distance running as full-time hobby will turn a fat man or woman into a lean marathoner. We base our belief in the fat-burning properties of exercise on the assumption that we can increase our energy expenditure (calories-out) without being compelled to increase our energy intake (calories-in).”
This assumption is wrong. We ended up buying into this exercise-more-eat-less story because it feels intuitive, correct, and reinforces our beliefs. We didn’t ask for evidence and none has been forthcoming in the intervening years.
Is it a matter of balancing calories?
No. Weight gain is a gradual process. So once you notice your jeans are getting tight, you can make some smart decisions and cut calories and increase physical activity right? “If it were true that our adiposity is determined by calories-in/calories-out, then this is one implication: you only need to overeat, on average, by twenty calories a day to gain fifty extra pounds in 20 years.” Now think of all the food decisions you make in a day and how impossible it would be, without scientific instrumentation, to balance your food.
Wait, what about thermodynamics. The law that says energy can be transformed from one form to another but not created nor destroyed.
“The very notion that we get fat because we consume more calories than we expend would not exist without the misapplied belief that the laws of thermodynamics make it true. When experts write that obesity is a disorder of energy balance—a declaration that can be found in one form or another in much of the technical writing on the subject—it is shorthand for saying that the laws of thermodynamics dictate this to be true. And yet they don’t.
All the first law of thermodynamics says is that “if something gets more or less massive, then more energy or less energy has to enter it than leave it. It says nothing about why this happens. It says nothing about cause and effect. It doesn’t tell us why anything happens.”
Experts think the first law is relevant because it fits neatly with our existing theories about why we get fact—those who consume more calories than they burn will gain weight. Thermodynamics tells us that if we get fatter and heavier, more energy enters our body than leaves it. But the important question, at least from an obesity perspective, is why do we consume more calories than we expend?
One of the other problems with thermodynamics argument is the assumption that the energy we consume and the energy we exert have little influence on each other—that we can change one without impacting the other.
The literature says that animals whose food is suddenly restricted tend to reduce energy expenditure both by being less active and by slowing energy use in cells, thereby limiting weight loss. They also experience hunger so that once the restriction ends, they will eat more than their prior norm until the earlier weight is obtained. (This is the same problem Bistrian and Blackburn encountered earlier).
Another problem with Thermodynamics is that it doesn’t address why men and women fatten differently. This means, at least at some level, bodily functions and possibly genetics play a role.
When we believe, as we do, that people get fat because they overeat, we’re putting the ultimate blame on a weakness of character and leaving biology out of it. This implies that we can generally tell, just by looking at the waistline, which people have strong self-control.
In the early 1970s, George Wade studied the relationship between sex hormones, weight, and appetite by removing the ovaries from rats. The impact was dramatic: the previously skinny rats ate voraciously and became obese. “The rat eats too much, the excess calories find their way to the fat tissue, and the animal becomes obese,” offers Taubes. He continues, “this would confirm our preconception that overeating is responsible for obesity in humans as well. But Wade did a revealing second experiment, removing the ovaries from the rats and putting them on a strict postsurgical diet. Even if these rats were ravenously hungry after the surgery, even if they desperately wanted to be gluttons, they couldn’t satisfy their urge.” The rats still got just as fat, just as quickly. And that is the start of our understanding of why we actually get fat.
The animal doesn’t get fat because it overeats, it overeats because it’s getting fat. The animal is unable to regulate its fat tissue.
A follow-on experiment, where the rats were injected with estrogen after the surgery, resulted in normal behavior. That is, they did not become slothful or obese. Biologically, one of the things that estrogen does is to influence an enzyme called lipoprotein lipase (LPL). When cells want fat they express their interest by “expressing” LPL. If the LPL comes from a fat cell, we get fatter. If the LPL comes from a muscle cell, it gets pulled in and digested as fuel. LPL, according to Williams Textbook of Endocrinology, “is a key factor in partitioning triglycerides (i.e., fat) among different body tissues.”
One of Estrogen’s roles is to inhibit the activity of LPL “expressed” by fat cells. The rats in Wade’s experiments over-ate because they were losing calories into fat cells that were needed in other places. The fatter the rat got, the more it had to eat to feed the non-fat cells. When the body is unregulated, it creates a cycle of getting fatter and fatter.
This, as Taubes says, “reverses our perception of the cause and effect of obesity. It tells us that two behaviors—gluttony and sloth—that seem to be the reasons we get fat can in fact be the effects of getting fat.” It also tells us that influencing LPL (either positively or negatively) has a dramatic effect on how fat we get.
LPL also explains why men and women get fat in different spots and why exercise doesn’t work. In men, LPL, activity is higher in the gut and lower below the waist. In women, LPL is highest below the waist. Bad news though, after menopause, LPL in a woman’s abdomen catches up to the men. As for exercise, while we’re working out LPL activity decreases on our fat cells and increases on muscle cells—so far, so good—because this prompts the release of fat from our fat tissue so that muscles can use this as energy. When we stop exercising, however, the situation reverses. LPL activity on the muscle cells shuts down and LPL activity on fat cells picks up. The fat cells natural tendency is to get back to their previous state.
