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.

If you tell a lie big enough and keep repeating it, people will eventually come to believe it.*

Joseph Goebbels (pictured left)
Reich Minister of Public Enlightenment and Propaganda

The history of our race, and each individual’s experience, are sown thick with evidence that a truth is not hard to kill and that a lie told well is immortal.

Mark Twain, Advice to Youth

I’ve always loved the above two quotes because their sentiments are so on the money.  It is sad but true that the bigger the lie, the more people are willing to unquestioningly accept it.  And the greater the mass of people who accept the lie, the easier it is to persuade others to join the growing crowd.  In such a way does a great lie snowball into a great ‘truth.’

Nutritionally I can’t think of a bigger lie than the one claiming that fats in general and saturated fats in particular are bad for us.  This lie is so deeply embedded in the minds of most that you couldn’t blow it out with a stick of dynamite.  Especially in the minds of academics, and more especially in the minds of most dietitians.  Not all, but most. Nutritionally, it is truly the Big Lie.

Despite the fact that they all tenaciously cling to the Big Lie, the evidence disputes it.  But, “a lie told well is immortal.”  Over at Whole Health Source Stephen Guyenet wrote a post recently looking at the observational data about saturated fat and cholesterol levels and heart disease.  Most of the Big Lie devotees worry obsessively about saturated fat intake while the great mass of observational data shows little, if any, correlation.  A couple of years ago, I wrote a long post about the invalidity of observational studies as proof of much anything, but in that post I neglected to mention that although observational studies can’t show that correlation equals causation, they probably are valid in demonstrating the opposite: if there is no correlation, there probably isn’t much of a case for causation.  So, if there isn’t a lot of correlation between saturated fat intake and elevated cholesterol and/or heart disease, is doubtful that saturated fat intake is causal.

I just came across a paper – a research editorial, to be correct – in the Journal of the American Dietetic Association (JADA) that, did I not already have a close and abiding relationship with Jameson, would drive me to drink.  In fact it probably did drive me to drink just a little more.  Now the JADA is the journal edited by and written for Registered Dietitians, and, as a consequence, it has an RD feel to it in terms of content.  It usually hews to the low-fat, high-carb party line, but every now and then it publishes a paper on some facet of low-carbohydrate dieting.  The particular article that caused my heartburn is titled Low-Glycemic Load Diets: How Does the Evidence for Prevention of Disease Measure Up?

This article annoys me on many levels, the first of which is that it even talks about glycemic index (GI) and glycemic load (GL).  I’ve written previously about why I don’t believe the glycemic index to be a particularly valid way of characterizing carbohydrates. And I don’t think the glycemic load concept is much better.  What’s wrong with simply counting carbohydrates?  It provides more benefits and doesn’t encourage the consumption of fructose, a harmful sugar with a low glycemic index.  The reason the glycemic index and glycemic load have been so embraced by the academic community is because they simply can’t bring themselves to admit that the low-carb diet is a superior diet for weight loss, lipid control, blood pressure lowering, blood sugar stabilization, GERD ridding, etc. than is their beloved low-fat diet.  So instead of manning up and admitting that they had been wrong for the past 40 years, they tart the venerable low-carb diet up in academic sounding garb and call it the glycemic load diet and hope no one notices the subterfuge.

It’s perfectly acceptable to talk about low glycemic load diets bringing about health benefits without anyone saying, Whoa, you’ll croak your kidneys. Or, Whoa, you may lose weight, but you’ll clog your arteries.  No, the low glycemic load diet is perfectly innocuous in any company.  No pompous academic will give you grief if you simply use the word ‘glycemic.‘  Try using the term ‘low-carb’ in the halls of Academe, however, and you may be in for some withering stares.

The author of the ‘research editorial‘ drones on about a handful of studies that have looked at the efficacy of low-glycemic-load diets in preventing the development of type II diabetes and other metabolic conditions in healthy subjects.  All of the studies discussed have various problems: not large enough, not long enough, less than optimal dietary questionnaires, etc.  Given the watery results of the studies describe, the article then ends on a bizarre note.

Despite the limitations of the available studies, there is increasing evidence that low-glycemic-load diets could prevent diabetes, cardiovascular disease, and some cancers, including endometrial cancer and esophageal adenocarcinoma.

Say what?

Yep, each of these statements is backed up by a citation or two.  It would seem to me that the ‘research editorial’ would have been much more interesting and meaningful had it focused on the results of these cited studies instead of the ones it did.

Nonetheless, the author soldiers on (and this is the part that really torques me):

In light of these findings, adherence to a low-glycemic-load diet, provided it meets current dietary recommendations including those related to dietary fat content and portion control, seems prudent. [Italics mine]

Ah, the Big Lie rears its fearsome head.  Doesn’t matter how well the diet works or what diseases it might prevent, we don’t want to follow it unless we meet those current recommendations on fat.  No sir.

Do you think the author of this drivel has ever really thought about what food is made of?  It seems unlikely.

Food is made of fat, protein and carbohydrate.  That’s it.  Food also contains water, vitamins, minerals and other nutrients, but only fat, carbohydrate and protein provide calories.  And when a diet is constructed of these things – especially one that toes the line as far as portion control is concerned – trade offs have to be made.

If you keep the calories the same, and you decrease one of the three components, you’re going to have to increase one of the others.  Let’s look at how the brain of a lipophobe would cypher this.  Okay, we need to cut the fat, so that’s the first thing we’ll do.  We’ll cut fat, and we’ll really cut saturated fat.  But now we’ve got to get our calories back up, so we’ll add low-glycemic carbohydrates to do that.  But, uh oh, when we add that many carbs, even though they are low-glycemic-index carbs, we increase the glycemic load.  We can’t really do that if we want to prevent all these diseases.  We’ll increase the protein.  But, wait, we can’t increase it too much or we’ll damage the kidneys. (A myth, of course, but they all believe it.)  And it’s hard to increase the protein without increasing the fat because most good sources of protein contain fat, even, God forbid, saturated fat.  So if we up the protein, we up the fat.  But fat is the devil in disguise, oh yes it is; it’s the devil in disguise.  Can’t go there.

See what I mean.  If you are a lipophobe, there is no solution. It could be called the Lipophobe’s Conundrum.  And that’s why I’m glad I‘m not a lipophobe, so I don’t have to worry about it. I haven’t bought into the Big Lie.  All I need to do is cut the carbs and let everything else take care of itself.

*Below is the Goebbel’s quote in full.  Interesting to note that Dr. Joe’s ideas are still alive and well and in full use by many of our own politicians.

“If you tell a lie big enough and keep repeating it, people will eventually come to believe it. The lie can be maintained only for such time as the State can shield the people from the political, economic and/or military consequences of the lie. It thus becomes vitally important for the State to use all of its powers to repress dissent, for the truth is the mortal enemy of the lie, and thus by extension, the truth is the greatest enemy of the State.”

I so often come across such breathtaking nutritional ignorance foisted off as legitimate information that I’m left feeling like the girl in this photo. I wrote about this woeful ignorance on the part of the medical community in my last post.  Now it’s time to take a look at the misinformation many registered dietitians dispense as a matter of course.

I have subscriptions to many magazines, most of which I save up to read while I’m on airplanes so I can trash them after I read them and lighten my load as I travel.  A couple of days ago I was on a flight from Newark to Seattle casually paging through a golf magazine when I came upon one of these well-meaning (I’m sure) but totally incorrect little bits of advice.  The only saving grace is that I’m sure the vast majority of people reading this magazine will totally ignore this advice and go on doing whatever it is they’ve been doing.  But the advice is so abominably wrong that it cries out for exposure.

I’m sure the magazine needed a little space filled up so the editor charged one of the magazine’s staff writers come up with a fluff piece to fit the space required.  The editor may have specified that the piece be nutritional in content because the add right below it is for Planter’s NUT-rition line of nut products “specifically designed to give you the taste you want and the energy you need.”

So, the staff writer contacts a registered dietitian and picks her brain.  Based on the dietitian’s responses, it was slim pickings indeed.

The shtick of the piece is that the snacks favored by a handful of professional golfers were to be analyzed by the dietitian.  The piece starts out thus:

Here’s how Tour pros satisfy those mid-round munchies – and how you can stay energized for all 18 holes.

Here is a bit of the actual piece that I scanned.  I was unable to find a link to the article.

Then it’s off to a pro by pro (there are snacks from seven pros) analysis and the idiocy begins.

Tiger Woods is first.  His favorite snack is a peanut butter sandwich.  Our registered dietitian, Sharon Richters, babbles (or raves, as the article puts it) about the good fats and protein in peanut butter then cuts to the pure idiocy:

The bread has carbohydrates.  Whole-grain bread gives you longer-lasting energy, and regular bread gives a quick jolt of energy.  It’s the perfect golf snack.

The white-bread, brown-bread double whammy.  What wonderful nutritional advice.  Somehow this woman has got it in her head that carbohydrates, and only carbohydrates, provide energy.  It gets worse.

Canadian golf pro Mike Weir snacks on a homemade energy bar made of granola, honey and a bunch of other stuff.  Says our registered dietitian:

Honey is OK as a sweetener, although agave is healthier.

I suppose agave is ‘healthier’ (a totally grammatically incorrect construction, by the way) than honey if you choose to disregard scads of medical evidence and choose instead to believe consuming more fructose makes you healthier.  Honey, like table sugar, is half fructose whereas agave nectar is about 90 percent fructose.  I don’t know about you, but I would prefer to minimize my fructose intake.

English golfer Paul Casey allegedly throws back walnuts during his rounds.  Not so good, says Ms. Richter, RD.

Walnuts alone will not provide enough energy.  You’re on the course for hours at a time, so I suggest adding carbohydrates for energy.  Fruit is always a good idea – bananas are easy to carry around and eat, and coconut water is a good source of carbs.

Jesus wept.

It takes a certain genius to cram so much misinformation into such a little space.  Let’s deconstruct.

Why is it that so many people – especially registered dietitians, it seems – believe that carbohydrates are the only source of energy available?  This notion is widespread.  You need energy, therefore you’ve got to eat carbs.

Walnuts contain over twice the energy than the do same dose of pure carbs.  And this energy – in the form of fat – provides a much longer burn time than would a similar dose of carbs.  So if one is on the course “for hours at a time” why on earth wouldn’t a ready source of fat such as walnuts be a vastly better snack than a comparable amount of carbs?

The energy in foods is represented as the caloric content. According to the USDA tables, a medium banana provides 105 calories, most of which comes from sugars.  One ounce of walnuts – which isn’t much of a snack – contains 185 calories, most in the form of monounsaturated and polyunsaturated fats along with a little protein and almost no carb.  Most people using walnuts as a snack would throw back a few ounces over the course of a round of golf, so you tell me which is the best energy source.

And when walnuts or other low-carb, high-fat snacks are consumed, insulin remains low, allowing the body to access stored body fat for any extra energy that might be needed.  If the snacks are high-carb – as this woman suggests – insulin levels rise, making it more difficult for the fat cells to release fat, causing the cycle of more hunger, more carb consumption, and more insulin.

To continue with this nonsense, tell me please when coconut water became a good source of carbs?  The USDA tables tell us that a full cup of coconut water provides a measly 46 calories that come primarily from the 6 or so grams of sugar contained therein.  Doesn’t sound like much of an energy source or a carb source to me.

Do these people learn this in school?  Do they just make it up because it sounds good?  Where are their brains?  It took me about 30 seconds to search the USDA database of foods to find these numbers, so why couldn’t the authors of this drivel have done the same and saved themselves the embarrassment of having this nonsense in print under their names?  It beggars belief.

I once read that golfers are the least intelligent of all professional athletes.  I don’t know if that’s true or not, but let’s say it is.  I’ve seen Paul Casey interviewed a number of times, and he seems – from my limited observation – to speak with the same degree of intelligence as most other professional golfers I’ve heard.  So let’s assume Paul Casey is in the middle of the pack intelligence-wise of all professional golfers.  Professional athletes – as a group – are not at the top of the intelligence list in general.  By this reasoning, we might say that Paul Casey operates at not the highest level of intelligence, yet he has sense enough to pick walnuts as a snack instead of bananas and coconut water.  What does this say about the level of intelligence of the people writing this article?

