The subtitle of this post could just as easily have been: Feed your mitochondria right.

The two videos below pretty much tell the whole sad tale of doctors and nutrition.  Taken together, they confirm the widespread notion that doctors, in general, know very little about nutrition and seem to be proud to keep it that way.

This first video has made the rounds on the internet.  I’ve had it sent to me or recommended to me a dozen times, but I had never watched it until just a few days ago.  I was put off because of its length, which, at a little over 17 minutes, seems like an eternity in internet viewing time.  But I hope anyone reading this post doesn’t make the mistake I did and avoid watching because of the length.  It is a spectacular talk given by Dr. Terry Wahls, a female physician who was struck down by a relentlessly progressive neurodegenerative disorder.  She describes how she was able to restore her health by revamping her diet in in a way designed to properly feed her mitochondria.*  The transformation is almost unbelievable, especially considering the disease she was battling.  If you haven’t already seen this video – watch it.  I guarantee you’ll be glad you did.  And while you watch, pay careful attention to what her diet doesn’t contain much of.

Click here to view the embedded video.

After you’ve seen the above video, take a look at the one below.  It is a little over 2 minutes long and was developed to give doctors – who, for the most part, don’t give a flip about diet – advice they can pass along to their obese or overweight patients.  Watching the longer video above first will give you more context to better appreciate the one below and show you just how lame mainstream medicine can be.

This video came from Medscape, a subscription service for doctors to keep them abreast of all the latest and greatest news and updates from the world of mainstream medicine.

Click here to view the embedded video.

Pitiful, isn’t it?

Links:

The Medscape article containing this video.  (Although Medscape is a free subscription service for physicians, non-physicians can sign up as well.  For free.  Register if you would like to see the article, which is nothing more than a transcript of the video above.)  It is amazing to me that an online newsletter designed for physicians would regurgitate dietary information from a newsweekly and pass it off as serious medical information.  Especially in such a condescending and patronizing way.  The whole thing is infuriating.

The list of the 22 nutritional ‘experts’ who came up with the dietary rankings mentioned.

The US News and World Report article that inspired the video.

Power, Sex and Suicide  A pretty thorough book on mitochondrial function that is accessible to the non-scientist.  I read this book 6 or 8 years ago and learned a fair amount about mitochondrial DNA.  I had been interested in the issue of mitochondrial rehab for a while, and this book filled in some, but not all, of the blanks.  A good place to start if your interested.

Why Are Cells Powered by Proton Gradients?  Full text of a paper written by Nick Lane, the author of the above book, discussing how mitochondria work by creating an energy gradient across the inner membrane.  Accessible to non scientists.

Source of photo of mitochondria at top of post.

* Mitochondria are the little sausage-shaped organelles inside the cells that convert the energy stored in food to ATP, the energy currency of the body. I think the idea of correctly feeding mitochondria is an important one.  If your mitochondria don’t work well, you don’t work well.  I’ve got a couple of posts in the works on this subject of just what does keep the mitochondria fit and what happens when they become unfit.  And what it takes to rehab them if broken.  Based on my own pretty extensive review of the scientific literature over the past few years coupled with my clinical experience, I have a few minor quibbles with Dr. Wahls’ notions of what constitutes a perfect diet for the mitochondria, but I’ve got to say that her results speak for themselves.  I just think her diet could be even better with a little judicious tweaking.

The first week of January is the traditional time for overweight people to start a diet.  For years I’ve told my patients (and anyone else who would listen) to fight the holiday eat-a-thon and start the new year at the same weight they started the month of November.  During the time between Thanksgiving and the end of the year, so the media typically reports, the average weight gain is anywhere from five to ten pounds per person.  A study in Nutrition Reviews showed the weight gain to be much less on average but a little over five pounds in those who are already obese.  This same study confirms a belief I’ve had for many years.

The best and easiest way to stay slim is to never become obese in the first place.

What I mean by making this seemingly obvious statement is that when a person goes from being normal weight to being overweight it is an indication that something metabolically has gotten broken.  At this point, no one knows for sure what gets broken, but many (and I count myself in this ever growing group) believe the damage occurs in the mitochondria, the organelles within the cells that are the energy furnaces.  Once whatever it is that gets broken breaks, it is difficult from that point on to lose weight and maintain weight loss without effort.

The study I mentioned above showed that the non-obese didn’t really gain anything over the Thanksgiving through New Year’s holidays, and I’m sure it’s not because they didn’t go face down in the fudge.  They didn’t gain because their metabolic systems were working properly.

MD and I both had our struggles with excess weight starting a few of decades ago.  We were both thin, both ate whatever we wanted, and both never gained weight.  Until, that is, our metabolic systems became damaged.  Once that happened, we ballooned, then lost, then have fought it since.  We both have kept our weight under control for years now with a few exceptions here and there by judiciously following a low-carbohydrate diet.  Since we’ve both stayed pretty much in the normal weight range for at least the last several years, we decided to try an experiment over the holidays.  And not over the entire Thanksgiving to New Year’s stretch but for a fairly short stretch between Dec. 20-Jan 2.  We had planned to make a multi-state trek to visit relatives over this period, so we decided that while we were traveling, we were going to eat like normal Americans just to see what would happen.

We didn’t go out of our way to overindulge in anything.  We had a maybe two hamburgers with the bun and had two or three orders of fries (I’m talking about during this entire period – not every day).  We had a Christmas cookie or two, downed several pieces of fudge, drank a bunch of eggnog, ate some fruitcake, and had a couple of bowls of ice cream.  And MD had a little more wine than usual while I probably doubled up on my Jameson.  Other than those indulgences we ate what would be considered sensibly by most people.  We ate some mashed potatoes, grits (we were in the South), beans (not the green bean variety), more fruit than usual and meat of one sort or another.  Pictured below is my plate (which I doubled down on) on New Year’s day.

As you can see, I ate ham, cheese grits, black-eyed peas, curried fruit, and corn bread.

The point of this exercise was to see what would happen to us if we followed a sort of modified typical American diet.  We avoided trans fats and vegetable oils as much as we could and had absolutely no soft drinks.  We had no breakfast cereals of any kind and took it easy on the wheat, but we did eat a little bread occasionally.  Except for the bits of fudge and other Christmas goodies we consumed – all of which were homemade using butter and/or lard as the fat source – we didn’t really go overboard on the sweets.  Our fructose intake was doubtless considerable less than that the average American, especially during that time of year.

So what happened to us during this couple of weeks of much better than average typical American dieting?

We gained weight!  And a fair amount of it.

I don’t know exactly how much we each gained because neither of us ever weighs – we go more by how our clothing fits.  (We didn’t plan on starting this little experiment before we left or we probably would have weighed.  We started it once we were already on the road.)  When I left on the plane, I wore a freshly laundered pair of jeans that fit loosely around my waist and that scrunched up a bit when I tightened my belt.  When we flew home, I wore the same pair of jeans (also freshly laundered), and they were tight around my waist and my belly actually spilled over a little.  MD had the same experience except her weight distribution was a little different.

If I had to guess, I would say we both gained somewhere around five or six pounds.  We were clearly at the top of the range of weight gain as described by the study I linked to earlier, and it happened in two weeks not the six weeks as it did in the study.  Which would indicate that we fall into the obese category, since the obese are the ones who most readily gain weight over the holidays.

But we aren’t really obese, or at least weren’t when we started.  But we obviously have the same metabolic defect that the obese have.  Our metabolic machinery has been damaged.  And even though we’ve keep our weight under control for years, the problem is still there, lurking in the weeds, ready to strike the moment we drop our defenses.

The take home message here is, to paraphrase Wendell Phillips, eternal vigilance is the price of thinness.  At least after you’ve once become obese.

So, MD and I are back on a rigid version of our own program, we are taking Metabosol, and, with the exception of a party we attended last night, are eschewing booze until we get back to our regular sizes.  Some of my GERD symptoms re-appeared during our modified debauch and I was thankful I had an old bottle of out-of-date Protexid to see me through.  One day of solid low-carb, and no more GERD, thank God.  And already after just a few days our clothing is starting to fit again.

If you are one of the many who are committed to a program of weight loss and rehabilitation this January, know that MD and I are right in there with you.

I want to forewarn you, though, that you’ve got to get your head right if you seriously plan to succeed.  Don’t be a Tara Parker-Pope.

I’ve had a number of people send me the link to her long piece in last week’s New York Times Magazine (Parker-Pope is a health columnist for the New York Times) about her struggles to lose weight and to maintain her weight loss once she is finally able to shed a little.  In the article she describes her despair as she tried first this program then that to lose weight.  She fits perfectly the description of so many patients I’ve dealt with over the years.

Once your metabolism is broken, it’s difficult  to lose weight (other than the first time or two you try it) and even more difficult to keep it off.  In order to be successful, you’ve got to make a real commitment and stick to it.  You can’t drift here and there as Parker-Pope has done looking for some magic regimen that is going to ‘melt the fat away.’  It ain’t going to happen.  It takes a lot of hard work and resolve to see it through.  Even with a low-carb diet.

As you can see from the vintage ad above, Tara Parker-Pope is not the first to look for a miracle cure for excess ‘flesh.’  But she is at a bit of a disadvantage in that by virtue of her position she can pick up the phone and call the head of nutrition at Harvard, Yale, Johns Hopkins or any big institution and ask for advice for a column she’s writing.  Unfortunately, the advice she will get from most of these people is totally the mainstream academic party line and more than likely incorrect.  And, if she’s like many patients I’ve dealt with, as soon as she discovers that whatever she is doing entails real work, she will start looking for the next magic fix, only to be disappointed in that.  She will, as she describes, roller-coaster around weight-wise, quickly regaining whatever she loses, and end up fat, sad and miserable.  The only difference between Tara Parker-Pope and the millions of other people out there in her shoes is that she has a powerful platform to express the despair and hopelessness she feels to a large readership.  (I noticed that for a few days her piece was the most emailed of all the articles in the New York Times, which speaks to just how many people are struggling.)

The underlying message of her piece is that she has tried everything, and it has all been for naught.  Her obesity is a condition beyond her control because she has worked with all the greatest minds in the academic world of obesity treatment and has ended up fatter than when she started.

