Of all the dangerous ideas that health officials could have embraced while trying to understand why we get fat, they would have been hard-pressed to find one ultimately more damaging than calories-in/calories-out. That it reinforces what appears to be so obvious—obesity as the penalty for gluttony and sloth—is what makes it so alluring. But it’s misleading and misconceived on so many levels that it’s hard to imagine how it survived unscathed and virtually unchallenged for the last fifty years.

It has done incalculable harm. Not only is this thinking at least partly responsible for the ever-growing numbers of obese and overweight in the world—while directing attention away from the real reasons we get fat—but it has served to reinforce the perception that those who are fat have no one to blame but themselves. That eating less invariably fails as a cure for obesity is rarely perceived as the single most important reason to make us question our assumptions, as Hilde Bruch suggested half a century ago. Rather, it is taken as still more evidence that the overweight and obese are incapable of following a diet and eating in moderation. And it puts the blame for their physical condition squarely on their behavior, which couldn’t be further from the truth.

Gary Taubes from Why We Get Fat

While trying to catch up on my reading before piles of Financial Times, New York Times and Wall Street Journals consume our living space, I came across a review of Donald Rumsfeld’s book, Known and Unknown.  The title of which was taken from one of his orotund responses to a reporter about the various kinds of knowledge we have.  Said he:

There are known knowns. These are things we know that we know. There are known unknowns. That is to say, there are things that we know we don’t know. But there are also unknown unknowns. There are things we don’t know we don’t know.

Mr. Rumsfeld believes the last of the above, the things we don’t know we don’t know, is the most problematic.  I disagree.  I think the first gets most people in trouble most of the time.  And this includes Rummy himself.

It ain’t so much the things we don’t know that get us into trouble. It’s the things we know that just ain’t so.

So opined Henry Wheeler Shaw (AKA Josh Billings), who said it a lot more memorably well over a century ago in a quote often misattributed to Mark Twain, Will Rogers and others.

One of the things countless people ‘know’ that just ain’t so – or at least that ‘just ain’t so’ as they think they know it – is that people get fat because they eat too much or exercise too little.  In the minds of many, it’s all a matter of calories in versus calories out.  Which is a really meaningless statement of the problem, but which leads inexorably to the conclusion that people get fat because they are either gluttonous or lazy or both.  The so-called Gluttony and Sloth model for obesity.

Why is the calories in vs calories out notion so meaningless?  If more calories come in than go out, you gain weight, and if more calories are expended than come in, you lose weight.  Seems reasonable.  It’s a bewitching notion, because it is absolutely true but at the same time absolutely meaningless.  It tells us nothing.  Let me digress to explain using a painful example from my own past.

Almost 20 years ago I singlehandedly dragged my family into the restaurant business.  I bought a franchise for a Mexican food place. (If you’re interested, you can read more about it here.) I recruited (read: dragooned) all our children to operate it, and despite all our best efforts, the venture ended in disaster.  But during the run, I spent a lot of time in the restaurant.  And one of the constant conversational threads was why it was or wasn’t busy at any given time.  We would have a Saturday afternoon during which few people came in.  As a consequence, the next Saturday we would schedule a skeleton crew, and we would be slammed.  Then someone would realize that there was a Razorback football game in Little Rock that weekend, which would explain it.  Or so we thought. Sometimes for no apparent reason we would have people swarm in.  There would be a line out the door with more showing up by the minute.  We would all be working like dogs to get everyone served, all the while saying to ourselves and to one another: What the #$&**!!# is going on? Why are we so packed?

Now imagine if during one of these rushes, one of us had said, It’s really quite simple:  we’re so crowded because there are way more people coming into the restaurant than there are people leaving.  We all would have looked at the person uttering such nonsense as if he/she were the village idiot.  But the statement is absolutely 100 percent correct.  That’s why we were so busy.  More people coming in than going out.  But it doesn’t really answer the question at hand.  What we want to know is why so many people are coming in?  A Razorback game? A big sale at the department store next door? A good review in the paper that we weren’t aware of? A bus full of people broken down outside the front door?  Why are there so many more people coming in than going out? If we could figure out the why, then we would have an easier time scheduling staff.*

It’s the same with the calories in/calories out notion.  If you’re fat, you’ve been taking in more calories than you’ve been expending.  No one would argue that.  At least no one with good sense.  But the question is, why?  Why have you been taking in more than you’ve been expending?  That’s the question you want to have answered, because only when you discover the answer can you figure out why you’re fat and what to do about it.