Before you attack me for casting aspersions on the intelligence levels of anyone, please realize that the above is tongue in cheek.

Let’s look at one more, then I’ll quit.

Golfer Luke Donald chows down on Chocolate Chip Peanut Crunch Clif Bars and dried apricots during his rounds.  Our dietitian likes the idea of apricots.

Dried fruit is a good source of carbohydrates.

Gotta get those carbs in.  I suppose that these people are blissfully unaware of our millions of years of evolutionary history.  A time during which we humans cut our teeth on protein and fat while pretty much hunting to extinction most of the large game animals on the planet.  Why do they persist in the notion that the only way we can get energy is via carbohydrates?  Do they think we noshed on carbs as we hunted the wooly mammoth and the cave bear into non-existence?

The Clif Bar is a bit high in sugar, but it doesn’t have a lot of junk in it.

Hmm.  Interesting.  “A bit high in sugar, but doesn’t have a lot of junk in it”?  What, pray tell, is sugar, if not junk.  Sugar is nothing but empty calories, half of which are fructose.

I’ve got to quit before I do permanent damage to my forehead from beating it against the desk.

It should go without saying that nutritional ignorance and misinformation abounds.  You can get it from all sources, including, sadly, your own doctor.  I doubt that many readers of this blog would be swayed from their nutritional course by the kind of drek written in this golf magazine, but others probably are.  We’ve all got to be vigilant and work to stamp out nutritional idiocy wherever we find it.  It’s a real jungle out there filled with clueless people with titles of one sort or another ready to snare the unwary with this dopey stuff.  Don’t fall victim.

Synchronicity strikes again.  The seeds of this post were sown when Gary Taubes emailed me about a study published in early 2009 in the New England Journal of Medicine (NEJM) that I had seen at the time, briefly skimmed and tossed aside as worthless.  Gary agreed that the study was of little value, but notice that it contained a peculiar statement by the authors, an interesting admission about HDL, the lipophobe’s favorite lipoprotein.  And not only had the authors made this strange admission, but so had another prominent lipophobe who wrote the accompanying editorial.

I pulled the study, read it more thoroughly and still found it mediocre at best.  But I did come across the strange HDL statements that Gary had mentioned. (More about which later.)

As I was shaking my head over the amount of money spent on what was a truly abominable study, the synchronicity occurred.  I got a ding that I had a new email.  It was a notice from the American Heart Association telling me that this august body had deemed the very study I was holding in my hands as one of the ten most important papers published in 2009.  The sheer stupidity of it nearly took my breath away.

Before we get into the study – which we won’t get into very deeply because, believe me, there’s not much depth – I want to use a parable to show just how silly this study is.

Let’s set our story in the wonderful country of Stupidland where a debate has been raging about the feeding of dogs.  A vociferous old woman who kept dogs had been insisting that different breeds of dogs eat different amounts of food  The majority of the populace were of the opinion, however, that all breeds eat the same amount (it is Stupidland, after all) and looked down their noses at those who  believe a chihuahua may eat less than a collie.  To put an end to the bickering, scientists at Stupidland U ( who were believers in the all-dogs-eat-the-same doctrine) decided to do a definitive study.  They went to the Stupidland pound and procured a German Shepherd, a Labrador Retriever, an Irish Setter and an Alaskan Malamute.

They provided the four dogs with pleasant accommodations and all the food they wanted to eat.  The scientists carefully measured every gram of food eaten by each dog and recorded it.  At the end of the two year study, they reviewed the data and confirmed what they already suspected to be the case: the different breeds of dogs ate just about the same amount.  They did notice one little disparity, however: the larger dogs ate a little more than the smaller dogs, but they were able to correct for that by controlling for size.  Their paper proving that different breeds of dogs ate the same amount of food was accepted for publication in one of Stupidland’s most prestigious scientific journals, The Stupidland Journal of Veterinary Medicine.  Buried deep within the paper was a sentence few noticed stating that size was a biomarker for food consumption by dogs.

The Stupidland press picked up on the study and headlines proclaimed that all breeds of dogs eat the same amount.  The mainstream Stupidlanders nodded their heads sagely; they, after all, had been right all along.  But the old woman, who didn’t actually live within the borders of Stupidland, but who lived close enough to cause trouble, kept insisting that different breeds of dogs didn’t eat the same amounts.  She had a beagle and she had a Great Dane, and she had kept careful records of the food consumption of both. She insisted that the Great Dane not only ate more than the beagle, but that it ate a huge amount more. She would bend the ear of anyone who took the time to talk to her, and her data was so persuasive that she was beginning to make converts.  Just as the population of Stupidland was once again starting to wonder about the dog breed verses food enigma, the Stupidland Heart Association came out with its annual bulletin announcing that the paper by the brilliant scientists from Stupidland U showing that all breeds of dogs ate the same was the most important paper of the year.  The old woman’s first impulse was to attack the Stupidland Heart Association for its sheer stupidity, when suddenly a sense of calmness and clarity settled over her.  She experienced a spiritual awakening (just as did the Grinch in another tale) and finally realized the real meaning of Stupidland. She took her dogs and moved far away, leaving the denizens of Stupidland alone to marinate in their stupidity.

The paper that inspired this parable was published in Feb 2009 in the New England Journal of Medicine and titled Comparisons of Weight-Loss Diets with Different Compositions of Fat, Protein, and Carbohydrates.  (This is another one of those studies the editors feel is so important that they provide the full text free of charge as a public service.)  The authors include Frank Sacks, George Bray, Steven Smith and an entire rogue’s gallery of lipophobes.  All the usual suspects, as they say.

What the NEJM study sets out to demonstrate is that different breeds of dogs different weight-loss diets of varying macronutrient compositions all bring about the same loss of weight.  According to these authors, it doesn’t matter if you go on a low-carb, high-fat diet or a low-fat, high-carb diet, you’ll lose the same amount of weight.  Doesn’t matter how the protein, fat and carbohydrate stack up in your weight loss diet, you’re going to lose the same amount of weight.  So, you can go to the bookstore, stand by the diet-book shelf, close your eyes and pick.  Whatever diet book you end up with won’t matter because you’ll lose the same amount of weight regardless of which one you choose.  And, even more importantly – again, according to the authors of this study – whichever diet book you select will help reduce your heart disease risk factors.

As Dave Barry says: “I AM NOT MAKING THIS UP.”  It’s right there in black and white in a study done at Harvard and published in the New England Journal of Medicine.

What’s more, the American Heart Association (AHA) deemed this study to be one of the top ten most important studies published in 2009.  And they put it #1 on their list.  Now they said that they listed these ten studies in no particular order – and you can call my cynical -  but I’m just betting that they put this one right at the top for a reason.

Said the president of the AHA, Dr. Clyde W. Yancy

We all thought the statement made in that study was pretty profound. It really dismissed the notion that there’s something clever about weight loss, [showing] that it really is about calorie consumption or, to make it even more straightforward, portion control. You can spend a lot of time wringing your hands about which diet and the composition of which diet, but it really is a simple equation of calories in and calories out.

Give me strength.

My disgust aside, you may be thinking:  Why isn’t the study valid?  If they did analyze all those diets and found them to bring about the same results, what’s the problem?

The problem is that the diets they used in the studies were similar.  They didn’t vary all that much in carbohydrate.  The diet with the highest carb intake contained 65 percent of calories as carbohydrate while the lowest carb diet was made up of 35 percent.  To put this into the gram figures we’re all used to, the highest-carb diet contained 325 gram of carb while the lowest-carb version contained 175 gram of carbohydrate.  Now, as those of us who have ever followed a low-carb diet know, 175 gram of carbohydrate does not a low-carb diet make.  Granted, it’s lower in carb than the diet with the 65 percent of calories as carb, but it doesn’t even approximate a low-carb diet.  As I’ve written before, you’ve got to get the carbs substantially below 100 g per day before good things start happening metabolically.

What this study has done is to study roughly similar diets for two years and pronounce that all produce about the same results.  What the authors (and, apparently the AHA) want you to take away from this study is that real, honest-to-God low-carb diets don’t perform any better than low-fat, high-carb diets.  Which, as most of us know from bitter experience, is not the case.

There are major problems in doing studies such as this one that make their outcomes suspect.  And these problems aren’t necessarily the fault of the researchers – they are simply a fact of life.

When you try to do a dietary study by recruiting people who want to lose weight then randomizing them to a particular diet, you are asking for trouble.  If you run the study out over a long period of time – two years, for example, as this study did – you are asking for even more trouble.  People go into diets with a lot of enthusiasm and pretty rigorously stick to them at first.  But as time goes on, people tend to cheat a little, then cheat a little more and pretty soon find themselves pretty much trending back toward and finally squarely back on whatever their regular diet was before they started the study diet.  (Sadly, it’s not just subjects in studies who follow this pattern, but is the fate typical of most dieters.)  For this reason, after time, all the people in all the different arms of the study are eating about the same thing.  This is why you always see the charts showing weight loss and macronutrient composition start out wildly diverging then converge as the end of the study draws near.  In other words, they all end up consuming the same diet, so they all end up with about the same result.

How can researchers overcome this dismal outcome.  Well, you can put out the call for people who really believe in low-carb diets to fill one arm of the study.  And recruit people who love the Ornish diet for another, and the Zone for another.  These subjects are more likely to stay enthused and stick with their respective regimens for the duration of the study.  But then you haven’t randomized your sample and you will be accused of generating worthless data because your sample groups self selected.

The other way, of course, is to randomize subjects into various diet groups, then put them under lock and key for a year or two and feed them like you would lab animals.  Another impractical solution from a cost perspective if in no other reason.

It’s extremely difficult – virtually impossible, I would say – to conduct accurate studies on diet over a long period of time with a large number of subjects.  Consequently, it is nonsensical to rely on the data from such studies to make the case for anything other than how difficult these studies are to carry out.  I certainly don’t think for all the reasons above that the study in question merits being listed as one of the top ten studies of 2009 by anyone, much less the AHA.

In their discussion of this mishmash of questionable data, however, the authors did make a most interesting statement.  Almost an admission, if you will, of the superiority of a lower carb diet.  This statement is what Gary emailed me about.

(Before we go on with this, I have to make this aside.  HDL and LDL and IDL (intermediate density lipoprotein) and VLDL (very low density lipoprotein) aren’t really cholesterols.  Even though we often refer to them as LDL cholesterol and HDL cholesterol, they really aren’t.  These different groups of letters refer to transport proteins that carry cholesterol through the blood, not to cholesterol itself.  Cholesterol is cholesterol.  It is a specific molecule that doesn’t change.  Cholesterol is a waxy lipid (fat) that virtually every cell in the body synthesizes (because is it so important).  Cholesterol, like all fats, is not soluble in water and therefore can’t dissolve in blood (which is a watery substance), which means that the body has to package cholesterol in a form in which it can be transported from place to place in the blood.  The body attaches a specific protein (a lipoprotein) to cholesterol to make it dissolve in the blood.  The names LDL, HDL and the rest refer to the specific type of lipoprotein being discussed.)

Here’s what the authors wrote:

There was a larger increase from baseline in the HDL cholesterol level, a biomarker for dietary carbohydrate [my italics], in the lowest-carbohydrate group than in the highest-carbohydrate group (a difference in the change of 2 mg per deciliter at 2 years)…

Even Martijn Katan, a lipophobe if there ever was one, and the author of a number of anti low-carb diatribes that I’ve taken to calling the Katanic Verses echoes the same fact – carbohydrates drive HDL down – in an editorial he wrote about the above paper.

…compliance was assessed with objective biomarkers.

The authors used the difference in the change in HDL cholesterol levels between the lowest- and highest-carbohydrate groups to calculate the difference in carbohydrate content between those diets.