My contention is that if she would undertake a low-carb diet composed of whole foods (with maybe a shake or two thrown in here or there) and stick with it judiciously she would ultimately achieve success.  At least considerably more success than she has achieved thus far.  But if she followed the best low-carb diet known to man and lost to her ideal weight and body fat percentage, she would still have to continue to watch what she eats for the rest of her life if she were to want to maintain her new slim self.  MD and I just proved that over the past couple of weeks.
I have never been able to understand the mindset of people who think that once they lose to their ideal weight and body fat percentage they can then go back to their old way of eating without regaining all the weight they originally put on by their old way of eating.  It baffles me even more that people can lose considerable amounts of weight on a given diet, then go back to their old way of eating, regain all their weight, and view it as a failure of their weight loss diet.  But they do.

I always took a detailed dietary history of all my patients.  Many had been through two or three (or more) weight loss programs before they came to see me.  I would ask them about all the different programs they had tried, and they would list them out.  And most had had some measure of success on one or more (if not all) of these programs, in many cases having lost anywhere from 60-80 or more pounds, but they, almost to a person, considered these programs failures because they had regained their lost weight.

These people, like Tara Parker-Pope, MD and me, and anyone else who has crossed the Rubicon into the land of obesity have dysfunctional metabolic systems that will probably never be completely normal again.  They, like we, will always have to exercise vigilance to maintain what we maintained so easily before the damage took place.

As I wrote above, the easiest way to deal with obesity is to never become obese in the first place.

Which brings me to a real pet peeve of mine.  I want to go for the throats of people who let their kids eat and drink tons of sugary crap and justify it because their kids don’t gain weight from it.  Who knows when the irreversible damage begins to occur?  I feel the same about adolescents and young adults who seem to feel invincible and are face down in all kinds of crap all the time because they never gain weight.  And they assume, stupidly, that they never will.  But when they do, most will struggle with it for the rest of their lives.

In preparation for my own weight loss, I went back an reread a few of my old posts to gain inspiration.  If you are in the let’s-lose-weight boat this month with MD and me, you might want to read them, too.

Here is one of my favorites about a good friend who really committed to losing weight and turned her life around.  The post also tells you why you should gain control not just for yourself but for others.

Another old post gives some psychological insights as to why it can be difficult right now to give yourself over to a low-carbohydrate diet and some psychological tools to make it easier.

Here is one that gives a few more psychological tools to make dieting easier.

Years ago I wrote a regular column for a now-defunct low-carb magazine.  This piece on what it takes to really make a low-carbohydrate diet work may help with your struggles.

There are the two fairly recent posts on all the tips and tricks you can use to start (or restart) a low-carbohydrate diet.

I’m frequently asked on radio, TV and print interviews what my daily food intake is.  A couple of years ago I decided to do a photo diary of a week’s intake of food during a normal week.  The food I ate that week pretty much mirrors the food I eat now with a couple of exceptions.  The quality of the cooked food is better now because almost everything we eat at home is prepared sous vide for obvious reasons.  I go through periods from time to time in which I really like to have shakes for breakfast.  Then I burn out on them and almost can’t bear the thought.  During the non-shake periods I typically eat three eggs and three or four slices of bacon (Mangalitsa bacon if I can get it) every day for breakfast.  During my week’s photo log, I was in a shake phase, so realize that I am not now in shake phase, so it’s bacon and eggs, but that’s about the only difference.  The week’s diet you’ll see if you take a look is what keeps me at my normal weight.  It’s pretty much what I’m back on now minus the booze and a few of the little extra carb tidbits. Plus, I’m scrupulously avoiding wheat just to see what happens.  As soon as I lose the few pounds I picked up and my jeans are loose again, I’ll be back to this diet in full.

• Photo food diary day 1
• Photo food diary day 2
• Photo food diary day 3
• Photo food diary day 4
• Photo food diary day 5
• Photo food diary day 6
• Photo food diary day 7

If you, like we, have been noshing on more carbs than normal over the holidays, then start anew with us this January.  As I have discovered this first few days, the time I spent dallying with carbohydrates over the previous couple of weeks has reinvigorated my long dormant urge to eat even more carbs.  I’m sure I’m not the only one in this boat.  We all have to remember that this urge is one we have to overcome first by effort and ultimately by habit.  I’m back on track.  Hope you are as well.

Over a half decade ago Professor Jared Diamond, in his Pulitzer Prize-winning book Guns, Germs, and Steel, famously wrote

“The adoption of agriculture, supposedly our most decisive step toward a better life, was in many ways a catastrophe from which we have never recovered.”

Dr Diamond was referring, of course, to the devolution of human health that took place as mankind suffered the corporal transformation driven by the mismatch between hunter-gatherer genes and an agricultural diet and lifestyle. Smaller stature, decreased cortical bone thickness, obesity, increased incidence of infectious diseases, dental caries, periodontal disease, vitamin deficiencies, and even famine – all common in agriculturists – were not, for the most part, the lot of pre-agricultural man.

Humanity doubtless gained more than it lost in this hunter to farmer changeover when viewed in a big-picture sort of way.  Farming made possible larger communities filled with workers, workers who, for the first time, made specialization of labor a possibility.  And fewer people could till the fields and provide food for the many, freeing the others to pursue the arts, business, politics, and warfare.

Stephen Budiansky, author of one of my favorite books, Covenant of the Wild, describes how domestic animals formed a pact with humans in which the animals traded a period of safety and survival for their lives.  Had this covenant not been made, it is highly likely – virtually a certainty – that cows would now be extinct.  Big, slow, stupid and tasty, had they not been amenable to domestication and entered into the covenant with their domesticators, cattle would have been hunted to extinction long, long ago.  But they did – however unwillingly – make the covenant and so exist by the tens of millions today.  The deal they cut was a phenomenal deal for cattle as a species, but not a particularly good deal for the individual cow when the time comes to pay up at slaughter.

Homo sapiens entered an almost mirror image of this same covenant when they domesticated cereal grasses.*  We gave up our independence and mobility for the promise of a constant and plentiful food supply.  But, as with our covenant with domestic animals, there is a catch.  And this time it’s with us.  Humans emerged from this deal with the short end of the stick.  In the same way as did cattle, we made a good-for-humans-as-a-species/bad-for-the-individual-human trade.  Like it or not, we traded the health of the individual human for the overall good of mankind and the development of civilization.

We traded a diet based primarily on fat and protein with a little carbohydrate thrown in from roots, shoots and tubers for one centered predominantly on carbohydrate.  The main source of the carbohydrate was cereal grains, chiefly ancient forms of wheat, the predecessor of the wheat that now occupies a large part of the human diet everywhere.  Ancient forms of wheat didn’t do our forebears a lot of good, and, according to Dr. William Davis’s new book Wheat Belly, the modern forms of the grain do us even less good.

Before we get to the problems modern hybrid wheat causes us, let’s take a look at the afflictions a diet of primitive wheat visited upon our predecessors.

The ancient Egyptians consumed a diet that would be considered optimal by many people today.  Both wealthy and poor Egyptians consumed primarily bread and a type of cloudy, almost gruel-like beer.  To these staples were added a variety of vegetables (mainly onions), and a small selection of game, fish and meat.  The bread was made from coarse ground, whole grain emmer wheat, a primitive, high-protein wheat.  Sugar didn’t come on the scene until about 1000 AD, so the Egyptians used honey sparingly (it was expensive) as a sweetener along with figs.  In short, these people consumed a diet the vast majority of modern nutritionists would prescribe to people to prevent obesity, heart disease, obesity and the rest of the diseases associated with the Western diet.

But, as their mummified remains and their contemporary artwork demonstrate, the ancient Egyptians were often fat and were riddled with heart disease, dental caries, bad periodontal disease and no doubt diabetes and hypertension.  Many people have argued that since only the wealthy were mummified, the mummy data applies only to them, and since the wealthy ate more red meat, the rates of obesity, heart disease and the other disorders common to them didn’t apply to the rest of the population.  Even the common man, however, was often portrayed as obese in Egyptian artwork, and despite greater consumption of meat, the main staple of even the wealthy was bread and beer. And it didn’t do them a lot of good.

The 5,300 year old mummy of Ötzi the Iceman found in the Italian Alps showed a bad case of dental caries and periodontitis along with a stomach-full of einkorn wheat (another primitive variety). Said the researchers who examined Ötzi:

Although the Iceman did not lose a single tooth until the his death at an age of about 40 years, he had an advanced abrasion of his teeth, profound carious lesions, and a moderate to severe periodontitis.

In particular, the molars of the upper jaw showed loss of alveolar bone as a sign of periodontitis (inflammation of the ligaments and bones that support the teeth), while evidence of “mechanical trauma” was found on two teeth.

…the most surprising find is the high frequency of cavities.

These dental pathologies are a sign of change in the Neolithic diet.

We already know that he was eating grains, such as einkorn or emmer. The contained carbohydrates clearly increased the risk of developing dental diseases

One would assume these findings would be common among the rest of Ötzi’s contemporaries, who doubtless consumed a similar diet.

Sadly, these same findings are also common among modern man who consumes a more malign version of primitive wheat.

Until I read Dr. Davis’s book Wheat Belly, I didn’t really think much about wheat other than its being a major source of carbohydrate in the American diet.  It never had occurred to me that the wheat we eat today is not the same wheat of our great-grandmothers cooked with nor probably even our grandmothers.  And it really hadn’t dawned on me how pervasive wheat is in the diet.  Since reading Michael Pollen’s The Omnivore’s Dilemma I had been conscious of the amount of corn in our modern diet, but I hadn’t thought much about wheat.  As Yogi Berra supposedly said, “You can see a lot just by looking.”  So I went out and looked.  And I can tell you that we are much more Children of the Wheat than we are Children of the Corn.

In most grocery stores, an entire aisle is devoted to nothing but bread in all its forms.  Then there is typically another large aisle full of cakes, cupcakes, cookies, pies, tarts, sweet rolls, bagels, croissants, brownies, and other sweet baked goods.  The vast majority of the cereal aisle displays products containing primarily wheat.  And if you look at processed foods of all kinds, you’ll find wheat in there.  If you make or buy gravy, roux, or just about any kind of sauce, you’ll find it’s thickened with wheat flour. (MD bought some demiglace a few days ago, and noticed as she was removing it from the container that even it had added wheat.) Then there is the aisle full of different beers, many of which are made with wheat.  These are just a few of the items you can find containing wheat in a grocery store; don’t even get me started on restaurant fare.  Wheat is everywhere – corn should be so lucky.

When I was roaming around looking for pictures of dwarf wheat (more about which later), I came upon the website for the Kansas Wheat Commission that listed a few facts about wheat.  Here are several that caught my eye.