Gary Taubes has done the figuring and writes about it in his new book, Why We Get Fat And What To Do About It (WWGF).  As most readers of this blog know, a few years ago Gary wrote a long, detailed book on what we can call the Carbohydrate Theory of disease, titled Good Calories, Bad Calories (GCBC).  Now he has come out with what many think is a slimmed-down version of GCBC, called by some GBGC-Lite. But it’s not really a lite version of GCBC – it’s something much different.  I call it GBGC-Fat.  I would append the term ‘fat’ because it’s about fat – adipose tissue – and why so many of us struggle so mightily to rid ourselves of superfluous wads of it.

WWGF is a great primer on fat gain, fat loss and just about everything having to do with obesity.  I read GCBC three times, starting with the first manuscript version and ending with the actual book.  I’ve done the same with WWGF, so I can assure you that it is not a rewrite of GCBC, but is mainly new material presented in a much easier to assimilate way.  As many people have discovered, trying to get their doctors or other non-believers to read GBGC is a tough sell.  Few, who aren’t already converts, can summon the will to dig in to a book that large.  The new book is much less intimidating than GCBC, but just as compelling.  Even the title is better and more seductive.  Who wouldn’t want to know why we get fat?

In his efforts to ferret out why we do get fat, Gary, an obvious follower of the Samuel Johnson admonition that we more often need reminding of old truths than instruction in new ones, looks to the pre WWII scientific literature for the ‘old truths’ that are still valid. One of which is that carbohydrates fatten both livestock and people.  If you think about it, it’s difficult for the current crop of academics to intuitively grasp this notion, because they have been inculcated from the time they entered kindergarten with the ‘dietary fat is bad’ mantra.  That kind of deep-seated learning is hard to shake.  Especially so, since when today’s academics were students, their mentors, who had built their own careers (all way post WWII) on the very same mistaken notion about fat, wouldn’t likely have provided much inspiration for their young charges to change.

So, why do people get fat?  Let’s look at it as Gary does and start from the beginning.

When we talk about obesity, we’re talking about the excess accumulation of fat.  The excess fat is stored in the fat cells (adipose cells), which, collectively make up the adipose tissue.  With that as our starting point, where do we go?

If we ask how the fat gets into the fat cells, we will discover that all the pathways of fat storage were worked out years ago and are so uncontroversial that they’re described in detail in every biochemistry and physiology textbook currently in use.  It’s well known that the metabolic hormone insulin stimulates an enzyme on the surface of the fat cell that moves the fat into the cell.

So if insulin moves fat into the fat cells, it would seem that a lot of insulin would move a lot of fat into the fat cells.  And indeed it does.  Given this, the rational person trying to figure out the previous step in our progression would ask What causes a lot of insulin?  Or the rational person, should he/she have been steeped for a lifetime in the marinade of ‘fat is bad’ might ask, What about fat?  If there is a lot of fat in the blood as a result of fat in the diet, wouldn’t that fat get into the fat cell?  If so, then doesn’t dietary fat lead to fat?

A good question, but the answer is no.  Type I diabetics can have a lot of fat in their diets and in their blood, but if they have no insulin, they can’t store that fat.  In fact, most pre-diagnosis type I diabetics lose enormous amounts of weight despite eating ravenously because without insulin they can’t store the fat.  So dietary fat itself – even large amounts of it – won’t find its way into the fat cell without the help of insulin.

When you hack through the thicket of all the biochemical pathways involved in the metabolic process, you find that insulin is the primary force involved in the storage of nutrients.  Insulin is the body’s storage hormone: it puts fat in the fat cells, protein into muscle  cells and glucose into it’s storage form, glycogen.  Insulin, along with its counter-regulatory hormone glucagon (the Yin and Yang of metabolism), are involved in nutrient partitioning – the process of stashing nutrients away in different parts of the body and/or harvesting them for the body to use as energy.