Now the differences weren’t all that spectacular, but the drop in HDL in those on the higher carb diet was there and noticed by the researchers.

I find this extremely revelatory because if there is one lipid parameter a lipophobe loves, it’s HDL.  And here you have an entire cluster of lipophobes admitting that HDL varies as the inverse of carbohydrate intake.  Take any of these folks individually – or, heck, take ‘em together – and they’ll tell you that low-carb diets are bad because they give you too much fat.  Yet they admit that their beloved HDL goes up when carbs go down.  Doesn’t make a lot of sense, does it?

When these folks compared these fairly similar diets they found that all of them reduced the risk for heart disease.  They used the fact that HDL went up on the lower-carb diets to deem them heart healthful; and they pronounced the higher-carb diets as heart healthful, too, because the LDL declined on those.

As Yogi Berra said: “You can observe a lot by just watching.”  And they watched LDL go down on the higher-carb diets and HDL go up on lower-carb diets.  But the reverse of the Yogi-ism is also true: you can also fail to observe if you don’t watch.

This refusal to watch is what really gets my dander up.

The researchers whose names are listed at the top of this paper are all affiliated with prestigious institutions.  I am quite sure that there is not a single one of them who is unfamiliar with the work over the last 15 years or so of Ronald Krauss, the researcher who made the discovery of the differences between LDL particle sizes. (The same Krauss, by the way, who published the paper about the meta-analysis of saturated fat and heart disease much in the blogosphere currently.) Krauss and his team showed that large, fluffy LDL particles aren’t particularly harmful whereas the small, dense LDL particles are the ones that cause the problems.  He also discovered that increasing carbohydrate in the diet caused LDL to shift to a smaller, denser pattern while decreasing carb and adding fat made LDL change to the larger, fluffier non-problematic kind.  (You can read a nice review of LDL particle size in this article published in the popular press.)

If you reduce carbs and add fat to the diet, not only does your HDL go up, but your LDL makes a particle size change for the better.  However, when you increase carbs and reduce fat, your HDL goes down and your LDL goes down too, but it changes for the worse. So even though the high-carb, low-fat diet decreases LDL, it doesn’t decrease risk – it increases it because even though LDL is lower, it is made up of a dangerous particle size,which negates any possible value of the fall in LDL.  All of these researchers know this.

Why didn’t they check LDL particle size on these subjects?  Had they done that, they would have found that those subjects on the higher carb diets would have lowered their HDLs and althought they lower levels, would have shifted to more of the dangerous, smaller, denser LDL particles.  They couldn’t have then made the case that not only did all diets work the same where weight loss was concerned but they all decreased heart disease risk.  They would have had to say that although all diets brought about the same degree of weight loss, the lower-carb diets clearly reduced the risk factors for heart disease the most.  And that’s an admission I suspect they didn’t want to make. Therefore they refused to observe.

I don’t know what the deal is with these folks.  Why don’t they simply tell it as it is?  Do the long-term lipophobes who have ridiculed low-carb diets for years and built their careers on the rickety edifice of the low-fat diet not want to admit they were wrong? That’s understandable, I suppose, but what about the young ones?  Why are they stampeding over the low-fat cliff like Gadarene swine?  Do the younger lipophobes not want to offend the older ones?  Why do they fail to reconcile their theories with what amounts to basic biochemistry and physiology?  Whatever the reason, they are fighting a losing battle.  Ultimately the truth will out and when it does, all these people who have tenaciously clung to the low-fat, high-carb fantasy will be – like the phrenologists and other failed theorists of the past -  so much detritus in the history of medicine.  And their books and papers will be displayed as curiosities of the boneheaded thinking of an earlier day. A sad but fitting fate.

Photo: Set of phrenological heads, England  circa 1831
via The Pollo Web

In the early 1980s MD and I were laboring away in anonymity in our clinics in Little Rock, Arkansas.  By that time I had gone through my thin-to fat-to thin again metamorphosis, and I was starting to treat patients for obesity.  My own transformation had been fairly striking, a fact not lost on many of my overweight patients, a number of whom were seeking my professional advice on treating their own weight problems.  I was still doing a fair amount of general primary care medicine, but more and more of my time was being diverted to helping people lose weight.

When I, myself, had gotten fat, I had tried a few diets that were then being extolled (including the Pritikin diet) and had experienced pretty much the same thing most people did with these diets:  I lost a few pounds, drifted from the diet, and regained the lost weight plus a little.  I then started thinking seriously about obesity as a medical problem, and, in an effort to learn all I could about it, I turned to the medical textbooks on my shelves.  Unfortunately, none of them contained any information I found particularly enlightening.  The texts went into great detail about the risks associated with obesity and the many diseases that it either caused or made worse, but, other than recommending caloric restriction, none really discussed the treatment.  None really discussed (at least not to my satisfaction) what happens metabolically that makes people store excess fat.

I next turned to physiology texts, which didn’t help a lot, either.  I then grabbed my old medical school biochemistry textbook (I hadn’t been out of med school all that long at the time, so it was fairly current) and struck gold.  I started tracing out all the pathways for fat storage and noticed that in virtually every one insulin turned up somewhere.  Then I started reading about all the pathways involving insulin and realized that excess insulin had to be the agent driving the storage of excess fat.  I then went back to the physiology texts, reread them in light of my new found knowledge, and discovered that they reinforced what I had learned from the biochemistry text. I just hadn’t realized it, until I had made the insulin connection. (I drew out all the different pathways insulin worked through on piece of paper that we’ve saved, but I can’t lay my hands on it right now.  If I find it, I’ll post it.)

This was long before the days of Google and online searches; in fact, it was at least two years before I owned my first computer.  So I did what you did in those days: I trekked to the medical library at the med school, ran a search on insulin and obesity through their system, and came up with a handful of papers. The research into this field was quite new and sparse back then, but I learned about the newly proposed theory of insulin resistance, which answered my question as to why anyone would ever develop excess insulin levels in the first place.

Then I asked myself the big question:  If I have too much insulin (and I was guessing I did – it wasn’t something you measured in those days unless you were in a scientific lab), how do I get it down?  There were only two conclusions.  Don’t eat.  Or don’t eat carbohydrates. The latter seemed to make a lot more sense over the long run.

I remembered the Atkins diet.  I had read his book ten years before, but that was before I went to medical school and was while I was still rail thin.  (Why did I read it?  Because it was a huge bestseller, much in the news, and I wanted to see what all the fuss was about.)  I dug out my copy and reread it.  Nowhere was insulin mentioned in the original book.  He talked about some mysterious fat mobilizing substance (FMS, as he called it), which couldn’t be insulin because insulin doesn’t mobilize fat – it stores it.  The references cited in the back of the Atkins book for FMS listed scientific papers written in German. But, by then, I was on to insulin, so I didn’t bother trying to seek them out.

I decided to design a diet for myself with lowering insulin in mind.  What I came up with (with MD’s help) was the basis for what ultimately became Protein Power.  I lost weight like crazy.  Many of my patients noticed my weight loss and started clamoring for me to help them to become thin.

At the time I started treating patients with the low-carb diet, cholesterol was just starting to be demonized.  For the first time, people were concerned about their cholesterol levels (and at that time, the upper level for normal for total cholesterol was 220 mg/dl, 20 units higher than it is now) It was the era Taubes discusses in his great paper The Soft Science of Dietary Fat and that Tom Naughton shows in his movie Fat Head.  Low-fat diets were the rage.  The 8-Week Cholesterol Cure, a book about eating giant oat bran muffins daily and taking sustained-release niacin was in the writing and destined to be a mega bestseller.  The fear of fat was settling in on America.

And here I was starting to put patients on low-carb, high-fat diets to help them lose weight.

Back then I had bought into the lipid hypothesis and truly believed excess cholesterol did indeed lead to heart disease.  As a consequence, I was a little squeamish about putting people who might actually be at risk for heart disease on the diet.  I had read the biochemistry texts, and I knew that insulin stimulated HMG Co-A reductase, the rate limiting enzyme in the cholesterol synthesis pathway;  and I also knew that glucagon (insulin’s counter regulatory hormone) inhibited that same enzyme.  So, in theory, lowering insulin and increasing glucagon with diet should work to treat elevated cholesterol.  But, knowing those things theoretically didn’t really give me a whole lot of solace when it came to taking care of real flesh and blood patients who were entrusting their well being to me. (The picture at the top left of this post is one of the handouts I used in my early practice to demonstrate the many effects of too much insulin.)

Stupidly, when I started on the diet myself, I didn’t check my own labs, so I didn’t really know what happened to me.  The patients that I did put on the diet were typically women who were premenopausal (a group who rarely develop heart disease), so I didn’t worry about them.  I checked everyone’s labwork, but no one’s was really out of whack lipid-wise at the start of the diet, so I didn’t have a lot to go on data-wise.  The few who did have minimally elevated cholesterol tended to lower it over the first six weeks (I rechecked everyone at six weeks), so I figured the theoretical underpinnings of the diet were okay.  But I was still uneasy.

I had visions of myself in the witness box with a sneering plaintiff’s attorney saying to me:  So, Dr. Eades, are you telling the members of this jury that you put the deceased – whom you knew to have high cholesterol – on a diet filled with RED MEAT! IS THAT WHAT YOU’RE TELLING THIS JURY, SIR? YOU, SIR, CAUSED THIS MAN’S FATAL HEART ATTACK, DID YOU NOT?

But more than being worried about this scenario, I didn’t want to do anything harmful to anyone.  I knew it would be difficult to live with myself if I thought I had killed someone or caused a heart attack out of pure negligence.

You’ve got to remember that at this time there was no one in his/her right mind recommending a low-carb diet.  There was Atkins, of course, but he had been totally discredited in the eyes of the medical profession by that time.  It wasn’t until over 20 years later in 2004 that he and the low-carb diet got even minimally rehabilitated.  I was very uneasy to say the least.

Then four patients came into my clinic, one almost right after the other, who changed my life.  In my actual practice, I’m kind of old school and always refer to my patients as Mr, Miss or Mrs. But for purposes of this post, I’m going to refer to them by a bogus first name just to make it easier to keep track.

The first of the four patients we’ll call Angie.  She was referred to me by MD, who was working at a different clinic than I at the time.  Angie came into see MD for nausea and vague abdominal pains, symptoms that, along with tenderness in her upper right abdomen, led MD to suspect gall bladder disease.  Angie was a 32 year old woman who was mildly overweight and had vague abdominal pain, but no other remarkable findings.  MD drew blood on her and sent her for a gall bladder ultra sound.  The ultra sound came back negative, but her blood work was a doozy.   Her total cholesterol was over 300, and her triglycerides were about 1900.  MD called me and said “Have I ever got the patient for you.”  This was what I had been waiting for.  A patient who was female and pre-menopausal with terrible lipids.  I figured I could treat such a patient without any risk of her developing heart disease over the short term, and I planned to recheck lipids way sooner than the normal six weeks.  Since her lipids were so out of the ordinary for one so young, I asked MD to repeat them, fasting, have the results sent to me and to send Angie to see me after her repeat labs had come back.

When I got her labs, I knew the first reading wasn’t an error.  In fact, they were a little worse than when MD checked them the first time.

Total cholesterol: 374 mg/dl (all values in mg/dl)
LDL: ?
HDL: 28
Triglycerides (TG) 2080

(There was no value for LDL because LDL is a calculated number and can’t be calculated when the triglycerides are over 400 mg/dl.)

Upon examination I found a pleasant mildly overweight young woman who had no real physical signs except for mild tenderness in the right upper quadrant of her abdomen when I really pushed on it.  She had no family history of heart disease and she didn’t smoke – both pieces of information that made me feel better about what I was preparing to do.

(Not only were her lipids a mess, Angie’s liver enzymes were way abnormal as well.  I now know that she had non-alcoholic fatty liver disorder, but we (the medical profession) didn’t really recognize that as a common disease back then.  I’m sure her liver was inflamed to some degree, which explained the mild pain she was experiencing.)