Wheat is the primary grain used in U.S. grain products.  Approximately three-quarters of all U.S. grain products are made from wheat flour.

More food is made with wheat than any other cereal grain.

U.S. Farmers grow nearly 2.4 billion bushels of wheat on 63 million acres of land.

About half the wheat grown in the United States is used domestically.

A little back-of-the-envelope calculating using the above statistics tells us that each of us in the United States consumes about four bushels of wheat per year.  Another statistic from the linked website states that each bushel of wheat makes about 90 one-pound loaves of whole wheat bread.  So, we all eat the equivalent of 360 loaves of bread per year, or approximately one loaf per person per day. That’s a lot of wheat, in fact, it’s almost approaching ancient Egyptian levels. (Moreover, since MD and I don’t eat any, that means two other people out there are each eating two loaves per day.)

It would be bad enough if we consumed all this wheat as emmer or einkhorn or other primitive varieties, but we don’t.  We get most from a hybrid of Triticum aestivum – our great grandmother’s wheat – called dwarf (or semi-dwarf) wheat, which now comprises more than 99 percent of all wheat grown worldwide.

As Dr. Davis tells it, the hybridization of wheat came about in an effort to improve yield, which is now about tenfold greater per acre than it was a century ago. Older strains of wheat were taller and more prone to damage from wind and rain.  And

When large quantities of nitrogen-rich fertilizer are applied to wheat fields, the seed head at the top of the plant grows to enormous proportions.  The top-heavy seed head, however, buckles the stalk.  Buckling kills the plant and makes harvesting problematic. A University of Minnesota-trained geneticist…is credited with developing the exceptionally high-yielding dwarf wheat that was shorter and stockier, allowing the plant to maintain erect posture and resist buckling under the large seed head.  Tall stalks are also inefficient; short stalks reach maturity more quickly, which means a shorter growing season with less fertilizer required to generate the otherwise useless stalk.

In the photos below you can see the difference between wheat grown in the Middle Ages and the dwarf wheat grown today.

Dr. Davis writes that modern wheat is approximately 70 percent carbohydrate by weight.  The carbohydrate is in the form of a starch called amylopectin A.

The most digestible form of amylopectin, amylopectin A, is the form found in wheat.  Because it is the most digestible, it is the form that most enthusiastically increases blood sugar.  This explains why, gram for gram, wheat increases blood sugar to a greater degree than, say, kidney beans or potato chips.  The amylopectin A of wheat products, “complex” or no, might be regarded as a supercarbohydrate, a form of highly digestible carbohydrate that is more efficiently converted to blood sugar than nearly all the other carbohydrate foods, simple or complex. [Italics in the original.]

But what about the much vaunted whole grains.  Won’t ‘whole grain’ bread or wheat products be better?  Not according to Dr. Davis:

…the degree of processing, from a blood sugar standpoint, makes little difference: Wheat is wheat, with various forms of processing or lack of processing, simple or complex, high-fiber or low-fiber, all generating similar high blood sugars.  Just as “boys will be boys,” amylopectin A will be amylopectin A.  In healthy, slender volunteers, two medium-sized slices of whole wheat bread increase blood sugar by 30 mg/dl (from 93 to 123 mg/dl), no different from white bread.  In people with diabetes, both white and whole grain bread increase blood sugar 70 to 120 mg/dl over starting levels.

And aside from the blood sugar and, consequently, insulin problems caused by the consumption of too much wheat, there are other problems.  As with almost any food, the newer the food, the greater the likelihood that it will be problematic to some humans who consume it.  Since dwarf wheat has been around for less than 50 years, it should come as no surprise that it does indeed cause it’s share of problems.  Dr. Davis spends the better part of his excellent book detailing many of these problems and describing his clinical experience in helping many of his patients shuck their wheat habit.  He describes the increase in celiac disease over the past 50 years and believes, as I do, that celiac disease is a continuum.  The severe form of it that is recognized as celiac disease is pretty easy to diagnose (if a doctor has sense enough to look for it), but there are milder forms that manifest themselves as anything from mysterious rashes that come and go to diarrhea and other GI disturbances to arthritic aches and pains. And we can’t forget a number of other afflictions that may well have their basis in wheat intolerance that include osteoporosis, acne (bagel face?), neurological disorders, and the creepily- dubbed ‘man boobs.’

It’s good to learn in Wheat Belly that Dr. Davis has finally shucked his bred-in-the-bone cardiologist’s antipathy toward fat in general and saturated fat specifically and has come over to what most of his peers must view as the dark (read: low-carb) side:

The fat phobia of the past forty years turned us off from foods such as eggs, sirloin, and pork because of their saturated fat content — but saturated fat was never the problem.  Carbohydrates in combination with saturated fat, however, cause measures of LDL particles to skyrocket.  The problem was carbohydrates more than saturated fat.  In fact, new studies have exonerated saturated fat as an underlying contributor to heart attack and stroke risk. [Italics in the original.]

Dr. Davis wraps up his meticulously researched book with a straightforward plan to help free the reader from the tyranny of wheat, while at the same time providing instructions for a delicious and satisfying wheat-free diet.  He furnishes an extensive list of wheat-containing foods that should be avoided and imparts his caveats about going facedown in products advertised as being gluten-free.  And best of all, he provides a short section filled with matchless wheat-free recipes for many meals that would otherwise be wheat-laden. (MD and I have tried a few of these recipes and found them to be superb.  I especially enjoy his wheat-free granola recipe even though I go a little easy on the rolled oats part of it.)

Wheat Belly hit the New York Times Bestseller list shortly after it came out (and has been there for two weeks now), which I can tell you from experience, is not an easy thing to do.  As a result (because being on the NY Times list means a book has had big sales numbers), the wheat producers have not taken their hits lying down.  They’re fighting back with full venom, because a book like this one can do them serious economic damage. Expect it to get worse. (Remember all those shelves in the grocery stores stuffed with wheat-containing products? They don’t want to see that go away.)  You can read about some of their tactics here and read Tom Naughton’s interviews with Dr. Davis here and here.

I can’t recommend this terrific book highly enough.  Wheat Belly is fully referenced and indexed (unless you somehow got the little freebee paperback review version that I received from the publisher), and is a must have for the library of any serious low-carber or anyone concerned about health.

*MD and I wrote about this domestication of humans by grains in The Protein Power LifePlan.  In that book we referenced an interesting paper by a couple of Australian researchers on the hypothesis that the addictive nature of cereal grains helping this domestication along.

A little over two years ago I wrote a post on Pentabosol, a weight-loss supplement we and our research partner developed and made available for a number of years.  In that post I mentioned that MD and I were contemplating actively marketing Pentabosol again.  We reformulated the product and changed its name to Metabosol, but our timing was all wrong because at about the same time, we wound up launching our SousVide Supreme project as well.  Never having been in the appliance business, we had not even the most minimal idea as to how much time that venture was going to take.  As a consequence, the weight-loss product project took a back seat and more or less fell between the cracks.  Now that things on the sous vide front requiring our direct attention have slowed down a bit (for us, not for the company) we decided to turn our attention to the nutritional supplement and made an annoying (to us) discovery that may benefit you. (More about which later.) In case you don’t go back and read the old post, let me quickly review the Pentabosol (Metabosol) story.

Pentabosol

NOTE: DUE TO OVERWHELMING DEMAND, WE HAVE JUST RUN OUT OF ALL OF OUR SUPPLIES OF METABOSOL.  THANKS FOR YOUR INTEREST.

MD and I have taken care of overweight patients using low-carb diets in our medical practice for decades.  Our patients had pretty spectacular results with their low-carb diets, but like dieters everywhere, they all wanted to lose weight faster.  For years we had been searching for some kind of nutritional product that could give a boost to our patients’ weight loss without their paying the price of unpleasant side effects.  As a consequence, we ruled out anything with phenylpropanolamine, ephedra, and all the stimulant type products.  Although we used prescription medicines occasionally, we weren’t really sold on them because of the side-effect issue and because we didn’t know what, if any, would be the long-term effects.  We were seeking something that was a natural supplement that had no stimulant effects and that actually worked.

As is my wont, I trawled through the medical literature looking for solutions.  It soon became obvious that although there were a number of natural substances (non stimulants) promoted as weigh loss supplements, these products were not particularly effective.  We looked at all these different supplements and, along with our partner, laid out all the mechanisms by which these products worked.  We then teased out those that drove pathways congruent with the pathways through which the low-carb diet worked.  And we came up with a couple of hypotheses.  First, we thought that these products individually might work a lot better than their study results had shown if used along with a low-carbohydrate diet (virtually all had been studied using low-calorie, high-carb diets), and, second, that these few substances taken in combination might have a synergistic effect not present when taken individually.  We came up with a supplement mixture that we thought might help people following low-carb diets lose weight more quickly.

We decided to make these supplements available to patients in our practice who wanted to boost their weight loss.  We provided them with a written list of supplements that they could gather at most health food stores (since we didn’t carry any of these supplements in the clinic).  The patients who elected to try the regimen did well, but we really had no control group, so we didn’t know with certainty whether our supplement conglomeration worked or not.  We had some difficulty getting a lot of patients to both try the regimen and stick with it once they started, because of the expense and the inconvenience.  The bag of supplements would set them back about $150 a month and required their taking multiple pills multiple times daily.

We felt that our little pilot study, such as it was, justified spending the money to both develop an actual product and to have it clinically tested.  We found a manufacturer to produce a product that was less expensive and more convenient than the handful of pills our patients had been taking daily.  We also sought out and found a facility that did contract clinical testing of products.  And we discovered what the drug companies have known for a long time – randomized, double-blind, placebo-controlled studies, the gold standard of clinical trials, are not inexpensive.  After giving the idea a lot of study, we sucked up and invested the money.

We established the protocols and launched the study.  Subjects were randomized into two groups, both of which went on moderately low-carb diets and both of which were instructed to perform the same type and amount of exercise. One group went on the supplement that we ultimately named Pentabosol, while the other went on a placebo that looked and tasted the same as Pentabosol.  (As an aside, I can tell you that we must have been brain dead when we contracted for this study because by the time all the subjects were recruited and randomized, the actual trial ended up taking place through the Thanksgiving holiday – for sure not the best time to be doing a weight loss study. I have no way of know, of course, but I suspect that had we waited until the first of the following year to do this study, we would have had even better results.)  After the last subjects completed the six week study, the testing facility broke the double-blind codes, analyzed the data, and the director of the lab gave me a call.