So what regulates all of this?
Insulin. The LPL on fat cells is regulated by the presence of insulin. The more insulin our body secretes, the more active the LPL becomes on the fat cells, and the more fat that, rather than being consumed as fuel by the muscle cells, gets stored in fat cells. As if designed to ensure we get fatter, insulin also reduces the LPL expressed by the muscle cells (to ensure there is lots of fat floating around for the fat cells). That is, it tells the muscle cells not to burn fat as a fuel.
Insulin also influences an enzyme called hormone-sensitive lipase, or HSL. And this says Taubes, “may be even more critical to how insulin regulates the amount of fat we store. Just as LPL works to make fat cells (and us) fatter, HSL works to make fat cells (and us) leaner. It does so by working inside the fat cells to break down triglycerides into their component fatty acids so that those fatty acids can then escape into the circulation. The more active this HSL, the more fat we liberate and can burn from fuel and the less, obviously, we store. Insulin also suppresses this enzyme HSL and so it prevents triglycerides from being broken down inside the fat cells to a minimum.” This also helps explain why diabetics often get fatter when they take insulin therapy.
Carbohydrates primarily determine the insulin level in the blood. Here quantity and quality are important. Carbs ultimately determine how fat we get. But most people eat carbs so why are some fatter than others? We all naturally secrete a different level of insulin — given the same food people will secrete different levels of insulin. Another factor is how sensitive your cells are to insulin and how quickly they become insensitive. The more insulin you secrete—naturally or with carbohydrate rich foods—the more likely it is that your body becomes insulin resistant. The result is a vicious circle.
Not all foods containing carbs are equally fattening. The most fattening foods are those that have the greatest impact on our insulin and blood sugar levels. These are the easily digestible carbs. Anything made of refined flour (bread, cereals, and pasta), starches (potatoes, rice, and corn), and liquids (beer, pop, fruit juice). “These foods,” says Taubes, “flood the bloodstream quickly with glucose. Blood sugar shoots up; insulin shoots up; We get fatter.”
Here is Taubes in a 70-minute video explaining more.
In Robert Lustig’s view, sugar should be thought of, like cigarettes and alcohol, as something that’s killing us. But can sugar possibly be as bad as Lustig says?
Lustig’s argument is that sugar has unique characteristics, specifically in the way the human body metabolizes the fructose in it, that may make it singularly harmful, at least if consumed in sufficient quantities.
The first symptom doctors are told to look for in diagnosing metabolic syndrome is an expanding waistline. This means that if you’re overweight, there’s a good chance you have metabolic syndrome, and this is why you’re more likely to have a heart attack or become diabetic (or both) than someone who’s not. Although lean individuals, too, can have metabolic syndrome, and they are at greater risk of heart disease and diabetes than lean individuals without it.
Having metabolic syndrome is another way of saying that the cells in your body are actively ignoring the action of the hormone insulin — a condition known technically as being insulin-resistant. Because insulin resistance and metabolic syndrome still get remarkably little attention in the press (certainly compared with cholesterol), let me explain the basics.
You secrete insulin in response to the foods you eat — particularly the carbohydrates — to keep blood sugar in control after a meal. When your cells are resistant to insulin, your body (your pancreas, to be precise) responds to rising blood sugar by pumping out more and more insulin. Eventually the pancreas can no longer keep up with the demand or it gives in to what diabetologists call “pancreatic exhaustion.” Now your blood sugar will rise out of control, and you’ve got diabetes.
Not everyone with insulin resistance becomes diabetic; some continue to secrete enough insulin to overcome their cells’ resistance to the hormone. But having chronically elevated insulin levels has harmful effects of its own — heart disease, for one. A result is higher triglyceride levels and blood pressure, lower levels of HDL cholesterol (the “good cholesterol”), further worsening the insulin resistance — this is metabolic syndrome.
When physicians assess your risk of heart disease these days, they will take into consideration your LDL cholesterol (the bad kind), but also these symptoms of metabolic syndrome. The idea, according to Scott Grundy, a University of Texas Southwestern Medical Center nutritionist and the chairman of the panel that produced the last edition of the National Cholesterol Education Program guidelines, is that heart attacks 50 years ago might have been caused by high cholesterol — particularly high LDL cholesterol — but since then we’ve all gotten fatter and more diabetic, and now it’s metabolic syndrome that’s the more conspicuous problem.
This raises two obvious questions. The first is what sets off metabolic syndrome to begin with, which is another way of asking, What causes the initial insulin resistance?
Sugar scares me too, obviously. I’d like to eat it in moderation. I’d certainly like my two sons to be able to eat it in moderation, to not overconsume it, but I don’t actually know what that means, and I’ve been reporting on this subject and studying it for more than a decade. If sugar just makes us fatter, that’s one thing. We start gaining weight, we eat less of it. But we are also talking about things we can’t see — fatty liver, insulin resistance and all that follows. Officially I’m not supposed to worry because the evidence isn’t conclusive, but I do.