I gave her a fairly rigid version of what became the Protein Power diet.  I explained exactly what she should eat and what she shouldn’t and sent her on her way with my home phone number and my beeper number (this was before the days of cell phones). I told her to call me if she had even the slightest problem and to return to the office in three weeks for a recheck no matter what. And I gnawed my nails.  I had the staff call her after a few days to see if she was doing okay.  She reported that she was fine.

I got no emergency calls from her and in three weeks she returned.  Her right upper quadrant pain had vanished as had her nausea.  She reported that she had never felt better.  She had even lost nine pounds (which was a fair amount for her since she wasn’t that overweight to begin with).   I rechecked her labs and waited anxiously for them to come back from the lab the next day.  When they did, I was stunned.

Total cholesterol: 292
LDL: 192
HDL 70
TG: 149

I had hoped for a change for the better, but I hadn’t in my wildest dreams expected this kind of change.  I kind of figured that her triglycerides and cholesterol would come down slowly over several months, not that they would drop like rocks in only three weeks.

The second of my life-changing patients was a casual friend of mine who came to see me about a week after my experience with Angie.  He was a 55 year old guy we’ll call Lynn who worked in advertising.  I had gotten to know him when his company created some brochures for our clinic.  He came to see me for an insurance physical.

He arrived, we chatted, and then I looked him over.  I poked and prodded and listened at all the appropriate places.  He seemed fine. He was a thinnish white male who was just starting to develop a little (and I mean little) paunch.  I would never have even noticed it had he not been sitting there with his shirt off.

Talk turned to my own weight loss, and he asked me if I could put him on a diet to help him lose his little pot belly.  I said ‘Sure,’ and told him about my meat, cheese, salad and green vegetable diet.  I told him that I had lost my weight eating a ton of steak and had continued to do so.  He was thrilled because he loved steak and had been avoiding it because of everything he had been reading about red meat and heart disease.  I had our nurse draw his blood for the lab part of his physical and sent him on his way.

The next day I was going through all the results from the bloodwork that had been drawn the day before when I came upon his.  I nearly dropped my teeth.

Total cholesterol: 312
LDL: ?
HDL: ?
TG: 1515

(There was a note on the lab sheet that said they were unable to determine the HDL because the serum was too lipemic (cloudy with fat)?!?!)

I thought, Whoa!, a 32 year old premenopausal woman is one thing, but a 55 year old male right in the middle of major-heart-disease-risk age is something else.  And here I had put this guy with totally disrupted lipids on a red-meat diet, which, according to current medical thinking, would almost guarantee to make the situation worse.  I put in an immediate call to his office and was told he had left that morning for vacation for two weeks.  (Why he had neglected to even mention this trip when we talked for 30 minutes the day before baffled me completely.) I asked for the number wherever he was.  His secretary told me that he was on a Caribbean Island and couldn’t be contacted.  I told her that if he called in to have him call me immediately.

My fears were somewhat assuaged because I figured, hey, the guy is on vacation, he’s not going to diet anyway.  Why should I worry?

He called me the day he got back and before I could get a word in told me “Hey, your diet works great.  I lost five pounds while I was on vacation.”  As it turned out, he was on a Caribbean Island, but it was a resort of some sort.  As part of his deal, all the food was provided.  He had chowed down on steak just about every day.

I was mortified.  I told him about his labs and told him to get into the clinic the next morning to have his blood rechecked.  He came in.  Here are his labs taken 15 days after his first ones.

Total cholesterol: 195
LDL: 124
HDL: 26
TG: 201

I was really stunned this time.  How could these values change this much in just 15 days?

He wanted to stay on the diet, so I told him to go for it. But I kept an eye on him.

Not long after this experience I had a very nice lady, named Jesse, who was the mother of a friend of mine come to see me.  She had had labwork done somewhere else and her cholesterol had come back as 735 mg/dl.  Her doctor had put her on a cholesterol-lowering medicine, but she was still distressed because she had a friend who remarked to her, “I didn’t know you could even be alive with a cholesterol that high.”  I examined her and found her to be a very mildly overweight 72 year old lady with no signs of anything out of the ordinary.  I rechecked her blood.

Total cholesterol: 424
LDL: ?
HDL: ?
TG: 1828

Along with these lipid labs, her fasting blood sugar came back at 154 mg/dl.  So, not only did she have major lipid abnormalities, she had blood sugar that was in the diabetic range.

I gave her instructions on the diet and told her to stay on her cholesterol-lowering meds until we checked her again in three weeks.

Three weeks later:

Total cholesterol: 186
LDL: 118
HDL: 27
TG: 201

I was surprised this time, but not stunned.  Along with these mega improvements in her lipids, Jesse’s fasting blood sugar was 90.

I told her she could go ahead and discontinue her cholesterol-lowering medications because her cholesterol was normal.  She looked at me kind of funny and said, “I stopped them when I started the diet.  That’s what I thought you said to do.”

The last of my four patients came along about two weeks after Jesse.  This woman, we’ll call Betsy, was famous in Little Rock.  Actually, she wasn’t the famous one – her husband was – but she got plenty of notoriety herself.  And just in case you’re wondering, it wasn’t Hillary.

She came to see me because she had picked up a little excess weight and wanted to get it off.  I went through my normal workup and found Betsy to be a moderately overweight woman with no other physical signs of ill health.

Her labs told another story.

Total cholesterol: 416
LDL: ?
HDL: ?
TG: 2992

(Like Jesse’s and Angie’s labs, Betsy’s didn’t show HDL because the serum was too lipemic.)

After three weeks on the program, Betsy lost 11 pounds and came through with the following labs:

Total cholesterol: 177
LDL: 122
HDL: 36
TG: 94

By then, I was kind of getting used to these seemingly miraculous lipid improvements, so I was no longer stunned.  But it did confirm that I was on the right track.

After my experiences with these four patients, all of whom came to see me over about a three month period, I became convinced that my theorizing about the potent effects of reducing insulin was based in reality.  Over the ensuing years, I saw many, many more patients with disturbed lipid metabolism whom I successfully treated with low-carb, high-fat diets, but these four, coming as close together as they did in the early days of my feeling my way along in my low-carb career, gave me the conviction to press on.

I am eternally grateful to them.

Applebee's Quesadilla Burger

One of my readers sent me a link to a segment on ABC News with Charlie Gibson showing just how disgustingly slanted and inaccurate mainstream media reports can be.

Gibson leads into the segment about two reporters who underwent self experimentation on the adverse effects of unhealthy eating.  The reporters, ABC’s Yuji de Nies and Jon Garcia, set out to see what would happen if they consumed a giant meal containing over 6,000 calories.  Here is the result as they reported it.

Click here to view the embedded video.

Pretty brutal, eh?  But let’s shine the piercing light of good sense on what is going on here.  As you might expect, the reality is vastly different from that portrayed by ABC.

First off, let’s look at the actual nutritional content of the food eaten.  As reported in the piece, the total energy content of the meal was 6,190 calories, which included 187 grams of saturated fat.  These were the only parameters reported.  I took the time to go through the links in the article accompanying the video to find exactly where these foods came from.  Here’s what I found.

The burger is an Applebee’s Quesadilla Burger (served with fries, of course); the snack is The Cheesecake Factory Fried Macaroni And Cheese; and the dessert is Uno Chicago Grill Mega-sized Deep Dish Sundae (listed as cookie below).  How do I know these are the exact ones?  These were the ones referenced in the CSPI’s List of Most Unhealthy High-Calorie, Fat and Salty Restaurant Foods That May Clog Your Arteries.  After seeing the photos and comparing to what I saw on the video, these selections are the ones the reporters ate.

I then tracked down the Nutritional Facts for the foods involved (here, here, here and here) and put them into an Excel spreadsheet.  Take a look.

The first thing you might notice is that the total calorie count is 5,708, which is considerable, but is actually 482 calories fewer than the 6,190 reported.  Second, and this is a biggie, the saturated fat content of this meal is only 88 grams, not the 187 grams reported.

The reporters stretched the truth a little in that they reported as if the Mega-sized Deep Dish Sundae were a single treat to be consumed by one person at a sitting.  I’m sure it could be so eaten, but it’s actually designed for four people to share.  The Nutritional Facts list the calories per serving as 690 and the saturated fat as 17 grams.  I’ve used the amounts in all four servings, i.e., one entire four-person dessert, in my spreadsheet.

As you may have noticed, the total carb content of the meal is 745 grams, which converts during digestion to a little over three cups (3.1 cups to be exact) of sugar.  The ABC report, of course, failed to mention the carb content of the meal and ignored any immediate effect this huge intake of carb might cause.  One of the reporters, Jon, claimed that he was ‘sluggish’ and ‘tired’; the implication being that this sluggishness resulted from his huge saturated fat intake.  No mention, naturally, of the enormous amount of carbohydrate and the large increase in insulin release it might cause.  From what I can see from the video, Jon looks to be sporting a little abdominal obesity, which would imply a degree of insulin resistance and hyperinsulinemia.  People with this disorder tend to over secrete insulin in response to carb intake causing an overshoot and reactive hypoglycemia (low blood sugar), which will indeed result in sluggishness.

It’s pretty impressive when the lab tech holds up the tube of blood taken after the meal and compares it to the one taken before the meal.  There is a lot of fat swimming in the serum, that’s for sure.  What the producers of this piece (and, sadly, the doctors commenting although they should know better) want you to take away from all this by the way they set it up is that all that saturated fat went directly into the blood.  And how can you argue with them?  It’s there for all to see.

Problem is, that’s what blood samples look like after almost any meal, especially one that contains carbohydrates.  The fat you see isn’t the fat the two reporters ate; it is the fat the liver has made from the carbohydrate.  It’s the same picture a tube of blood would show after either of the two doctors had eaten a high-carb, low-fat lunch.

The blood samples were taken two hours after the meal.  Dietary carbohydrate is absorbed directly into the blood and makes a pass through the liver where it stimulates the production of triglycerides, the fat you see in the blood.  Fat, especially long-chain saturated fat digests very slowly, and doesn’t reach the blood until much later than the two hour mark.  While carbs go directly into the blood, fats take a different route.  The process that breaks down dietary fat into its component fatty acids is a lengthy process as compared to the breakdown of carbs.  Once the fat has broken down, it has to combine with bile salts to make it into a form that is water soluble and can be taken up by the intestinal cells.  Once taken up, unlike carbs, which are sent directly to the bloodstream, fats go into the lymphatic system, a much smaller and more static transport system than the vasculature.  Once in the lymphatics, fats make their way to the thoracic duct, which empties into a large vein in the upper chest.  The lymphatics are small vessels and take a long time to move their contents along since there is no heartbeat pushing them as there is with blood.  As I say, the fat in the blood you see on the video didn’t come from the saturated fat in the diet, although that was definitely the implication.

But what about the ultrasound showing the blood vessels had changed?  Wasn’t that because of the fat?

I’m afraid not.  The fat from the diet wasn’t in the blood vessels yet, so it couldn’t be the dietary fat causing the change.  So what was it?

How about a little normal physiology.  Let me explain.  The body gets blood where it needs to get it by opening certain blood vessels while closing others.  Let me give you an example.  Have you ever jumped into cold water to go swimming and noticed that not long after jumping in you have to urinate?  What happened?

Your arms and legs have a radiator effect.  Since these appendages have little padding the blood circulating there is exposed to the cold water, and if nothing is done, the cold water cools the blood creating a big problem.  Your body compensates by shutting down the circulation to the skin and areas close to the surface in your arms and legs and shunts that blood to your core.  Your core already has plenty of blood when this happens, so it has to get rid of some.  It does so by sending it through the kidneys where the liquid portion is filtered out and becomes urine.  Suddenly your bladder is full and you have to go.

The body has the ability to direct blood wherever it needs by its manipulation of blood vessel size.  Where do you think blood is needed after an almost 6,000 calorie meal?  That’s right.  The digestive tract.  It takes a lot of work to deal with 6,000 calories, and a lot of work requires a lot of oxygen, which comes from the blood.  So after a heavy meal, the body shunts extra blood to the guts where the works is being done.  It does this by opening or dilating the arteries carrying blood to the intestines and by narrowing the blood vessels in other parts of the body.