It was a memorable call.  He started out by saying: “Well, I’ve got some good news for you and some bad news for you.  Which do you want first?”

Being the eternal optimist, I said, give me the good news.

He said:  “You have got a phenomenal product.  It works like nothing we’ve ever seen.  It works better than some drugs we’ve tested.”

The people on the supplement had lost almost double the weight (71 percent more, to be exact) than those taking the placebo.

As you might imagine, I was thrilled. But not all that surprised based on our reports from our own patients.

“So what’s the bad news?,” I asked.

The bad news, he told me, was that we didn’t have what he thought was a commercial product.  He said that he had to practically horsewhip some people to keep them on it.  He said he thought it didn’t matter how efficacious a supplement was if people wouldn’t take it.

He had a point.  And, admittedly, the first primitive version of our product was pretty rough.  The product … is a powder that you dissolve in water (cold or hot like a tea) and drink.  The early study version mixed about like sand mixes with water.  You had to put it in the water, then swirl the water in the glass while you drank the stuff.  And it didn’t taste all that great.

After badgering our manufacturer to make the product better but obtaining only marginal improvements, we began seeking other manufacturers.  We finally found one that specialized in powders and finally had a product manufactured that was tasty and mixed well.

Metabosol

NOTE: DUE TO OVERWHELMING DEMAND, WE ARE OUT OF OUR SUPPLY OF METABOSOL.

A couple of years ago MD and I decided we needed to give Pentabosol a makeover.  A complaint we had heard over and over was that Pentabosol contained sucralose, an artificial sweetener.  At the time we first made the product, we had no choice.  We did have a choice, I suppose, in aspartame, but we elected to go with sucralose.  The product required a sweetener because one of the components is extremely tart, and without sweetening the product would have been unpalatable.

We  spent some time with the manufacturer and discovered that we could freshen the taste, improve mix-ability, add another flavor and use a natural sweetener instead of sucralose.

We decided to name the new and improved product Metabosol.  It contains all the same active ingredients in the same proportions as Pentabosol, but is naturally sweetened, giving it (to my palate, at least) a cleaner taste.  Those who have tried both products like the taste and consistency of Metabosol better.  And like the fact that there are a couple of flavors: berry and citrus.

How you can take advantage of our lack of attention.

As I mentioned at the start of this post, we did all the improvement work and got Metabosol all ready to launch but put it on the back burner because of our commitment to the sous vide project.  We just got a call from our able assistant, Kristi, who said, guess what? all the Metabosol is going out of date as of the end of May.  This May.  As in about two weeks.

So, if any readers out there would like to give Metabosol a try, it can be ordered through the Products section of our website absolutely free.  With absolutely no strings attached.  All we ask is that you pay for UPS shipping.  And because we don’t have all that many containers left, please only two per person.  Let’s make sure that anyone who wants to can give it a try.

I want to end with a few caveats.

First, we did only one study on Pentabosol / Metabosol.  That study showed significantly increased weight loss in the subjects using the product.  But I’ll be the first to tell anyone that it takes more than one study to prove anything.  We (or someone else) might do a second study and find less or more weight loss.  As far as I know, there is no other study out there evaluating the efficacy of the exact combinations contained in Metabosol.  There is one other study – a pilot study – showing a significant weight loss in subjects following a similar, but much more expensive supplement regimen.  We’ve had over 250,000 people use Pentabosol with a substantial reorder rate, which would indicate that it works.  But we have only the one study.

Second, the Metabosol you will receive is almost out of date.  It shouldn’t be a problem, but the manufacturer is required to put a two year expiration on supplements.  We will ship only while the product is still in date, so once the end of May comes, we will take the product off our website until we have a new batch, which will then be at the regular price.

Third, as studied, Metabosol was shown to work only when combined with a low-carb diet and moderate exercise. (We had to control for diet and exercise.) It was designed to enhance the rate of weight loss in those following low-carbohydrate diets and who exercised moderately, and the study indicated that it did.  We have no idea if Metabosol would work without diet and exercise and we don’t recommend that you use it in that way.  It is not a magic bullet.  As we all know, weight loss is a difficult proposition at best – Metabosol is simply designed to help you get to your goal a little faster.

Now, if I haven’t scared you off with all the disclaimers, give it a try on us.  And we would love to learn how it works for you, so don’t hesitate to let us know.

Note: We try to get all of our products shipped the same day the orders come in.  But Kristi, our able assistant, is leaving for a long weekend (it’s her birthday today, so we’ve let her escape the asylum for a bit) and won’t be able to get these Metabosol orders shipped until Monday morning, May 23.

THANKS FOR YOUR INTEREST.  WE HAVE RUN OUT OF OUR SUPPLIES OF METABOSOL.

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.

The first Dietary Goals for the United States (DGUS) were released in 1977 to not a lot of fanfare.  At that time, the great unwashed masses hadn’t really heard much about the word cholesterol, a substance the DGUS recommended that we should limit to 300 mg per day.  Doctors didn’t routinely screen for it, and if they did, they didn’t pay much attention to it.  In fact, at that time – as I recall, anyway – the upper limit of normal for total cholesterol was 240 mg/dl.  I was in medical school back then, and I don’t really remember any emphasis on cholesterol or blood lipids.  I think we had one lecture on it in biochemistry, given by a nebbish little professor we called Mighty Manford (his first name was Manford), who labored away in the obscurity of the biochemistry department. It’s hard to believe in today’s world of lipophobia that as little as 30 years ago, no one much cared about cholesterol.

One of the major players in bringing cholesterol to the public’s awareness was Time magazine. Its piece on cholesterol in the March 26, 1984 issue was a devastating hit piece on both dietary cholesterol and dietary fat.  Both – the article explained – were a main driving force behind the development of heart disease.

Reading this article today, it’s amazing how it drips with misinformation.  At the time, however, most people – physicians included – accepted it as gospel.  Sadly, even today, many physicians who should know better believe in and act in accordance to the bountiful misinformation contained in this piece.

I could write a blog longer than the article (and it’s a long article) describing and dissecting all the many errors, but I’m going to go over just one.  And that one just briefly.  But before I get to that, let me show you just a few of interesting small parts of the article beginning with the very first sentence:

Cholesterol is proved deadly, and our diet may never be the same.

Hmm.  Dietary cholesterol has been proved pretty benign.  But the writers are correct about our diet being changed.

And take a look at this:

For decades, researchers have been trying to prove conclusively that cholesterol is a major villain in this epidemic [heart disease].  It has not been easy.

Have you ever seen a better example of the confirmation bias at work.  We know cholesterol is a problem, and we’re going to prove it no matter what it takes.  So what if the evidence keeps blowing up in our faces, if we work hard enough, we can by God prove what we know to be true.

Although most cholesterol found in the body is produced in the liver, 20% to 30% generally comes from the food we eat.

Actually, the figure is about 15 percent that comes from the food we eat.  Most cholesterol is made in the liver, but not all.  Virtually every cell in the body has the ability to make cholesterol, because it is so important to survival.

The main thrust of the article is about a study demonstrating that lowering cholesterol levels brought about a decrease in cardiac death rate.  Here it is presented in the breathless prose of the Time writers:

That was the reason for the N.H.L.B.I, study. The elaborate, ten-year program recruited 3,806 men between the ages of 35 and 59, all of whom had cholesterol levels above 265 mg per deciliter of blood (the average for U.S. adults is 215 to 220). Half the men were put on daily doses of cholestyramine, an unpleasant, cholesterol-lowering drug that was mixed with orange juice and taken six times a day. One participant likened taking it to swallowing “orange-flavored sand.” Among its side effects: constipation, bloating, nausea and gas. The other half received a similarly gritty placebo. Researchers had decided to use a drug rather than diet to lower cholesterol, because it would have been virtually impossible to control or measure the diet of so many men over so long a period. By the end of the study, the cholestyramine group had achieved an average cholesterol level 8.5% lower than that of the control group and had suffered 19% fewer heart attacks. Their cardiac death rate was a remarkable 24% lower than that of the placebo group.

The lesson is plain, says Dr. Charles Glueck, director of the University of Cincinnati Lipid Research Center, one of twelve centers that participated in the project: “For every 1% reduction in total cholesterol level, there is a 2% reduction of heart-disease risk.” This, says Project Director Basil Rifkind, is the evidence scientists have been waiting for. “It is a turning point in cholesterol-heart-disease research.”

Pretty powerful stuff, you might think.  Which is just what the authors of this article must have wanted you to think.  After all, a failed study doesn’t produce cover stories.

There are more than a few flies in this anti-cholesterol ointment, however.  Let’s take a look at what Gary Taubes writes about this study in Good Calories, Bad Calories:

In January 1984, the results of the trial were published in The Journal of the American Medical Association.  Cholesterol levels dropped by an average of 4 percent in the control group – those men taking a placebo.  The levels dropped by 13 percent in the men taking cholestryramine.  In the control group, 158 men suffered non-fatal heart attacks during the study and 38 men died from heart attacks.  In the treatment group, 130 men suffered non-fatal heart attacks and only 30 died from them.  All in all, 71 men had died in the control group and 68 in the treatment group.  In other words, cholestryramine had improved by less than .2 percent the chance that any one of the men who took it would live through the next decade.  To call these results “conclusive,” as the University of Chicago biostatistician Paul Meier remarked, would constitute “a substantial misuse of the term.”  Nonetheless, these results were taken as sufficient by Rifkind, Steinberg and their colleagues [those who had been searching for ‘proof’ for decades that cholesterol causes heart disease] so they could state unconditionally that [Ancel] Keys had been right and that lowering cholesterol would save lives.

Aside from the lack of any real meaningful data, the authors tried to palm off what they had found from a drug study as being applicable to diet.  Again, from Good Calories, Bad Calories:

Pete Ahrens [a cholesterol researcher at Rockefeller University] called this extrapolation from a drug study to a diet “unwarranted, unscientific and wishful thinking.”  Thomas Chalmers, an expert on clinical trials who would later become president of the Mt. Sinai School of Medicine in New York, described it to Science as an “unconscionable exaggeration of the data.”  In fact, the LRC investigators acknowledged in their JAMA article that their attempt to ascertain a benefit from diet alone had failed.

But that certainly didn’t keep them from trying.

Although there were several people mentioned in the Time article who were examples of the benefits of healthful, low-fat living, the star of the piece had to be Fred Shragai.