If we have a lot of insulin, the insulin dominant-pathways (the storage pathways) hold sway, and fat is partitioned away in the fat cells; if insulin is low, then the glucagon-dominant pathways (the energy-release pathways) take over and start moving fat out of the fat cells, so it can be consumed by the body as fuel.  This is how it is supposed to work.  We eat.  Insulin comes out and stores away the energy.  We go for a while without eating, insulin goes down and glucagon comes out to retrieve our stored fat so we’ll have a continuous energy supply.

Problems arise when this system goes off the rails, which most commonly happens when people develop insulin resistance, a problem of disordered insulin signaling.  Insulin talks, but the cells don’t listen.  So insulin keeps talking louder until the cells finally get the message. In other words, the pancreas keeps producing insulin and the blood levels continue to rise until the cells finally get the message.  But it’s a message that has taken a lot of insulin force to deliver.

If all the different types of cells developed resistance to insulin at the same rate, we wouldn’t have as much of a problem.  But they don’t. Different cells develop insulin resistance at different rates.  Typically the first cells to become insulin resistant are the liver cells.  The liver cells are continuously producing sugar and dumping it into the blood.  Insulin shuts this process down.  If the insulin level drops to zero, as it does in type I diabetes, the liver dumps a huge load of sugar in the blood causing all the blood sugar problems associated with this disease.  Under normal circumstances, just a little insulin stops the liver cells in their tracks.  But if these cells are resistant to insulin, much more is required to get them the message to turn off the sugar spigot.

In most people, the fat cells develop insulin resistance later, which creates the problem.  If insulin levels are high to control the liver’s sugar factory output, then these elevated insulin levels are sending a strong message to the non-insulin-resistant fat cells.  The message is take this fat and store it.  High insulin not only drives fat into the fat cells, it prevents it from getting out.  Fat is packed into the fat cells and kept there.

Between meals when insulin levels would normally fall, allowing the liberation of fat to feed all the body’s tissues, insulin remains high in an effort to keep the liver in check.  Fat can’t get out of the fat cells, and the tissues begin to starve.  Even though there is plenty of stored fat, the body can’t get to it because elevated insulin is preventing its release.

Starving tissues send a message to the brain, saying ‘we’re hungry.’  The brain responds by increasing the drive to feed.  We eat, and the carbs we eat are consumed by the cells for immediate energy, and insulin stimulated by the dietary carbohydrate drives the fat into the fat cells where it is trapped with the rest of the fat already there.  The fat cell mass gets larger and larger, and we become obese.

The above scenario explains a lot.  Why can some people eat like crazy and not get fat?  Perhaps because they develop insulin resistance in their fat cells just as they do in their liver cells.  They don’t get fat, but they typically have all the other insulin-driven problems of the obese: high blood pressure, elevated triglycerides, increased risk for heart disease, etc.  And all while staying skinny.

How about morbid obesity?  Easy.  Those people don’t develop insulin resistance in their fat cells until late in the game, if ever.  They continue to push fat into the fat cells and become more and more obese until they weight 400-500 pounds or even more.  The average person will finally develop fat cell insulin resistance before the morbid obesity stage.  When this happens, weight and level of obesity stabilize and stay the same, almost irrespective of how much is eaten.

We now know why we get fat.  Excess insulin drives fat into the fat cells increasing the fat cell mass, ultimately leading to the state we call obesity. If we keep walking this progression back, the next question has to be, Why do we make too much insulin?

We make too much insulin because we eat too many carbohydrates, especially sugar and other refined carbohydrates.  With that statement, we’re starting to edge into controversial territory, but it’s only territory populated by the ignorant.  The hard science is emphatic that carbs are a pure insulin play.  Eat them and your insulin goes up.

Some people with a little learning may be quick to point out that protein drives insulin up as well.  This is true, but with a catch.  Protein drives both insulin and glucagon up, so you don’t have the pure insulin effect.  Only carbs will give you that.  With carbs, insulin goes up while glucagon goes down.  With meat and other proteins, the effects of the elevated insulin are muted by the concomitant rise in glucagon. (Glucagon isn’t called insulin’s counter-regulatory hormone for nothing.)