Now, think back to the video of the woman whose blood vessel (in her arm) is being examined by ultrasound.  When it’s compared to the previous ultrasound, the one before she ate, notice how much faster the heart is beating.  (The little swishing sounds you hear, each of which represents a heart beat, are spaced much closer together.)  The heart is beating faster because the body is working to digest an enormous amount of food, and this work stresses the heart in the same way that running down the street would stress the heart.  Work is work.

The digestive tract needs extra oxygen to do its work, this extra oxygen can get there only via the blood, so the intestines require more blood than normal.  This extra blood gets shunted there by opening the arteries that feed the gut and narrowing those that go other places where a lot of blood isn’t needed at the moment.  Such places as, say, a relaxed arm.

Anyone with a smattering of knowledge of normal physiology (and apparently an open mind) could predict that the artery in a relaxed arm would narrow after a heavy meal and that that artery would be back to normal six hours later (which it was so reported in this video).

What you’re seeing in this video is normal physiology at work interpreted as being abnormal by a couple of lipophobic doctors who should (and probably do) know better.  It makes for dramatic theater, but their interpretation is nothing but prevarication or ignorance or both.

But had they reported the truth, there would have been no story.  Kind of sad, isn’t it.

Instructor teaches Friedewald equation and bad cholesterol

This week sees the publication of yet another study showing the superiority of the low-carbohydrate diet as compared to the low-fat diet.  This study, published in the prestigious American Journal of Clinical Nutrition, demonstrates that subjects following the low-carb diet experience a decrease in triglyceride levels and an increase in HDL-cholesterol (HDL) levels; and that these changes are accompanied by a minor increase in LDL-cholesterol (LDL), which prompts the authors to issue a caveat.

Yes, although just about all the parameters that lipophobes worry about improved with the low-carb diet, the small increase in LDL has caused great concern and has prompted the authors to gravely announce that this small increase is troublesome and should be monitored closely in anyone who may be at risk for heart disease.  Since most people who go on low-carb diets do so to deal with obesity issues, and since obesity is a risk factor for heart disease, it would appear that this small increase in LDL often seen in those following a low-carb diet could put these dieters at risk.  Does it?  We’ll see.

Let’s take a look at the study. But before we do, let’s digress for just a bit and look at low-carb diet studies in general.

As we’ve discussed in these pages before, there are a couple of ways to do dietary studies in which on diet is compared to another.  You can compare a low-carb diet to a low-fat diet in a way that reflects what happens in real life.  For example, you could randomize your study subjects into two groups, then give those in one group a low-carb diet book (Protein Power, maybe) and those in the other a low-fat diet book (an Ornish or McDougal book, perhaps).  You would instruct both groups to follow their respective diets and come back periodically for evaluation.  When these kinds of studies are done, the low-carb diet invariably brings about more weight loss and greater changes for the better in just about all parameters.  But the folks who are proponents of low-fat diet cry foul.  Why?  Because in virtually all of these studies the subjects on the low-carb diet consume fewer calories than those on the low-fat diets.  Lower-carb, higher-fat diets are satisfying, and it has been shown over and over that those following such diets actually consume fewer calories while still feeling full than do those following ad libitum (eat all you want) low-fat diets.

So, the low-fatters attribute all the improvement in those on the low-carb diets as simply a result of their lower caloric intake.

If you want to eliminate this caloric-deficit difference from your study, then you design a protocol in which calories are the same in both the low-carb and the low-fat arms of the study.  This strays from the real-life way of looking at what is likely to happen when people buy diet books and follow them, but it does offer the advantage of getting rid of the calorie issue.

In these kinds of studies you randomize your subjects into either a low-carb or a low-fat diet group and put both groups on the same number of calories.  At the end of your study, you can see the differences between the two diets – if any – that are brought about without calories being an issue.

The study under our consideration today is of the latter type; it’s one in which both groups were kept on an equal number of calories, a so-called isocaloric diet.

Here’s the setup for the study titled Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo.

The researchers recruited 118 subjects who had abdominal obesity and at least one other metabolic syndrome risk factor and randomized them to either a low-carb or a low-fat diet for one year.

The diets were designed to be isocaloric with moderate energy restriction (≈6000 kJ/d [1433 kcal] for women, ≈7000 kJ/d [1672 kcal] for men). The planned macronutrient profile of the LC diet was 4% of total energy as carbohydrate, 35% as protein, 61% as total fat (20% saturated fat) with the objective to restrict carbohydrate intake to <20 g/d for the first 8 wk and to <40g/d (with the inclusion of an approved 20-g carbohydrate exchange) for the remainder of the study. The target profile for the LF diet was 46% of total energy as carbohydrate, 24% as protein, and 30% as total fat with the objective to restrict saturated fat intake to <10 g/d and <8% of total energy, with the inclusion of an approved food exchange (equivalent to the energy content of 20g of carbohydrate;) between weeks 9 and 52, so that the diets remained isocaloric.

Sixty nine subjects completed the study, and, fortunately, all the results reported in the paper were for the 69 completers, so we don’t have to worry about data contamination we would have gotten had the researchers done an intention-to-treat analysis.  We know how the people fared who actually hung in there for the entire study period, which is what we want to know.

And how did they fare?

Those on the low-carb diet lost 26 percent more weight than those on the low-fat diet (14.5 kg vs 11.5 kg), but the difference wasn’t statistically significant.  As you can see from the graph below of the weight loss between the two groups over time, the difference was widening, and we can extrapolate that the difference would have become statistically significant had the study gone on longer, but we can’t say for sure.

As for the other parameters, blood pressure, glucose, insulin, insulin resistance and C-reactive protein were the same for both groups.  There was a difference in lipid outcomes, however.

The LC [low-carbohydrate] diet also provided greater improvements in triglycerides and HDL cholesterol than did the LF [low-fat] diet, which occurred independently of differences in energy intake and weight loss. This finding is consistent with those of long-term ad libitum studies. High triglyceride and low HDL-cholesterol concentrations are 2 of the MS risk factors, a syndrome that is associated with an increased risk of type 2 diabetes and CVD. Elevated triglyceride concentrations have also been identified as an independent CVD risk factor, and the triglyceride:HDL cholesterol ratio is considered a strong predictor of future cardiac events and is a surrogate measure of insulin resistance. Our data show that the triglyceride:HDL cholesterol ratio was halved after the LC diet and was approximately double the improvement observed with the LF diet. A recent review suggests that biological markers typically associated with the MS are those improved by carbohydrate restriction, which suggests that LC diets may offer the greatest clinical benefits for overweight populations who are insulin resistant and have several metabolic risk factors.

So far, so good.  But now the other shoe is ready to drop.

Whereas the LC diet improved a range of cardiometabolic risk factors, greater increases in total and LDL cholesterol also occurred. Other studies that compared LC and LF diets reported similar findings, although the overall magnitude of the differences was smaller: 0.60 and 0.20 mmol/L in favor of the LF diet.

Let’s see how much the total cholesterol and LDL changed.

Those in the low-fat group started with an average total cholesterol of 212 mg/dl (5.5 mmol/L) and ended up a year later at same number.  These same subjects also started out with average LDL levels of 131 mg/dl (3.4 mmol/L) and ended up the same at the end of the study.  The low-carb dieters began the study with average total cholesterol levels of 209 mg/dl (5.4 mmol/L) and ended the study a year later with average total cholesterol levels of 232 mg/dl (6.0 mmol/L).  Their average LDL levels started at 124 mg/dl (3.2 mmol/L) and ended up at 147 mg/dl (3.8 mmol/L).

The authors of this study bestow great significance on this fairly minor increase in LDL levels in those subjects on the low-carb diet.  In their summary of the results of this study, they list the many benefits of the low-carb diet, then end on an ominous note:

However, these potential benefits may be counteracted by the detrimental effects of an increase in LDL cholesterol, which should be monitored…

The abstract of the study echoes this warning.

However, the increase in LDL cholesterol with the LC diet suggests that this measure should be monitored.

It was my impression that the tone of the authors was one of a little foreboding.  Kind of a ‘this looks too good to be true, and, hey, look at those LDL levels; it is too good to be true’ aura about it.  But is it too good to be true?  Is the rise in LDL seen in most low-carb diets the hidden stinger?  Is what all the lipophobes say true?  You know, the old ‘Well you may lose weight on those diets, but you’ll clog your arteries at the same time.’

It’s all hogwash, of course, but before we get to the heart of the explanation as to why, let me remind you that numerous studies have shown that whenever subjects go on low-carb diets, they end up increasing the size of their LDL particles.  Large, fluffy LDL particles are not only harmless, but may be protective.  If they are protective, what’s wrong with having a bit more of them?

At the same time, numerous studies have shown that low-fat diets usually decrease LDL levels, but do so while reducing the particle size.  Followers of such diets end up with lower levels of LDL made of smaller, denser, more atherogenic particles, which, in my mind, isn’t a good trade off.

The authors of our paper acknowledge this fact and cite some of this research, but they are still fixated – as are most lipophobes – on LDL levels.  They just can’t get their heads around the notion that there is more to cardiovascular risk and health than LDL-cholesterol.

Since these researchers placed so much emphasis on LDL levels in their interpretation of all the data from their study, I got to wondering how they measured LDL levels.  I looked in the Methods section of their paper and found the following:

Plasma glucose, C-reactive protein, serum lipids, and apolipoprotein B (apo B) were also measured by using standard methods (11).

The #11, of course, means that the description was in another paper that I had to go to the trouble of looking up.  I always find it annoying when authors do this when they could just as easily stick a short paragraph in their paper and save people who really want to read it critically a lot of trouble.

Tracking down the other paper in the Journal of the American College of Cardiology, I found the following:

The LDL-C was calculated according to the method described by Friedewald et al.

What this means is that the researchers did not measure LDL levels directly in their study subjects, but calculated them using the Friedewald equation.

For reasons we don’t need to go into here, LDL is fairly difficult (as compared to total cholesterol and HDL) to measure.  It can be done, but it’s expensive.  So instead of measuring it directly, most labs calculate it based on an equation derived by William Friedewald and others in 1972.

Friedewald realized that it was pretty simple to measure total cholesterol, HDL-cholesterol and triglycerides.  He knew that total cholesterol was the sum of all the various subfractions of cholesterol, which can be presented by the following equation:

Total cholesterol = HDL-cholesterol + LDL-cholesterol + VLDL-cholesterol

Rearranging this equation to solve for LDL gives us this one.

LDL = Total cholesterol – HLD – VLDL

Friedewald knew that it was easy to measure total cholesterol and HDL but difficult to measure the others.  His insight was that the triglyceride level if divided by five could give a close approximation of VLDL.  In running his experiments he also realized that this relationship held only if triglyceride levels were 400 mg/dl or under.  If they were over this, all bets were off.

So, Friedewald substituted triglycerides (TGL) divided by 5 for VLDL in the above equations, giving us the so-called Friedewald equation for calculating LDL.

LDL = Total cholesterol – HDL – TGL/5

And this is how it is still done in labs all over the world 27 years after Friedewald’s paper.   If you’ve had a lab report showing an LDL figure, I can guarantee it was calculated by the Freidewald equation and not measured directly.

What’s wrong with this if it works?  Nothing.  If it works.  Problem is, it doesn’t always work.  Friedewald himself found that in subjects with triglyceride levels greater than 400 mg/dl the equation didn’t hold.  Anyone reading this who has had a lipid test showing triglycerides greater than 400 will have note on their lab report saying that LDL couldn’t be calculated because triglycerides were too high.

I’ve always thought the same held true for triglycerides under 100 mg/dl, which would apply to almost everyone who sticks to a low-carb diet for any length of time.  Triglyceride levels of 40-90 mg/dl are not uncommon, and are, in fact, typical.  When Friedewald did his work, the triglyceride levels were mainly up in the 150 – 250 mg/dl range, and in this range his equations match pretty well to directly measured LDL levels, but all bets are off with triglycerides above 400 mg/dl and, I suspect, triglyceride levels below 100 mg/dl. MD and I did find this ourselves in a few patients that we did direct LDL measurements on in our practice.