Fred Shragai, 59, of Encino, Calif., is a good example. Fourteen years ago, the prosperous real estate developer had a cholesterol level above 300 mg. At the time, he smoked four packs of cigarettes a day, was overweight (202 lbs. on a 5-ft. 5-in. frame) and routinely put in five or six 14-hour, pressure-packed days a week at the office. Rich sauces and fatty meat were his standard fare for both lunch and dinner, and exercise meant reaching under the bed to grab from his stash of pretzels and potato chips. Shragai was a classic candidate for a heart attack, and at the age of 45, he had one. Nine years later he was hospitalized for an operation to bypass five seriously blocked coronary arteries. In desperation, Shragai enrolled himself in U.C.L.A.’s Center for Health Enhancement. By changing the way he lived, he was told, he could lower his cholesterol level and reduce his risk of another heart attack.

There was much to learn. Cholesterol, as Shragai found out, is packaged by the body in envelopes of protein, and only some of these packages are potentially harmful. The main culprit, LDL (for low-density lipoprotein), is the body’s oil truck, circulating in the blood, delivering fat and cholesterol to the cells. Studies have shown that the higher the level of LDL, the greater the risk of atherosclerosis. Another type of cholesterol package is called HDL (for high-density lipoprotein). It appears to play a salutary role, helping remove cholesterol from circulation and reducing the risk of heart disease. Shragai’s goal was to lower his level of LDL and raise his HDL.

Diet was a first step. To begin with, such cholesterol-rich foods as eggs and organ meats and most cheeses can directly add to the level of potentially harmful LDL. Fat has an even bigger impact, although the reasons are not well understood. Saturated fat tends to raise LDL levels. Butter, bacon, beef, whole milk, virtually any food of animal origin is high in saturated fat; so are two vegetable oils: coconut and palm.

Polyunsaturated fats, which are typically of vegetable origin, have the opposite effect; thus corn, safflower, soybean and sesame oils tend to lower the level of potentially dangerous LDL. Fish oils do the same. In the middle are the mono-unsaturated fats such as olive and peanut oils. These may lower LDL slightly, but tend to be neutral.

The amount of fiber in the diet also seems to influence cholesterol levels. “LDL cholesterol can be reduced 20% in people with high levels just by consuming a cup of oat bran a day,” says Dr. Jon Story of Purdue University. However, Story adds, “that does not mean you can go and eat whatever else you want.”

For reasons that are still under study, cholesterol levels are influenced by a number of life-style factors. For instance, regular exercise can significantly raise the level of protective HDL. Alas, a couple of push-ups a day will not do the trick, says Dr. Josef Patsch of Houston’s Baylor College of Medicine: “You need sustained aerobic exercise for 20 minutes at least four times a week to really benefit.” A less strenuous way to raise HDL levels may be to have a daily shot or two of alcohol. “The evidence is indirect,” reports Epidemiologist Stephen Hulley of the University of California at San Francisco, “but social drinkers have HDL levels as much as 33% higher than those found in teetotalers.” On a more sober note, U.C.S.F.’s Dr. Richard Havel warns: “Anyone who recommends raising HDL by drinking is playing with fire.” Stress too has a detrimental effect. Studies have shown that the cholesterol levels of medical students peak at exam time, while accountants hit their high point around April 15.

By applying these lessons, says Shragai, “my life was totally changed.” Today the man who used to love steak says, “I won’t touch it.” At a restaurant, “if I choose fish, I ask the chef to skip the butter or please to sauté it in wine.” Every morning, regardless of weather, the man who once spurned exercise goes for an eight mile, two-hour hike through the wooded mountain trails near his home. He no longer smokes. His workdays average between eight and ten hours, but he insists, “I can absolutely stay away from the tension now. If I feel the pressure, I take off. Business associates get used to it; I set my own pace.” Shragai no longer lives in fear of a sudden heart attack: his blood pressure and pulse rate are down, and most remarkable, his cholesterol level has dropped to an exemplary 195.

Do a little Googling on Fred Shragai and a few things turn up.  Apparently, Mr. Shragai, a Holocaust survivor, was quite an interesting character.  In addition to being a successful businessman, he donned a Santa suit and entertained children around Christmastime.  As described in a December 1990 article in Orange Coast Magazine,

Shragai, in his late 60s, stands 5 feet 5 inches and weighs 165 pounds, down from his former rotund 200-plus since the doctor put Santa on a diet.  His beard and twinkling blue eyes are his own, he says proudly.

The article describes Mr. Shragai’s joy in his long-term job as Santa to many of his area’s poor residents.  He would visit houses, tell stories and bring presents.

“I’ll do this as long as I possibly can,” Shragai says, his eyes twinkling behind his Santa glasses. “After all, Santa can’t just quit.”

Unfortunately, that wasn’t all that long.  Mr. Shragai died of a heart attack about two months later on Feb 8, 1991 at age 66.

You can read about his life in an article in the Guardian written by his daughter as she came to grips with his death.

Many people who were in Mr. Shragai’s condition – overweight, overworked and overfed – bet their lives that the promise made by the Time article would be fulfilled.  If they quit smoking, cut the fat from their diets, took up exercise and dropped their cholesterol levels, they would avoid an early death from heart disease.  As the Time article said about Mr. Shragai:

[he] no longer lives in fear of a sudden heart attack: his blood pressure and pulse rate are down, and most remarkable, his cholesterol level has dropped to an exemplary 195.

As if these changes undo the risk of heart attack.  We can see from Mr. Shragai’s unfortunate case that they don’t.

Basically, he bet his life – literally – on the recommendations of doctors who were responsible for most of the hype in the Time article.  It’s hard to say whether he won, lost or broke even on the bet, because we don’t know what the outcome would have been had Mr. Shragai continued on his previous path.  Or what would have happened had he gone on a low-carb diet instead.  Based on my years of experience, I would bet that he would have done better on the low-carb approach, but, as I say, there is no way to know for sure.

There are a couple of take-home messages from Mr. Shragai’s case.  The first is that we don’t really know what constitutes true risk for heart disease.  Reduction of blood pressure, weight and cholesterol levels – measures of risk in the estimation of most physicians – didn’t prevent a disastrous outcome.  The second, and, in my view, the most important is that when we make nutritional and lifestyle decisions, we are betting our lives that we’ve made the correct decision.  Even those maintaining their course are making the decision not to change.  Decisions precede actions, and actions definitely have consequences, which means decisions have consequences.

I’m betting my life that saturated fat is good for me and that carbs are bad.  I eat a ton of saturated fat and very few carbs (unless I’m being a very bad boy as I was last night when I indulged in some of my granddaughter’s birthday cake).  So, if Dean Ornish is right and I’m wrong, I could be in deep trouble and maybe live a dramatically shortened life.  But I don’t think so.  Why?  Because the indications that the low-carbohydrate diet is the correct diet for humans comes from so many different sources. (And that’s not even counting my years of hands-on care of many thousands of patients on such diets.)

If you look at the scientific literature, you find that the low-carbohydrate diet is, at worst, the equal of the low-fat, high-carbohydrate diet and at best triumphs over it in spectacular fashion.  If you look at the anthropological evidence, the health of early humans took a turn for the worse when agriculture (read: high-carbohydrate diet) came along.  Pasta, even whole-grain pasta, was the fast food of antiquity.  If you look at the evolutionary evidence, it’s pretty clear that the forces of natural selection molded us to function optimally on a higher-fat, higher-protein diet.  And, finally, if you just look at the human physiology and biochemistry involved, it is clear that a diet high in carbohydrates is not good for us.  Looking at all this graphically from one of my slides below, we can see that all the evidence vectors point to a low-carb diet as being the one most optimal for human health.  Can a low-fat, high-carb diet make this claim?  I don’t think so.  Though many misguided vegans try to make such a claim, their arguments are risible.

You can find a few studies that show a low-fat, high-carb diet performs OK, but where is the anthropological, evolutionary and biochemical data to confirm?  When deciding what diet to follow, remember: you’re betting you’re life.  Consequently, you should view the diet through the various lenses as laid out in the graphic above.  If a new diet looks acceptable through one or two lenses, but not the others, just stick with your low-carb diet and be done with it.

Had Mr. Shragai performed the above analysis, he probably would not have followed the diet he did.  As I wrote earlier, we have no idea as to what his outcome would have been had he gone on a low-carb diet instead of a low-fat one, but I can’t help but believe it would have been better.  Although Mr. Shragai’s case is that of but one individual, since this vapid 1984 Time article came out launching the jihad against fat and cholesterol, the entire country became unwitting subjects in a long-term experiment testing the hypothesis that a low-fat, high-carbohydrate diet is healthful.  And in the intervening 26 years, obesity has skyrocketed and type II diabetes has reached epidemic proportions, leading me and many others to say that the low-fat diet has failed.  At least as applied to large groups of subjects.

Let me sum up the take home message with an unrelated story that oddly illustrates the point.  When I was taking flying lessons years ago, the tower once told me to cross one runway we were stopped short of and proceed to the next one.  I goosed the engine and started across.  My instructor pushed on the brakes and stopped us and asked me what I was doing.  I said, “The tower told me to proceed to runway 15L.”  My instructor said, “Yes, but you didn’t look for traffic coming in on runway 15R (the runway we had to cross) before proceeding.  Here’s what you’ve got to learn.  If the pilot make a mistake, the pilot dies; if the control tower makes a mistake, the pilot dies.  Always check for yourself.”

Sobering words, but ones I remember.  The same applies to diet.  Don’t let Time magazine or anyone else tell you what to do.  It’s your life.  Don’t bet it heedlessly.

In 1976 the classic film Network starred Peter Finch as crazed anchorman Howard Beale who launched into his now-famous rant “I’m mad as hell…” on air and galvanized movie goers everywhere.  Even though Howard Beale is fictional, I often share his sentiments.

I got a call yesterday from an acquaintance who wanted to get together and talk to me “face to face.”  I’ve played golf and had a few drinks with this guy over the last couple of years, but that’s about it.  I agreed to meet him at a local coffee shop.

When we had our coffees in front of us – I, a full-strength, scalding hot Americano; he, a non-fat, decaf, double shot latte, just in case you’re wondering – we made small talk for a few minutes then he cut to the chase.  A look of despair came over him, and he confided to me that he was a type II diabetic and was in real trouble.  His doctor had been monitoring his HgbA1c levels for a couple of years, and lately they had been inexorably on the rise to the point at which drastic action was required.  What drastic action?  His doctor told him he was going to have to start insulin injections.