As Gary lays out the progression, carbs increase insulin, excess insulin drives excess fat into the fat cells, the fat cell mass grows, and we become fat.  This chain of cause and effect leads to the ineluctable conclusion that excess carbohydrate intake leads to obesity.  And each and every link forged in this chain is scientifically unimpeachable.

So if you are fat and want this progression to reverse itself, wouldn’t it make sense to reduce your carbohydrate intake?  All the science is valid.  But don’t just take my word for it. Gary writes of a former Harvard professor responsible for much of the early work in the field of the regulation of fat accumulation who summed it up like this:

Carbohydrate is driving insulin is driving fat.

If you put that in reverse, you should cut the carbs, reduce the insulin and lose the fat.  Seems simple, but here is where all kinds of controversy rears its head. Even the very smart Harvard professor who did the original work and uttered the above quote, when asked by Gary why there is so much obesity, responded that people didn’t exercise enough. Which also proves true what Saul Bellow wrote years ago:

A great deal of intelligence can be invested in ignorance when the need for illusion is deep.

As I’ve written numerous times in the pages of this blog, food is made of three things: fat, protein and carbohydrate.  When you decrease one, you typically increase the other.  If you cut the carbs, you’re going to increase the fat and protein in your diet.  And it’s the increased fat in particular that leads to all the controversy.

The current zeitgeist is that dietary fat, especially saturated fat, is bad.  And not just bad, but extremely bad.  So, even though they may understand that carbs drive fat storage, the ingrained fear of fat keeps many otherwise smart people from accepting the merits of the low-carbohydrate diet.  To escape the cognitive dissonance, they default to the calories in/calories out argument, which, as we’ve seen, is meaningless.  But they feel safe taking refuge in what they believe is a known known. More’s the pity since it will end up doing them about as much good as it did Rummy in the Iraq war.

Most rational people will find the above argument understandable and be able to connect the dots showing that carb intake leads to excess insulin leads to obesity.  The difficult concept for many to grasp, however, is the other problem with too much insulin: it prevents the stored fat from being accessed for energy. Normally adipose tissue acts as a reservoir of energy.  We eat, we convert the food we don’t immediately use into fat, and the body – acting via insulin – stashes it away for later.  When later comes, insulin falls, glucagon rises, and the body starts harvesting it’s stored fat to provide energy for all the cellular functions.  Then we eat, and the process starts anew.

In obese people it’s different.  They eat, they use the food for immediate energy needs and store the rest away.  In other words, they store excess energy away in their fat cells just like non-obese people do.  It’s the second part of the formula that is different.  In obese people, insulin is almost always elevated – even when they haven’t just finished a meal.  These chronically elevated insulin levels trap the fat in the fat cells, and, in fact, turn the fat pathway into the fat cell into a one-way street.  Fat can get in, but it can’t get out. If the fat does get out, the excess insulin tells the mitochondria not to burn it anyway, so it just gets sent back to the fat cells.

What does this mean for an obese person?

Let’s look back at the non-obese person to explain.  A non-obese person eats, uses the energy from the food and stores the rest.  During the time between meals and during sleep, the non-obese person draws on the stored fat to provide energy.  When the fat cell mass decreases to a certain critical point, the body signals the brain that the fat cells need a refill, so the brain initiates the hunger response.  The non-obese person eats, uses some energy for immediate needs, fills the fat cells with the rest, uses the stored energy as needed, and then the cycle repeats.

It doesn’t work that way in the obese.  Obese people eat, use the energy required for immediate needs and store the rest.  But–and this is the extremely important ‘but’– during the time between meals and during sleep, obese people can’t access their fat stores because their baseline insulin is too high.  When they can’t get to their stored fat, the lack of access to energy sets in motion all the same biochemical signals in the obese person that get sent in the non-obese, who have depleted the energy storage in their fat cells.  And these signals are converted by their brains into the drive to feed, i.e., intense hunger.  They have to eat to provide for their immediate energy needs because, thanks to chronically elevated insulin levels, they can’t get into to their own stored fat, even though it’s there waiting in massive quantities.