A paper published a few years ago in a pathology journal corroborating what we found. (Full text here.)

This paper is basically a case presentation of a 63-year-old man with a total cholesterol level of 263 (all results in mg/dl), an HDL of 85, a triglyceride level of 42, and an LDL level of 170.  The LDL level was, of course, calculated using the Friedewald equation.

For some unexplained reason the authors of this paper decided to repeat the lab results and got the same readings.  They then wondered if his very low triglyceride readings might be having an effect, so they measured his LDL levels directly and found that instead of the 170 predicted by the Freidewald equation, his actual LDL levels were only 126.

More recently a paper appeared in – of all places – the Archives of Iranian Medicine showing the same phenomenon.  These authors tested 115 subjects with low triglyceride levels.  You can get the full text of the paper, but a line in the abstract says it all:

Statistical analysis showed that when triglyceride is <100 mg/dl, calculated low-density lipoprotein cholesterol [LDL] is significantly overestimated (average :12.17 mg/dL or 0.31 mmol/L), whereas when triglyceride is between 150 and 300 mg/dL no significant difference between calculated and measured low-density lipoprotein cholesterol is observed.

The authors of this paper derived their own equation to be used in lieu of the Friedewald equation when the triglyceride levels are below 100 mg/dl.  I suspect that if we were to apply this equation to the labs of the 33 subjects who finished the low-carb arm of the study we started out discussing in this post, whose average triglyceride levels were under 100, the LDL levels would have averaged much lower than the 147 mg/dl they were calculated to be by the Friedewald equation.  If you subtract the 12.17 mg/dl that the Iranian paper estimates as the difference from the average triglycleride levels (an admittedly extremely unscientific and non-statistically valid way to do it), you find that the average drops to 135 mg/dl, which I doubt is significantly different than the 131 average of the low-fat dieters. If you did it the right way – subject by subject and then average – I suspect it would be greater yet.

The moral of this story is that if you have been following a low-carb diet and your triglycerides are low (or if your triglycerides are just low) and your LDL reading comes out a little high – or even a lot high, don’t let anyone mule you into going on a statin or undergoing any therapy for an elevated LDL.  Demand to have a direct measurement of your LDL done.  Or if you get an insurance physical and your triglycerides are low and your LDL up a little, fight to get a direct measurement so they don’t stick you with higher premiums because they think you’ve got an increased risk for heart disease.

What we do know based on the work of many is that low-carb diets change LDL particles to the large, fluffy, harmless variety.  Thanks to these other papers we also know that the LDL levels so many people end up with on their lab reports after being on low-carb diets for a while are artificially high.

Now when you hear people say that low-carb diets may help you lose weight but run your LDL levels up and increase your risk for heart disease, you’ll know this is just so much gibberish.  Sadly, your doctor will probably spout the same thing, and it will be up to you – who after reading this post will know more about this point than 99.9 percent of doctors practicing today – to educate your trained professional.

And if you are a researcher studying the effect of the low-carb diet on LDL, for crying out loud, hit your grant up for the extra few bucks it takes to get LDL cholesterol measured directly in your subjects so you won’t be in the embarassing position of having your data become worthless.

Dr. George Bray's model of obesity

In July 2008 I posted on Dr. George Bray’s critique of Gary Taubes’ book Good Calories, Bad Calories that appeared in Obesity Reviews.  Included in my post was a copy of Gary’s response.  Now Dr. Bray is back with a rebuttal to Gary’s response to his (Bray’s) original critique.  In conversation, Gary told me he has elected to drop the issue because the discussion is going nowhere.  Gary makes substantive points; Bray obfuscates the issues and will continue to do so.  I, however, am not going to drop the case.  Maybe I’ll have the last word here.

I want to go over Dr. Bray’s response to Gary’s letter in some detail because it is emblematic of all that is wrong with obesity research today and clearly demonstrates why we will never get anywhere until the people of Bray’s generation fade away. I don’t know that I’ve ever seen so many instances of one writer missing the point as often as Dr. Bray does in this short reply.  The entirety of his response is an example of either shoddy thinking or intellectual dishonesty.  Or maybe both. It brings to mind Mary McCarthy’s famous quote about Lillian Hellman: “Every word she writes is a lie, including ‘and’ and ‘the’.

(You can read Dr. Bray’s original critique of Good Calories, Bad Calories along with Gary’s response in my July 2008 post.  The full-text of Dr. Bray’s letter of reply we’ll be discussing in today’s post can be found here.  You should pull it down in pdf and print it so you can follow along.)

Right off the bat, in the very first line, Bray leads off with his first porkie.

In his nearly 5000-word response to my book review, Mr. Taubes has raised a number of issues.

Gary’s response was slightly under 2000 words.  You might think this just simply a typo, and normally I would too, but the entire piece is filled with so many inaccuracies seemingly designed to denigrate Gary’s response that I don’t think so.  Why even put the number of words?  Why not simply say: In his response to my book review…?  By quantifying the number of words the way he does, Bray casts a pejorative shadow on Gary’s response from the get go.

If you read Gary’s letter, you will see that he methodically refutes Dr. Bray’s criticisms of GCBC and identifies those issues in which he feels Bray misses the point.  In his response, Bray says Gary’s critique of his (Bray’s) review of GCBC

opened the door for [him] to contrast [Taubes’] hypothesis for obesity with [his own].

It’s a kind of disingenuous way for Bray to get his own hypothesis of obesity into play in what amounts to a review of Gary’s book, but let’s take a look at what he has to say.  First, he completely simplifies and basically mischaracterizes Gary’s hypothesis of obesity.  Here is Gary’s hypothesis of obesity and his proposed treatment as interpreted by Dr. Bray:

As you can see, it appears pretty simplistic, which, I’m sure, was the intent.  Not shown are all the feedback loops and intricacies Gary has described at length in GCBC .

In referring to this diagram, Dr. Bray admits that it is based on “two sentences from the letter,” which doesn’t seem like a lot out of a 5,000-word letter (or even the 2,000-word letter that it was).  Then he goes on to use three sentences to establish the basis for the diagram.  (See what Mary McCarthy meant about even ‘and’ and ‘the’?)

After giving short shrift to Gary’s hypothesis of obesity, Dr. Bray then goes on to lay out in great detail his own theory of obesity as represented by the Rube Goldbergesque diagram at the top of this post.  Bray’s entire hypothesis, for which he recruits leptin, insulin, the brain, glucocorticoids, and God knows what else to help make his point, is based on a faulty premise.  But it’s a faulty premise he has accepted uncritically.

His hypothetical model of obesity, he authoritatively states

starts with the First Law of Thermodynamics, which states that the change of energy in a closed system is the difference between the heat added to the system and the work done by the system.

Dr. Bray then restates this hypothesis (and the First Law) in the form of this equation:

Δ E = Heat (q) – Work (w)

Readers of this blog know this as the energy balance equation, which looks like this in its more familiar form:

Δ Weight (the Δ means change) = Energy in (food) – Energy out (exercise plus metabolism)

The fatal flaw in Dr. Bray’s hypothesis (which is a flaw we’ve discussed often in these pages) is that he doesn’t understand that the components on the right side of the equal sign are not independent variables.  They are dependent variables.  If one eats less, the rate of metabolism falls to compensate.  If one exercises more, the appetite increases, and one eats more to compensate.

Were these components truly independent variables, life would be easier (but we may not have survived).  According to Dr. Bray, Anthony Colpo, and countless others, however, these components are independent variables.  Eat less, say they, and you’ll lose weight.  Which is true, to a point.  But once the energy-out component of the equation kicks in, weight loss stalls, even if you are eating less, a fact everyone who has ever dieted knows.  Exercise more, they pontificate, and you’ll lose weight.  Which, again, works (maybe) in the very short term.  But once appetite kicks in, you unconsciously eat enough more to compensate for your increase in exercise, as anyone knows who has tried to lose weight by walking or other exercise alone without consciously restraining eating.

Now don’t get me wrong, it is possible to lose weight by decreasing food intake and increasing exercise.  It worked well in the concentration camps in WWII and in Ancel Keys’ starvation studies in the 1940s.  But in those cases, people were under lock and key.  It doesn’t work for the long term for the majority of people unless they are coerced.

This fairly obvious observation that the energy in/energy out components are not independent variables seems to elude most (if not all) obesity researchers, including George Bray.  These people persist on basing the foundation of any obesity treatment on the admonition to eat less and exercise more, which is a total folly.  Yet Bray and his ilk continue to clothe this folly in the garments of academic respectability and work to pass it off as the latest fashion in scientific thinking.

Dr. Bray believes that the reason so many people are fat is twofold. First, he thinks  humans have a ‘hedonic’ drive that inexorably pushes them to increase their food intake.  And, second, he reckons that this ‘hedonic’ drive also overrides the “appropriate negative feedback signals to stop eating.”  What stimulates this ‘hedonic’ drive?  According to Dr. Bray

It is caused by the pleasurable effects of high-fat, high-sugar foods.

Well, at least he’s half right on that one.  No one binges on pure fat.  It’s impossible because of feedback inhibition to eat a lot of pure fat at a sitting.  Try sometime to sit down and eat some butter all by itself.  See how much you can choke down.  I can guarantee you it won’t be much.  Then add a little sugar to the mix and see what happens.  Suddenly the butter is converted to frosting, and you can put away a lot of it.  What’s the difference?  It’s the sugar.  Sugar – and carbohydrates in general – override the stop-eating center in the brain.  That’s why all binge eaters binge on a combination of fat and carbohydrate.  That’s also why you can go out to dinner, eat ‘til your stuffed, not be able to eat another bite of any kind of meat or other real food, yet perk up when the dessert tray comes around.  As the old saying goes: there’s always room for dessert.  Why? Because your brain knows the stop-eating center will be overridden by the sugar and carb in the dessert.

Dr. Bray would have been more accurate had he said that the stimulus for the ‘hedonic’ drive is carbohydrate.

But he doesn’t.  He is trapped in the fat-is-bad paradigm.

In experimental animals, highly palatable food or a high-fat diet is one of the easiest ways to disturb this homeostatic system [as defined by Dr. Bray], and this may apply to human beings as well.

Dr. Bray seems to believe that we live in a toxic world in food terms.  We are unable to help ourselves, and are therefore destined to be fat because of our ‘hedonic’ drive.  We are helpless.  There is no cure save eating less and exercising more, which even he more or less admits doesn’t work despite his entire model being based on the idea.  As I have discussed in another post, Dr. Bray is a major proponent of drug therapy to treat obesity.

In a way, I agree with him about the idea that we live in a toxic world, one with all kinds of the wrong kinds of food available to tempt us 24/7.  Problem is that Bray and his ilk are a major part of the reason we live in such a world.  But that’s a topic I’ll leave for a future post.

Dr. Bray makes a bizarre case for why he thinks the majority of dietary studies show better results in those subjects following low-carb diets than in those consuming low-fat regimens.  I’m going to use his own words, so you won’t think I’m making this up.

the principal studies that directly support this model [Taubes’ theory on low-carb dieting] included the word ‘Atkins’ in their clinical trial. When similar low-carbohydrate diets were tested without using this ‘name’, the low-carbohydrate diets had no more effect than those to which they were compared.

There you have it.  All you have to do to make a diet work is include the name ‘Atkins’ in the title.  I wish MD and I had known that when we wrote Protein Power.

What is truly ironic about this nonsense is that in this very same issue of Obesity Reviews containing Bray’s rebuttal is a long review article titled Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities.  This article takes an in depth look at studies comparing low-carb diets to low-fat diets.  Here is the conclusion as written in the abstract:

There was a higher attrition rate in the low-fat compared with the low-carbohydrate groups suggesting a patient preference for a low-carbohydrate/high-protein approach as opposed to the Public Health preference of a low-fat/high-carbohydrate diet. Evidence from this systematic review demonstrates that low-carbohydrate/high-protein diets are more effective at 6 months and are as effective, if not more, as low-fat diets in reducing weight and cardiovascular disease risk up to 1 year.