The guy had begged his doctor for a reprieve, which he got until the end of the year, then called me in desperation.

I went through all the quotidian doctor questions and discovered that he was taking three different drugs for his blood sugar, a high-blood pressure pill, a medicine for his GERD and, it should go without saying, a statin.  I asked him about his typical diet, but I already knew the answer.  He ate pretty much what he wanted to eat, but he did try to avoid desserts because he knew sugar wasn’t good for him.  I then inquired as to whether his doctor had discussed diet with him as a part of his treatment.

He said the doctor had advised him numerous times to cut the fat from his diet.  His physician had told him that his diabetes put him at a greater risk for heart disease – which is indeed true – and that, consequently, he should cut the fat, especially the saturated fat, from his diet and live mostly on complex carbs.  He said he had tried, but just couldn’t seem to stick with it for any length of time.  With a What-can-I-do? kind of shrug, he divulged that he was a real meat-and-potatoes kind of guy who felt he would always be hungry if he couldn’t have a steak or a burger from time to time.

I asked if his doctor had perhaps suggested a low-carb diet when the low-fat diet hadn’t worked for him.  No, not really.  In fact, he, himself, had asked about the South Beach Diet since he had a friend who had done well on it.

“Absolutely not, replied his physician.  Too much fat.  Remember, you’re at increased risk for heart disease.  Besides, you don’t want to go on a fad diet.  You’ve got a serious health problem, so you need to go on a diet that might make you better.”

For the most part I face widespread medical/nutritional idiocy with a fair amount of equanimity, but every now and then, when I brood on the cost in human suffering this idiocy all too often causes, I want to do the Howard Beale and scream “I’m mad as hell.”  Problem is the idiocy is so widespread that my pitiful efforts to counter it are on par with King Canute’s trying to hold back the tide.  If I can make a little difference here and there, I suppose it’s worth the effort, so I keep trying.  But I still want to scream.

I started ruminating about all the misery this seemingly universal lack of nutritional understanding engenders when I read on Fred Hahn’s blog an email he posted from one of his readers.  In short order, I came across a brief anecdote in a book I was working through.  If that weren’t enough, I got a copy of Robb Wolf’s new book and read about his medical experiences.  Then, hard on the heels of that, the meeting with my friend almost put me over the edge.  I was ready to lean out the window and start screaming, “I’m mad as hell…”

First the email, which I have excerpted.  You can read it in its entirety here.

I also want to really thank you personally for being a part of a program that has saved my life.  That may sound dramatic, but here is my story.

I am 42 years old and 6 foot tall.  A little over ten years ago I was diagnosed with Type 2 diabetes and given medication to deal with it.  I was also told to lose some weight.  I weighed between 200 to 205 at the time.  I was also told to lower my fat intake and I could eat as much fruits and vegetables as I wanted.

Over the years, the weight stayed relatively consistent.  I am not athletic at all, but am fairly active.  However, the quantity of food has consistently gone down in my efforts to lose weight.  Additionally, my blood sugar has constantly gone up.

In these last two years, my weight started creeping up some.  As a result, I stated running fairly regularly.  It had no, or very little effect on my weight.  I pretty much stopped eating a regular dinner at night after work.  All I would eat is some yogurt or some fruit cups at night. Remember, I could eat all the fruit I wanted.  I still kept gaining weight, but my fasting blood sugar that I measured in the morning did come down a little.

On March 14th of this year, I weighed 215.  I was taking 4 different diabetes medications, one blood pressure drug, pretty much taking a Prilosec everyday for heartburn as well as Tums fairly regularly.  My doctor did not seemed concerned with the heartburn.  I assumed it was from stress at work.  I would also vomit fairly regularly.  I assumed from the various drugs, maybe stress.  My cholesterol as indicated from my blood tests when I visited my doctor were higher than recommendations as well as my blood pressure.  Neither super high, but higher than what is considered normal and healthy.

I visited all the normal diabetes type web sites and none of them said anything or recommended anything that seemed to offer anything of value.  I was mostly doing what they said.  Lots of fruits and vegetables, lots of whole grains, try to lower fats and some exercise.  Yes to all of the above.  Yet I continue to get worse.  I was beginning to believe this was just a part of aging and having diabetes.

How long was it going to be until I started having real health issues?  For the most part I very rarely get sick.  When was I going to start going blind, lose a foot or leg, have a heart attack, kidney failure, stroke out???  I was getting to be resigned that it was just a matter of time.  Inside my head I secretly hoped that I would have a fatal heart attack at a relatively young age so I would not have to deal with the real issues of diabetes.

On March 14th in a round about way, I found the Protein Power book.  It was opposite everything I knew to be true, yet it seemed more true about nutrition than anything I read before.  How could everybody else be so wrong?  I instantly started following it, cutting my carb intake to next to nothing or at least less than 30 grams a day.  Before stating this, knowing what I ate, I am fairly certain my carb intake was close to 60 to 70 percent of my total calorie intake.  I bought your book a couple weeks later.

I am sure you will not be surprised at all by the results.  As of this morning I now weigh a little over 190.  It has been close to 20 years since I have weighed that little.  I have stopped taking two of the diabetes drugs completely, one of the others I am taking 80% of what I was taking, the other I am down 30%.  I have not taken a single Prilosec or a Tums since I have started this change and this is the most stressful part of the year for me as it relates to work.  I have only vomited once and that was on March 16 or day 2.  Six weeks in, I had a doctor visit and blood test.  Blood sugar way lower, bad cholesterol way lower and in the normal range, good cholesterol way higher and also now in the normal range.

Five weeks after I changed my eating habits, I started my slow burn routines based on your book.  With some of the exercises I really struggled at first, but now am fairly comfortable with most of them.  I am still learning and refining a few things, but I can say my increases in strength are just as dramatic as my weight loss.  In the case of the chest press, the very first time I did it following your slow burn book instructions I did 3 reps at 100 pounds and was wiped out.  Yesterday, at 130 pounds I did 6 reps in a little over 2 minutes.  Time to increase the weight again.

As I said before, I was running fairly regularly for a few years.  Not that fast, and really, not that far, 3 to 4 miles in around 45 minutes.  Generally 3 or 4 times a week to do “some exercise” as recommended by my doctor and everything I had read about diabetes.  I have cut back on the running since I started your workouts, but when I do run, I run significantly farther and significantly faster than I have run in years.  I hated, hated, hated the running, but did it to do my exercise.  Now when I do run, it is almost fun.  I am so amazed at the changes in me.

So that is how you have had a part in saving my life.  I do not know how to say thank you any more than that.

Not long after coming across this email, I was reading a book on TRIZ, a methodological approach to engineering problem solving that can be applied to other realms, when I came across a report of a disturbing doctor-patient interaction.  The author is using this story to illuminate a problem solving technique called peeling the onion, which means to continue to dig deeper and deeper in the quest for a solution.  Instead of illuminating anything for me, it just made me mad as hell.

One day, I was sitting in my doctor’s office anxiously waiting to hear the results of my most recent cholesterol screening. The previous year my cholesterol had gone up just slightly, which was very depressing. I essentially had no exercise regiment prior to that, but afterward I went into fat-free mode and started walking 4 miles a day. In spite of my protests, a couple of years earlier my doctor had put me on a low dose of blood pressure medication. I don’t even like to take aspirin.

As a result of my hard work, I was certain my current cholesterol level would be outstanding. I couldn’t wait to hear the great results.

Unfortunately, the test results painted a different picture. My cholesterol level was 30 points higher.

“That’s impossible. I don’t eat beef brisket anymore… ever! I don’t eat any sausage, never go to McDonalds, buy fat-free everything, and walk 4 miles a day. It can’t be true.”

“Yeah, it sucks getting old doesn’t it? Aging is that one thing you can’t control. Even though you’re trying to eat better and exercising, which is a great thing, these efforts are obviously not enough.”

“What? Older? It has only been a year! Urrrrrrr…this doesn’t make any sense. It’s not fair.”

“I think we should put you on Lipitor.”

“No. I don’t want to take anymore meds. Let me think about it for a while. This makes no sense.”

When something makes no sense to you, your curiosity needs to kick into high gear. Well, this surely qualified as nuts to me. Yes, I was a year older, but… come on. The test results couldn’t be right. Most people would probably just do as the doctor ordered, but I almost never take anything at face value.

The author then goes on to describe how he “peeled back the onion” by doing internet searches for cholesterol and found that one of the supplements he had been taking for his joint pain – glucosamine – had been found in some cases to raise cholesterol levels.  He went off of the glucosamine, and as he tells it:

Two months later, my cholesterol was 30 points lower and back under the limit.
If I did not have a curious nature about most everything I would have been on another needless medication. It pays to peel the onion back.

I don’t think his glucosamine had anything to do with his cholesterol – the 30 point drop in his cholesterol was probably just the normal roaming range of his cholesterol levels over time. The take home lesson of this story is that this guy’s doc was ready to put him on an expensive medication with a number of pretty severe side effects because of one cholesterol reading above a particular number.  The doc wasn’t treating a patient, he was treating a lab value.  In this case the patient is a young man (mid 40s) with no history of heart disease, the very kind of patient for whom no benefit has ever been found for statin therapy.  Why, when this patient’s low-fat diet failed to lower his cholesterol, didn’t his doctor suggest a low-carb diet?  Studies have shown the low-carb diet to be more effective in solving lipid problems than the low-fat diet.  So why wasn’t it suggested.  Had this patient gone on his doctor’s statin of choice and not had his cholesterol fall, his doctor would have tried another statin.  Why not try another diet?

If you read the entire book, the author mentions throughout how his days of red-meat eating are over and makes numerous references to his much-despised (but in his mind, therapeutic) low-fat diet.  It’s really sad that he’s such a victim of medical ignorance.

I got a copy of Robb Wolf’s new book The Paleo Solution and started reading the first chapter, which describes Robb’s own story.  In short, he spent years as a vegetarian, getting sicker by the day.  All his physician’s told him that he was lucky he was able to follow the diet he was following because he would have really been much worse had he been following a standard diet.  Robb ultimately came around to the low-carb, high-meat Paleo way of eating and solved his own health problems.  When he went back to his various physicians to get blood testing – all of which was perfect for the first time – he was ecstatic.  He told his doctor he had completely changed his diet.