To use an analogy, it would be like being out of cash when you desperately needed it yet having a huge amount of money in the bank.  You hustle to an ATM machine and find your card won’t work.  It’s the same with the obese – they have plenty of energy to go without eating for months, but their fat ATM cards don’t work.  And since their fat ATM cards don’t work, the only option they have for immediate energy is to eat.

So fat people are fat not because they overeat – they overeat because they’re fat.

A real debt of gratitude is owed Gary for combing the old literature and ferreting out this notion.  As early to mid-twentieth century, researchers both in Europe and America had determined obesity is a disorder of fat accumulation, not a problem of ‘perverted appetite,’ self control, or gluttony and sloth.  Louis Newburgh, Ancel Keys, Jean Mayer and a few others were responsible for turning the herd thinking of academia in a different direction, and the ‘eat less, exercise more’ paradigm has been with us since. It’s doubtless not a coincidence that the obesity and diabetes epidemics have flourished as a consequence.  As I say, Gary deserves a lot of credit for resurrecting this old work and starting to turn opinion in the other direction.

In addition to the chapters describing and discussing the mechanisms by which we get fat, Gary has included other important material in his book.  One of my favorite chapters is the one titled “The Nature of a Healthy Diet.”  Although you wouldn’t know it from this title, the chapter fairly presents most of the arguments against low-carbohydrate diets and refutes them.  I’m sure many will find these refutations helpful in their dealings with naysayers, who seem compelled to point out non-existent problems with carb-restricted dieting.  There is one in particular that I plan to deploy at the next opportunity.  Since I have my own arguments against the rest of the anti-low-carb idiocy, it annoys me greatly that I didn’t think of this one myself.

Here is a scenario I often endure at a party or other get together after my identity as a diet book writer and low-carb expert has been revealed:

Other person, OP (typically an overweight female): I tried a low-carb diet once.

Me: (Dreading what’s sure to follow.) Oh, really.

OP: Yes, and it worked for a while, but I couldn’t stick to it.

Me: Oh, really?  Why not?

OP: Well, I felt tired and spacey headed.

Me: People sometimes experience those symptoms early on, but they usually resolve after a couple of weeks.  And there are steps you could’ve taken to prevent or minimize them.

OP: No, I don’t think so in my case.  I know my body, and I know what it’s telling me.  I’m just one of those people whose body needs carbs.  As soon as I started eating carbs again, I felt much better.

Me: (Fighting down the impulse to point out that she’s still fat…) Hmmm.  Maybe so.
Now, thanks to WWGF, I’ll know just what to say.  I’ll leave you with the relevant paragraph from the book along with my highest recommendation to grab a copy and read it.  I can promise you won’t be disappointed.

The more technical term for carbohydrate withdrawal is “keto-adaptation,” because the body is adapting to the state of ketosis that results from eating fewer than sixty or so grams of carbohydrates a day.  This reaction is why some who try carbohydrate restriction give it up quickly. (“Carbohydrate withdrawal is often interpreted as a ‘need for carbohydrate,’ ” says Westman.  “It’s like telling smokers who are trying to quit that their withdrawal symptoms are caused by a ‘need for cigarettes’ and then suggesting they go back to smoking to solve the problem.”)

* Full disclosure:  In the first draft of WWGF I read, Gary had used the crowded restaurant example to explain why the calories in/calories out explanation was so ridiculous.  It reminded me of our dismal times in the restaurant business, and I thought it was a brilliant way to demystify the problem.  In one of the later drafts I read, the restaurant example was missing.  I asked Gary about it, and he told me he and his editor had decided it wasn’t the best way to describe the situation.  I disagreed (probably because my financial wounds from the restaurant biz, though long past, were still painful) and told Gary I thought it was a terrific way to explain it and that if he didn’t use it, I would rip it off and use it as my own.  Although he has used the examples in lectures, Gary didn’t use it in the book, so, true to my word, I ripped it off as my own.