Dr. Bray lists five other issues about Gary’s letter to which he wishes to respond, but before he gets to the list, he makes one last flippant point.

I thus conclude that if any diet ‘cured’ obesity as their proponents often claim, there would be no obesity and thus no need for the next diet. Yet the past 150 years, since the publication of Banting’s first popular diet, have seen a continuing stream of new diet books.

The reason, of course, is that we dieting fish all swim in waters that have been polluted by Bray and his brethren, more about which in a later post.

Now to the list.

1.    Near the end of the letter, Mr Taubes suggests that my review of his book may be a ‘conflict of interest’. He says ‘I [Bray] may be defending what my scientific research has led me to believe’. If this is a conflict of interest, then all scientists have a conflict of interest.

This first short point of only three sentences tells you everything you need to know about Dr. Bray’s scientific credibility.  I have no problem with the first sentence.  The second sentence is purportedly a quote from Gary Taubes letter.  It isn’t.  It is a paraphrase…sort of, but put in quotation marks.  This is a real no no.  It was done so for a particularly egregious reason, which was for a set up for Bray’s final sentence.  But that sentence even further diminishes his credibility.  Scientists are supposed to constantly challenge their own hypotheses, not accept them as fact simply because they’ve spent their careers enraptured with them.   All true scientists don’t have this conflict of interest.

2.    The first paragraph of his letter dealt with lipoproteins that I said he had not covered. The issue was not the lipoproteins but their receptors, from which we have learned so much in the past 30 years.

This one is a real copout.  In Bray’s original critique he wrote:

As I read through Good Calories, Bad Calories, I found a number of errors of omission or commission that are important when relating diet to heart disease.  There is no mention in the Diet-Heart section of low-density lipoprotein-cholesterol (‘bad cholesterol’) or of high-density lipoprotein-cholesterol (‘good cholesterol’).

The issue may have been the receptors and not the lipoproteins, but as you can see from his direct quote above, that’s not how Bray characterized it.  Gary set him straight with a list of about two dozen pages and groups of pages where LDL and HDL were mentioned, yet Bray weasels instead of admitting his mistake.  When I read his first letter, it made me wonder if he had even read the book.

3.    In his letter he mentions doubly labelled water only to conclude that we knew this already from the 19th and early 20th century and he did not need to discuss it in his book. I would submit that we did not know that people under-report their intake by as much as they do and that overweight people under-report more than normal-weight people do.

Okay.  There’s a total non sequitur.  What does the second sentence have to do with the first?  Weird.  Was Bray on dope when he wrote this?

4.    Mr. Taubes say ‘the goal of science is to determine causality…’

(What Gary actually wrote was ‘The goal of science is to correctly determine causality,’ but who’s counting?)

Then Bray wades into this strange discourse about the theories of Karl Popper, whom he misnames as Hans Popper.  (Does this guy ever bother to look anything up?)

This is significantly different from the views of Hans Popper, the philosopher of science, whose search is for ‘reality’ rather than ‘causality’. Popper says ‘there is a reality behind the world as it appears to us, possibly a many-layered reality, of which the appearances are the outermost layers. What the great scientist does is boldly to guess, daringly to conjecture, what these inner realities are like. Popper also espouses the concept of ‘falsification’, which is at the heart of rationalist thought. To quote him again –’a false theory may be as great an achievement as a true one. And many false theories have been more helpful in our search for truth than some less interesting theories which are still accepted’.

If you can make sense of this gibberish, you’re a better man than I am.  All I know is that Bray misses Popper’s point about falsification in a major way.  (We discussed Popper and his theory of falsification in an earlier post.  And it ain’t anything like Bray makes it out to be. I seriously doubt he has even read Popper’s work.)

The last sentence of the above paragraph I find particularly interesting.  Writes Bray, apropos of nothing really:

And many theories have been more helpful in our search for truth than some less interesting theories which are still accepted.

I don’t know about the search for truth, but I can tell you that the inability of Bray and the rest of the academic obesity ‘experts’ to shake loose from their own ‘less interesting theories’ have led us into the obesity epidemic we’re in the throes of now.

Dr. Bray’s fifth comment, which I’m not going to reproduce in full, is a world-class case of totally missing the point.  After commending Gary for proposing an experiment to validate his hypothesis, he goes on to quote Gary’s rebuttal letter:

He says ‘the positive energy balance hypothesis of obesity asserts that the only way to lose excess fat is to eat less and/or exercise more – that without consciously inducing a negative energy balance we will not lose weight’. His hypothesis is ‘the carbohydrate/insulin hypothesis asserts that if we restrict carbohydrates in the diet/and or improve the quality of the carbohydrates consumed then insulin levels will be lowered, reducing the accumulation of fat in the fat tissue independent of the nutrition state of the subject’. I would take exception to his use of the word ‘consciously’ in his statement of the energy balance hypothesis. For example, the current level of oil prices may increase human energy expenditure through more walking as it decreases automobile use. This is not a ‘conscious’ choice in the sense used above but would have the same effect.

Say what?!?!?!

Let me get this straight.  Dr. Bray thinks if we walk more because we decrease automobile use as a consequence of the high price of gasoline that we’ll lose weight because we are unconsciously exercising instead of volitionally exercising?  As I say, he misses the point, which is that the two components on the right side of the energy balance equation are not independent variables, but are dependent variables.  It doesn’t matter if one walks as a part of exercise or because one can’t afford the gas, the body compensates by increasing food intake.

Dr. Bray ends his response by resorting to the old conservation of energy principle, which all the eat-less, exercise-more folks hew to.  They seem to believe that no one who advocates low-carb diets can understand the laws of thermodynamics when it is they themselves who don’t understand them as applied to diet.  There is nothing inconsistent with Gary’s theories of the cause and treatment of fat accumulation and the laws of thermodynamics.  It’s Bray and friends’ lack of understanding of these laws and/or their refusal to accept the dependent nature of the energy in/energy out components of the energy balance equation that are the heart of the problem.

This entire rebuttal of Dr. Bray’s reminds me of my own favorite lines from Good Calories, Bad Calories.  They are my favorite because I’ve seen first hand what they describe.

The institutionalized vigilance, “this unending exchange of critical judgment,” is nowhere to be found in the study of nutrition, chronic disease, and obesity, and it hasn’t been for decades.  For this reason, it is difficult to use the term “scientist” to describe those individuals who work in these disciplines, and, indeed, I have actively avoided doing so in this book.  It’s simply debatable, at best, whether what these individuals have practiced for the past fifty years, and whether the culture they have created, as a result, can reasonably be described as science, as most working scientist or philosophers of science would typically characterize it.  Individuals in these disciplines think of themselves as scientists; they use the terminology of science in their work, and they certainly borrow the authority of science to communicate their beliefs to the general public, but “the results of their enterprise,” as Thomas Kuhn, author of The Structure of Scientific Revolutions, might have put it, “do not add up to science as we know it.”

The result is an enormous enterprise dedicated in theory to determining the relationship between diet, obesity, and disease, while dedicated in practice to convincing everyone involved, and the lay public, most of all, that the answers are already known and always have been—an enterprise, in other words, that purports to be a science and yet functions like a religion.

Is it any wonder that Dr. Bray didn’t enjoy the book?

There is an old joke that goes something like this:

Question: What is Mozart doing in his grave right now?
Answer: De-composing.

The same question could be asked of the living right now who are working hard on their diets and seeming to go nowhere body weight-wise.

Question: What’s happening right now? Why am I not losing weight?
Answer: You’re Re-composing.

As you can see from the picture above, body composition matters a lot.  It’s not the particularly the weight you carry as much as how it is distributed that counts.  As I’m forever asking my female patients, What difference does it make if you weigh 200 pounds if you’re wearing a size 4?  Although that situation is unlikely, they get the point.

A soon-to-be-published study by Donald Layman and his team at the University of Illinois demonstrates this phenomenon nicely.  And shows that by increasing protein intake – even while keeping carb intake much higher than I would recommend – increases fat loss while increasing muscle and lean tissue mass.

Here is how the study was set up.

One-hundred thirty overweight men (58) and women (72) between the ages of 40 and 56 were recruited into the study.  None of the subjects smoked, took cholesterol-lowering drugs or had any medical condition that might affect the outcome of the study.  In other words, the study subjects were relatively healthy overweight middle aged people.

These subjects were randomized into two groups.  One group was started on a diet (PRO) containing 1.6 gm protein per kg body weight per day and under 170 g carbohydrate per day.  The other group went on a diet (CHO) composed of 0.8 g protein per kg per day (the minimum Recommended Daily Allowance (RDA) for protein) and over 220 g carbohydrate per day.

The diets for both groups were formulated to be equal in energy with  1900 kcal/day provided for males and 1700 kcal/day for females.  Total fat content was the same in both the PRO and CHO diets.

Diet differences between groups were designed to reflect direct substitution of foods in the protein groups (meat, dairy, eggs, and nuts) for foods with high-carbohydrate content (breads, rice, cereals, pasta, and potatoes).  The education guidelines for the CHO group followed the USDA Food Guide Pyramid and emphasized restricting dietary fat and cholesterol with use of whole-grain breads, rice, cereals, and pasta.  For the PRO group, the education guidelines emphasized use of high-quality, low-fat proteins including lean meats, reduced-fat dairly, and eggs or egg substitutes.  Both diets included 5 vegetable servings/d and 2-3 fruit servings/d.

This study is unusual in that it provided a comprehensive nutritional education program along with an intense degree of nutritional monitoring throughout the 12 months of the study.  Most nutritional studies give the subjects a lead in lecture or series of lectures, then pretty much leave them alone.  To help ensure compliance, these researchers met with the subjects weekly throughout the study.

Subjects were evaluated at the start, after a 4 month period of active weight loss and finally after an 8 month maintenance period.  The entire length of the study was 12 months.

At the end of the 4 month weight-loss period, subjects on the PRO diet fared substantially better than those on the CHO diet.  Fewer people in the PRO group had dropped out of the study, and those who remained experienced an increase in HDL-cholesterol and a substantial reduction in triglycerides as compared to those on the CHO diet.  Those subjects on the CHO diet had greater reduction in LDL-cholesterol than did those following the PRO diet, but those changes didn’t old over the full 12 months.

Most interesting was the finding that although both groups lost equivalent amounts of weight over the first 4 months (actually, the PRO group lost a little more, but not a statistically significant amount), those in the PRO group lost 22 percent more fat than the subjects in the CHO group.  Since weight was essentially the same in both groups, those in the PRO group maintained or lost less lean mass while losing fat.  Which means that, despite the weight being the same, those in the PRO group ended up smaller than those in the CHO group.

As I’m sure everyone knows, fat is lighter than muscle.  If you trade a pound of muscle for a pound of fat, the scales don’t change.  But size does change because a given weight of fat occupies much more volume than the same weight of muscle.  You can see from the photo to the right how much less space 5 pounds of muscle take up than does 5 pounds of fat.  Plus, muscle is more metabolically active in that it burns more calories, and it actually does something for you.  Muscle makes you stronger; fat just weighs you down.

I know that many female readers will not want to gain extra muscle.  They shouldn’t worry, however, because in the absence of exogenous anabolic steroids women won’t become ‘muscle bound’ or non-feminine appearing.  What generally happens is that the muscle replaces fat within the muscle.  We’ve all seen marbling in beef, which is fat within the muscle tissue.  With the extra protein, new muscle replaces this fat, and the muscle may even become a little smaller in females while at the same time becoming more dense and stronger.

Let’s take a look at a couple of graphs that demonstrate nicely the difference in fat loss with greater protein intake, even in the face of what I consider way too many carbs.

The graph on the top shows the difference in fat loss between those PRO and CHO subjects who completed the entire 12 months of the study irrespective of how much weight they lost.