“Doc! Have you ever heard of the Paleo diet?” I asked.  “How our ancestors ate for millennia?”

His answer was typical of what I would encounter in the years to follow.  “That is pseudo science.  There is no proof.”

When Robb describes the remarkable difference in his health to yet another doctor, he is told:

It must be something else.

Why do these stories make me mad as hell?  Not just because the people involved suffered as a consequence of medical hubris, incompetence and intransigence, but because so many millions of others do suffer miserably and aren’t lucky enough to escape their fates as these few were.

It’s difficult to imagine the number of people who go into doctor’s offices every day with weight problems, elevated blood sugar, high blood pressure, and abnormal lipids and are told with great authority to eat less and exercise more.  If the patient asks the doctor for a specific diet, the doc usually has the nurse give the patient the standard 1800 kcal low-fat diet sheet.  Depending upon the motivation of the patient, this diet may or may not be followed.  If the patient does suck up and follow the diet, many, of not most, will fail. When these poor folks come back for their recheck, their doctor then wants to put them on some sort of drug.  Believe me, the stories above aren’t atypical.  This is happening all across the country thousands of times every single day.

And I’m mad as hell because it doesn’t have to be this way.

There is another option.  These poor people could be given a low-carbohydrate diet to try.  Most of the doctors who prescribe the 1800 kcal diet (along with a recommendation to exercise more) could give people the choice.  A low-carbohydrate diet or a low-calorie diet.  But the vast majority of them don’t.  They simply opt for the low-calorie diet, then resort to drugs when it doesn’t work.

There is plenty of good research available now showing the low-carb diet to be at least the equal of the low-fat diet in virtually every parameter with most of the studies showing the low-carb diet to be superior.  With this research backing the efficacy of the low-carb diet, why don’t more doctors offer it as an option?  Naiveté? Stupidity? Pigheadedness? Who knows?  What I do know is that it’s a real problem.

Lately the web has been full of various health gurus (mainly those involved in weight training and/or bodybuilding) making the case that the only reason the low-carb diet works is that it is satiating and spontaneously causes its followers to restrict calories.  It’s the calories, say they, not the carbohydrate restriction that does the job.  I say, So what? Who cares as long as it works?  And countless studies have shown the low-carb diet to be as efficacious (if not more so) as the low-fat diet, so why isn’t it offered as an option?

If a doctor treats a patient with a specific drug for high blood pressure, and the patient’s blood pressure doesn’t respond, the doctor switches medications.  Most doctors will fiddle with the medicines to get the problem solved.  Why not do that with diets?  Why just go with the low-cal, then move immediately to drugs if that diet fails?  Years ago, during the interim in which low-carb diets were out of favor and not much good data existed on their efficacy, I could understand it.  But why now?

It seems that almost every week a new study is coming out showing the superiority of the low-carb diet.  Over the past couple of years we’ve had a trifecta of well-done studies published in major scientific journals demonstrating the effectiveness of low-carb diets.  There was even a meta-analysis published in Obesity Reviews, the most mainstream of mainstream academic journals** showing low-carb diets work better than low-fat diets.  So why don’t more doctors recommend them?

I’ve been infused with a little hope by a recent totally unscientific poll published in the Annals of Internal Medicine.  Readers (primarily physicians) were presented with the following poll.

Surprisingly, the majority answered that they would give a low-carb diet a try first.

The particular issue of the journal publishing this poll was the one containing one of the more recent papers on the benefits of low-carb dieting.  (I’ll post later on this amazing study that was designed to fail.)  As a consequence, I would bet docs taking this poll were skewed in the low-carb direction.  But who knows? I can always hope it means there is a light at the end of the tunnel, and that physicians are beginning to discard their low-fat tunnel vision.  The fact that this poll even exists in a major mainstream journal.  We should all take heart.

But until docs start changing diets that don’t work at the same rate at which they change blood pressure medicines, many, many people will suffer.  And I’ll continue to get mad as hell every time I hear about travesties such as the ones I wrote about above.  Too bad there aren’t diet reps that go into all the doctor’s offices like the drug reps do.  Maybe if there were, things would change a little faster.

Since most of you reading this blog visit your doctor from time to time, perhaps you can play the role of diet rep.  You can do it by telling your doc how your low-carb diet is working for you.  And you can provide literature just like the drug reps do to add substance to your report.  Here is a pdf file of the Obesity Reviews meta-analysis showing low-carb superiority. Meta-analysis of low-carbohydrate diets

So, be ambassadors for the low-carb diet so that more physicians might give it a try. If enough of you do that, your actions will provide a gentle but steady invigilation that will ultimately bear fruit. When physicians do gingerly recommend low-carb diets a few times, they’ll see the same astonishing results you have.  More and more will start recommending low-carb to their patients as a first line therapy, which will decrease the number of tales of woe I’ll have to sit through.  I can then dodder off into my dotage in a much more sanguine frame of mind.

If you haven’t seen it, here is a clip of the famous I’m mad as hell speech from Network.

Click here to view the embedded video.

** How mainstream is Obesity Reviews? It is the journal that published George Bray’s unfair and almost incomprehensible review of Gary Taubes’ book Good Calories, Bad Calories.

I’ve got to apologize in advance for the length of this post, but in order to thoroughly do what needs to be done, it took the space.

Readers of this blog who have been around for a couple of years have been through the Anthony Colpo (AC) fiasco with me.  For those of you who weren’t around at the time, I’ll give a brief – a very brief – overview of what happened so you’ll understand what this is all about.

I wrote a post in September 2007 describing two different diets and their outcomes.  The first was designed by Ancel Keys and was a 1500+ calorie low-fat, high-carb diet; the other, designed by John Yudkin, was a 1500+ calorie low-carb, high-fat diet.  The subjects following the two diets experienced drastically different results.

This post, for whatever reason, inspired AC, a trainer and self-taught nutritional guru from Australia, to go into mad-dog attack mode.  I wasn’t the first person he had gone after, but I became the first to fight back.

Around the same time AC took it upon himself to attack me, he had just published an online book on weight loss that he was beginning to promote called The Fat-Loss Bible.  A more cynical person than I might have thought AC picked this fight in an effort to get some free publicity for himself and his book.  If that was indeed his motivation, he may have gotten a little more publicity than he had bargained for.

I took a look at his book – which I hadn’t realized even existed prior to this kerfuffle – and found it to be much like the ad for the educational software pictured above to the left.  At first glance, it looked reasonable, but upon closer inspection, it had some problems.

I made the offer to readers to dissect AC’s book if that’s what they wanted.  Or I could ignore the whole thing and continue with my regular posting.  A majority in the comments section voted for me to dissect.  I dug into the book, pulled all the papers cited, but subsequently got involved in other stuff and forgot about AC and his book.  He more or less dropped from sight, but has surfaced lately.  I had forgotten all about him, his book and the whole situation, but his new antics have stirred a few readers to ask about the dissection that I promised but never came through with.

So, with that preamble, here it is.

The crux of AC’s objection to me (and a few other people, namely Gary Taubes, Richard Feinman and Gene Fine) is that I (and they) believe there is a metabolic advantage that becomes manifest during low-carb dieting.  AC has taken the position that my idea of the low-carb driven metabolic advantage means that people following low-carb diets can eat all the calories they want and lose massive amounts of weight as long as they keep their carbs reduced.  He accuses me of leading people astray by encouraging them to eat, eat, eat as long as carbs stay low.

I don’t know where he got this idea because I have certainly never said such a thing anywhere.  The metabolic advantage brought about by low-carb dieting is probably somewhere in the neighborhood of a 100-300 calories, which isn’t all that much.  This few hundred calories don’t even come into play until the 1500-2000 calorie range of consumption.  I’ve written about this numerous times and have always used these figures, so, as I say, I don’t know where the idea that I believe the metabolic advantage allows low-carb dieters to eat huge numbers of calories and still lose weight.

I don’t plan to go through The Fat-Loss Bible in its entirety or this post would take on the dimensions of War and Peace.  I’m going to limit my comments to Chapter 1, titled “Myth 1: Don’t Count Calories.”  This first chapter is the one that tells why AC so fervently believes there is no metabolic advantage.

AC sells his book online, but (at least the last time I checked) it can be downloaded only on a PC.  At the time this dispute started I had a PC, which I used to download the book.  Since then, my PC has given up its ghost and I now use Macs exclusively.  So, the copy I have is about two years old.  I don’t know if AC has changed it since; consequently, I don’t know if my critique applies to the book as it exists today.  AC changes his book all the time, updating here and there, and I don’t blame him for it.  I do it with this blog all the time.  I find typos in old posts and sentences that I don’t like.  I change these things all the time and the blog is the better for it, so I don’t blame him if he does the same thing.  But I just want everyone to know that I’m critiquing the book as it was when he launched his attack.

AC firmly believes that a calorie is a calorie is a calorie.  He believes that people lose the same amount of weight dieting irrespective of the composition of whatever diet they’re on.  He believes that a given person will lose exactly the same amount of weight on, say, a 1600 calorie diet whether that diet is a low-carb diet or a low-fat diet or any other kind of diet.  It is the calories that set the weight loss, not the macronutrient composition or any other factor.

I don’t know if AC came to this conclusion then went looking for studies to confirm his bias or if he came to this conclusion because of the studies he read.  The first chapter of his book contains a number of studies he trots out to ‘prove’ his idea that only calories count.

There have been many out patient studies that have shown a metabolic advantage and many that haven’t.  Overall a greater number of studies demonstrating a metabolic advantage exist than studies showing no such metabolic advantage.  The first part of the first chapter of The Fat-Loss Bible goes into great detail describing why such studies are worthless.  He makes a fairly plausible argument as to why people on low-carb diets might tend to overreport consumption while those on low-fat diets may underreport.  If correct, this difference in reporting would create the appearance of a metabolic advantage where none exists.

To solve this problem, AC turns to what he calls

strict ‘metabolic ward’ studies in which, for the entire duration of the study, the participants are confined to a research facility where they can only eat the foods supplied by the researchers.

On the surface this seems to make sense.  Put the subjects under lock and key, give them just the food you want them to eat, and see what happens.  You’re going to have some individual variation, but if evaluate enough subjects and they all end up losing the same amount of weight irrespective of macronutrient composition, then you’ve got some pretty good evidence that there probably isn’t a metabolic advantage.

But as obvious as this appears at first glance, there are problems with this approach.