The bottom graph shows the difference in fat loss in those who were able to maintain a weight loss of at least 10 percent of their starting weights.

As you can see, the fat loss in those in the PRO group were substantially greater than those in the CHO group even though both groups were on an equivalent number of calories.

The series of graphs to the right show what happened to lipid values in the subjects in both groups.  HDL-cholesterol went up more and stayed up in the PRO subjects.  Triglycerides went down more and stayed down in the PRO subjects.  Subjects following the CHO protocol tended to have a reduction in LDL-cholesterol as compared to those in the PRO group, but as the study continued, the LDL-cholesterol began to return to pre-study levels.  This finding has been replicated in many other studies.  A high-carb, low-fat diet reduces LDL in the short term, but the changes don’t last.

The authors of this study made some interesting points in the discussion part of the paper.

Across all 3 analyses [the data was analyzed in three different ways], the PRO group averaged ~21% greater weight loss and 27% greater fat loss than the CHO group.  Further, irrespective of the amount of weight lost, participants in the PRO group obtained greater improvements in body composition as reflected by greater FM [fat mass] loss and attenuated relative lean mass loss.

In addition to the beneficial effects of the PRO diet for changes in body composition, more participants in the PRO group completed the study (64%) than in the CHO group (45%) and attained ≥ 10% weight loss (31 vs 21%, respectively).  These findings demonstrate greater compliance with a moderate PRO diet designed within the DRI [Daily Recommended Intake] guidelines for macronutrients for long-term weight management than the CHO diets often advocated for weight loss.

This is information you can use with friends and family who are, for whatever reason, adverse to going on a real low-carb diet.  The beauty of this particular study is that all the protein, carb and fat recommendations are within the government-approved RDAs.  The PRO group had a protein intake that was at the upper end of the RDA for protein and carb at an amount that was far from the lower end of the RDA for carbs.  (Of course those of us in the know realize that there is no lower end requirement for carbs  – many people get by with zero or close to zero carbs.  But we’re talking the government here. So, nuff said.)  What this means is that you can encourage friends and family to go ahead and eat a government-approved diet yet still get some of the benefits of a semi-sort-of low-carb diet.  A real win win.

Multiple mechanisms have been reported to explain increased loss of body weight and body fat with higher protein diets.  Higher protein diets appear to increase satiety, increase energy expenditure, and/or maintain lean tissue with higher metabolic activity.

Improvements in body composition, including reducing body fat and maintenance of lean tissue, are critical for prevention of weight regain and long-term health status.  Evidence is accumulating that the RDA for protein is inadequate to maintain muscle mass in adults during aging, with a physically inactive lifestyle, or during energy restriction for weight loss.  The current RDA for protein represents the minimum protein needs for healthy young adults with adequate energy intakes.  During weight loss, energy restriction increases the protein needed to maintain muscle mass and protein needs expressed as percentage of the reduced energy intake nearly double.

Just to give you an idea of the amount of protein we’re talking about here, let’s take the so-called average person who weighs 70 kg (154 lbs) and calculate daily protein requirements based on the protocol of this study.  70 kg  X 1.6 g/kg/day = 112 gm protein per day.

If you want to use pounds instead of kilograms, use 0.73 gm protein per pound per day.  If you weigh 200 lbs, then the calculation would be 200 lbs X 0.73 gm/lb/day = 146 gm protein per day.  Since meat contains about 7 gm protein per ounce, this 146 gm could be gotten in about 21 ounces of meat per day.  So we’re not talking about a small amount.

I’ll leave you with the conclusions of the authors of this study, with which I mostly concur.

The findings of the current study demonstrate that although energy deficit is the major factor for body weight loss, the macronutrient composition affects body composition, blood lipids, and long term compliance.  Specifically, a PRO diet with protein at the upper end and carbohydrates at the lower end of the AMDR [Acceptable Macronutrient Intake Range] is more effective for reducing % Fat and improving dyslipidemia.

I can only add that were the protein kept high (along with the fat) and the carbs slashed to around 30-50 gm per day, the results would have been even more impressive.

When I put out the call for what people wanted to read about on this blog in 2009, numerous folks commented that they would like to know why it seems so much more difficult to successfully follow a low-carb diet the second or third time around.  Over the years I’ve noticed this phenomenon in myself and in many others whom I have treated or advised, so it’s truly a subject worthy of exploration.

I’m going to list the reasons experience has taught me below, starting with situations over which we have no control and ending with those over which we have total control.

Aging

We all get older every day.  Sadly, with aging, all systems deteriorate.  Some slower, some faster, but all get a little older and a little less functional every day.  If you achieve success on a low-carb diet and find yourself 70 pounds lighter, you’ll also find your self five or six months older.  If you regain that lost weight, then decide to start another low-carb diet to re-lose it, you will probably be a couple of years older than you were when you tried your first low-carb diet.  Just as it’s a little more difficult to pick up tennis at age 46 than it is at age 44, it’s a little more difficult to get everything moving with a low-carb diet when you’re a couple of years older.

Built-in survival mechanisms

Although most dietary recommendations are fairly simplistic, our bodies are unimaginably complex.  Not only do we have a complicated metabolism centered around and directed by the liver, we have multiple neurological and endocrinological feedback pathways between the liver-directed metabolic system and the central nervous system.  And we have gut hormones that get into the act sending signals of fullness or lack thereof.  It is an intricate system designed to allow us to survive on all kinds of food and to keep us alive as long as possible in the face of famine.  I like to think of this entire interconnected system as having its own memory.  It will allow you to fool it once or maybe twice, but then it gets wise.

Almost everyone who starts any kind of diet for the first time sees pretty rapid results.  Pounds seem to fall off quickly and effortlessly.  At a point down the way in the diet, it starts becoming progressively more difficult to lose more weight because the body starts catching on to what’s happening and starts fighting back.  This phenomenon seems to occur less with a low-carb diet because if it is a good quality low-carb diet, the body is getting all the nutrition it needs, so it doesn’t rebel quite the same as it does with some other nutritionally inadequate diets.  But it does rebel a little, nevertheless.  And worse, it remembers.

If you lose weight then regain it and restart a low-carb (or any other) diet, the body is not quite so willing to shed the first pounds as quickly as it did the first time.  It remembers.  If you, like many people I’ve met do, give low-carb a serious, diligent go for about a week, then fall off because of a party, wedding, etc. that you attend, then try again for another week before falling off, you program your body to hang in there for at least a week before letting loose its fat.  The body says, ‘Well, here we go again with another week of this nonsense.  Let’s hold steady on and we’ll be back to our regular high-everything diet within a week.  Let’s not go into starvation mode yet and starting getting rid of our fat.’  What you will find after a few turns of this cycle is that although the first time through with low-carb you may have lost six pounds the first week, the forth time through you will lose almost nothing the first week.  Then the doubt creeps in.  And you begin to wonder if the low-carb diet will really work for you.  It will, but you’ve got to get past the body’s diet memory for it to.

Increased insulin and leptin resistance

All the studies aren’t in yet on this issue for sure.  But, those that are (both animal and human studies) indicate that we become progressively more insulin and leptin resistant as we age.  This is especially true for people who have become overweight or obese and have maintained that state.  Sadly, it is also true for those who became overweight or obese and lost the excess weight, which is most of us.  The more insulin and leptin resistance we are, the more difficult it is to lose weight.  So, the increase in this phenomenon just from the years passing between the first go round and the second on a low-carb diet makes it a little more difficult the next time.

Hormonal dysfunction

Women who are wildly successful on a low-carb diet when they are in their 30s or 40s and premenopausal then try again when they are in their menopausal years often find it almost impossible to lose.  It requires fiddling with hormone levels by replacing with natural hormones and getting the system back into balance before a lot of weight can be lost.  It takes a while to do this.  Even if the hormones do get back to where they need to be quickly, it takes some time for the body to respond.  Often just getting the hormones balanced results in weight loss spontaneously without dieting.  But dieting helps the process along more quickly.

Now we get to the issues that we do have control over.  I don’t want anyone to be offended by this list or think I’m pointing any fingers because I’m not.  But I would guess that I’ve (MD and I as a team) taken care of more overweight people on low-carb diets than anyone alive today.  We’ve had thousands and thousands of patients in our clinics and we’ve dealt with many others second hand through books, lectures, etc.  And we’ve had many friends, relatives, friends of friends, associates, etc. whose care we have monitored.  In shepherding all these people (not to mention ourselves) on low-carb diets, we have learned a few things.   What follows is a summary of what we’ve learned.  Not about the biochemistry and physiology of low-carb dieting, but about the psychology of low-carb dieting.

Lack of commitment

It has been my experience that people just don’t seem to commit as strongly the second, third, etc. time around.  The first time, people make a major commitment.  They lose weight.  They feel better than they have in years.  They are excited.  Then they either stay continue on their low-carb diet and maintain or they don’t.  If they don’t, the weight comes back.  Then a couple of years later when it’s time to start again, they just don’t have the commitment they did the first time around.  And, due to the above reasons, it’s a little more difficult the second time around.  They never really get into the swing of it like they did the first time, and then the notion that maybe it won’t work starts to gnaw.  And then they start doing a ‘half-fast’ (if you get my drift) low-carb diet, which works okay for maintenance, but not for weight loss.  Discouragement sets in, and they bolt from the diet.  I’ve seen this cycle in action countless times.  Don’t fall into it.

People learn how to cheat in their first low-carb go round and remember how when they start again

The first time around on a low-carb diet is exciting.  You’re actually getting to eat all these forbidden foods – steak, eggs, real butter – that you’ve been taught make you fat and are losing weight like crazy.  It’s unbelievable.  But sooner or later, you get a little weary of steak, eggs and real butter, and you start looking to expand your food choices.  If you stay on your carb restriction, you start to figure ways that you can keep carbs low, but eat facsimiles of the high-carb foods you enjoyed before you started your low-carb diet.  You make the major discovery that low-carb brownies exist (or at least they call them low-carb brownies) so you give them a try.  Then you find out about low-carb waffles, pancakes, bagels, etc.  You discover that there is a whole low-carb world of what you’ve always thought of as high-carb foods.  You are in heaven.  You can have your cake and eat it, too, so to speak.  But around about this time, the weight loss starts to really taper off and maybe even comes to a halt.

A few years later, you’ve regained your lost weight plus some, remember how effortlessly you lost it on a low-carb diet, and decide to do it again.  But this time, instead of starting with the steak, eggs and real butter all alone, you stock your low-carb larder with low-carb brownies, bagels, chips, and other junk as well.  Strangely, the low-carb diet just doesn’t seem to work as well this next time around.

If you want to be successful the next time around on a low-carb diet, you’ve got to follow a low-carb diet.  And it takes commitment.  You’ve got to realize it’s going to be a little more difficult than it was the first time, and you’ve got to go on an honest-to-God low-carb diet filled with quality low-carb real foods.  And you’ve got to stick to it.  You want to hang in there until you get to what was called in the old medical literature the dynamic weight stage.  The dynamic weight stage is when weight is changing rapidly in either an upward or downward direction.  Anyone who has gained or lost a lot of weight has experienced this. You can gain rapidly once you get into this phase, but ultimately you stabilize and hit the static weight phase.  It works the same going the other way.  Once you get your weight loss momentum built up, you seem to lose effortlessly while in this dynamic phase.  This is where you want to be.  But you have to commit for a few solid weeks to get there.  You can’t just diddle with it, go on a few days and off, fill up on calorie-dense, low-or-no-carb junk, say you’re doing a low-carb diet, and wonder why you aren’t losing.  You’ve got to get up into the low-carb saddle and ride.

In the next post in this series of two, I’ll present some tips that have helped me enormously and have helped others achieve the level of commitment needed to see us through years of low-carb dieting.

In the above list of reasons I think the low-carb diet (or any diet) is more difficult the nth time around, I’ve probably forgotten something.  Which is why I rely on you and your comments to fill in the missing info.  If you have reasons I’ve not mentioned, send them in.  Don’t be shy.  Or if you disagree.  Let me know.  I’ll be eager to hear from you.