The first problem is a problem of measurement.  Newton derived his gravitational laws and everything scientists measured obeyed them.  These laws became sacrosanct.  If some observation didn’t conform to Newton’s laws, then the observation was faulty because Newton’s laws were infallible.  Those quirky movements of planets way out on the edge of the solar system were off a little from Newton’s predictions, but, hey, it’s got to be a measurement error somehow.  Then Einstein came along with his theory of relativity, and all the weird deviations conformed to Einstein’s laws.  Newton had been superseded.  Because the caloric differences brought about by a metabolic advantage (at least as I see it) are so small, weighing subjects in pounds and kilograms may miss it.

That’s the first problem.  But there is a problem much greater than that.  One that AC isn’t aware of because he doesn’t really have any real-world experience in doing nutritional studies in a hospital.

When subjects are studied in ‘metabolic wards’ they aren’t locked away and under constant observation.  In fact, often enough, they aren’t even in a hospital at all.  A ‘metabolic ward’ is simply a part of the hospital set aside to do nutritional studies.  And often it isn’t even a specific part of the hospital.  Subjects can be scattered about among the other patients.  Subjects can have visitors, can roam through the hospital, can even go to the cafeteria.  A ‘metabolic ward’ study can mean anything from: careful observation; to check into the hospital for a couple of days; to get trained on the diet then follow it at home; to check in, go to work all day, then come stay in the hospital all night. They are definitely not the strictly-controlled studies AC thinks they are.  He confuses them with ‘metabolic chamber’ studies, which are a horse of a different color.

The opportunities to cheat in a ‘metabolic ward’ study are, for the most part, as great as the opportunities to cheat in an outpatient study, especially since many of the subjects are outpatients most of the time.  There is a difference though.  When people are on outpatient studies they are more likely to at least admit their cheating and record what they cheat with than they are in ‘metabolic ward’ studies.  Some of the studies AC sites are formula diet studies in which shakes made of specific caloric and macronutrient composition are provided to subjects throughout the day.  (Or are given to them to consume outside the hospital at work or wherever.)  These are the kinds of programs you wouldn’t want to report cheating on.  And these subjects do without question cheat.  The fact that the data is reported as coming from a ‘metabolic ward’ study gives it a veneer of accuracy that it doesn’t really deserve.

AC gathered up a bunch of these ‘metabolic ward’ studies – 17 to be exact – that he uses to prove his point that there is no metabolic advantage and that only calories count.  He lists these studies in a chart (reproduced below), then proceeds to go through them one at a time.

On the ones that confirm his bias, he spends little time.  Just a brief description typical of this one describing the first study.

In a paper aptly titled ”Calories Do Count”, Kinsell and co-workers admitted five obese subjects to a hospital metabolic ward, then fed them liquid formula diets.  The diets ranged in protein content from 14 to 36 percent, fat from 12 to 83 percent, and carbohydrate from 3 to 64 percent.  The calorie content of the various diets was held constant for each patient irrespective of diet composition.  As they switched from one diet to another, each patient continued to lose weight at a similar pace.  Concluded the researchers: “…it appears obvious that under conditions of precise consistency of caloric intake, and essentially constant physical activity, qualitative modification of the diet with respect to the amount or kind of fat, amount of carbohydrate, and amount of protein, makes little difference in the rate of weight loss. [Italics in the original]

This is a great study to start with because it contains many, many flaws that AC is blinded to by his own confirmation bias.  It’s a terrible study.  Let me show you why.

Here is the first paragraph of the study.  And I’m not kidding.  This is directly quoted from the paper.

The accumulation of excess adipose tissue is a malady which affects many people.  That undue preoccupation with the pleasures of the table contributes to the disease has geen [sic] generally accepted in most quarters; or, to express the matter differently, majority opinion has held that the first law of thermodynamics applies to the human machine quite as predictably as it does to inanimate machines.  Despite this body of “official opinion” one finds many obese individuals who are either convinced that their food intake completely fails to explain their adiposity, or who spend time and money in the search for the magic potion or pill which will enable them to consume food in any quantity but still maintain or achieve a slim figure.

Do you think there might be just a little bias in this author and his co-workers?  From this first paragraph one sees by the reference to the first law of thermodynamics the set of the sail of these researchers.  Plus it’s pretty clear that these researchers don’t like overweight people and think obesity comes from a “preoccupation with the pleasures of the table…”  How do you suppose their data is going to turn out?

First of all, were these five subjects inpatients in a metabolic ward or did they just pick up their formula and take it home.  Did the live in the hospital or just spend the night?  No information is given.
Here is the sum total of the information given on the ‘metabolic ward’ status of the first patient described:

His weight on admission to the metabolic ward was 270 pounds.

Was he admitted to the ward where he stayed full time for the full 70 days of the study?  I doubt it, and I’ll describe why in a bit.  Or was he admitted for his initial workup then released to continue his diet at home.  I suspect the latter.  Whatever the situation, this is all the study says about it.

Here are the descriptions of how the rest of the subjects entered the study:

Second subject:

Weight on admission to the study was 227 1/2  pounds…

Third subject:

At the time the study was undertaken her weight was 199 pounds…

Forth subject:

At the time the study was undertaken, her weight was 211 1/2 pounds…

Fifth subject:

Patient GTAY was a 61 year old white female with a history of diabetes for more than 20 years.  She had received insulin in the past but could be maintained in a satisfactory diabetic control with diet and tolbutamide.  Milky fasting plasma was discovered in July 1962.  Other findings included evidence for coronary and peripheral atherosclerosis, and diabetic retinopathy.  She had partial removal of a goiter 40 years ago, but was essentially euthyroid during her stay in the metabolic ward.

The study in this patient was actually directed toward evaluation of her hyperlipidemia, but she is included in this report since she was maintained on quantitatively constant, eucaloric regimens containing high fat and high carbohydrate respectively, and also received both saturated and unsaturated fat.

This last patient wasn’t even accepted into the study as a subject for a diet study but more or less added after the fact.

There were five subjects in this study that lasted for anywhere from 65 to 77 days.  We can’t really tell which subjects went how long. Nor can we really tell if it was an inpatient study or just one where the subjects checked in.  Nor do we know how much weight each lost over how long a period.  We know the starting weights and that’s about it.

The data as displayed looks like data collected in an inpatient study, but the paper itself only implies that it is.  As you might imagine, inpatient studies are tremendously expensive, and, consequently, authors tend to make sure readers of the study know they are inpatient studies.  In this paper, we have to guess.

If these are truly inpatient studies for 65 to 77 days, we need to address another point: the quality of the subjects in such studies.  Who do you know who would have the time or inclination to spend two to two and a half months in a hospital full time?  People who are willing to spend the time in such facilities are usually not the most reliable. They are typically unemployed with little education and, for the most part, are imbued with a lack of understanding as to how important their rigid adherence to the protocol truly is.  I will be the first to say that not everyone who has ever volunteered for such a study falls into this category, but, unfortunately, many do. I’ll let a couple of the authors of these metabolic ward studies expound on this fact a little later.

The age range of these subjects is from 25 to 61. All of the subjects in this trial save one have serious medical problems and are under treatment with multiple drugs.  The one who doesn’t have serious problems is a 25 year-old male who has “been grossly obese since childhood.”  These are not the subjects you would want in a study of this nature.

The subjects getting the most calories got 1200 per day while those getting the least consumed 800 calories per day.  As I’ve written before, if calories are kept ultra low, all the calories – irrespective of composition – are going to be used for energy.  And under those circumstances, you would expect there to be no metabolic advantage.  And you would expect weight loss to pretty much follow a trajectory driven solely by caloric deficit, which is pretty much what happens in this study.  But it’s difficult to tell because of how terrible this study is presented.  There is a starting weight, but no ending weight for the subjects.  And, although the Methods section reports that the study lasted from 65 to 77 days, my calculations based on the data provided shows the study lasted from 64 to 82 days.  Which are we to believe?  Without an ending weight for the subjects and a precise number of days under caloric restriction, how do we really know how much they lost verses how much they should have lost given the number of calories they were getting?

And we have this other little tidbit thrown in when discussing the results of one patient, RTEA, who was a 26 year old female with “a history of resection of a cystic chromophobe adenoma of the pituitary…followed by radiation”:

Rate of weight loss was greater during the last 2 weeks on the high fat, high protein intake than during either of the other 2 dietary periods.  This probably does not have significance on view of the “stair case pattern” of weight loss.

Say what?  So they do have a subject that shows greater weight loss (and late in the program rather than early), yet they toss off the data with a bunch of weasel words implying that it probably isn’t significant.

I suggest you pull down the full text of this study at the bottom of this post so you can see for yourself how terrible it is.

I’m certainly not going to go through all 17 of the studies in this fashion because this post would then truly gargantic, but I wanted to go into this one at length to show that so-called ‘metabolic ward’ studies, those AC terms the ‘gold standard’ of medical research can be very, very flawed.  I, for one, would not want to be making any categorical statements based on the data contained in this study we just evaluated, that’s for sure.  If AC weren’t so blinded by his own confirmation bias, he would have laughed this study off.  If I had used it to ‘prove’ a metabolic advantage – based on the one patient described above who had more weight loss on the high-fat diet – he would have had a field day.

Next, let’s turn our attention to the Liebel et al study.  It’s number 11 down the chart if you’re counting.  Here’s what AC says about it:

Leibel and co-workers took 13 subjects, determined how many daily calories each needed to maintain his/her weight, then proceeded to feed them, in crossover fashion, diets differing in their macronutrient content.  Despite wide variations in protein, fat, and carbohydrate intake, the subjects maintained their weight irrespective of diet type.  This included two subjects who followed low- and high-carb diets (15 percent and 75 percent carbohydrate, respectively) for a minimum of 34 days each.

That’s it.  That’s AC’s commentary on the study.  I suppose readers are meant to believe that this study showed that it was all a matter of calories with no difference in terms of weight lost versus macronutrient composition of the diet.

The Leibel et al paper is a great one because it shows just how sloppy AC is in his presentation of data and, no doubt, in his own evaluation of the medical literature.

Go back and reread AC’s description of how the study was done.  Looks like Leibel et al did a hands-on study of these subjects, right.  Well, that’s not exactly how it worked.  Here is what really happened as reported by Leibel et al:

The records of all subjects studied by the Lipid Laboratory of the Rockefeller University Hospital between 1955 and 1965 who were fed lipid-formula diets of various carbohydrate (CHO) and fat composition were reviewed.

Leibel et al didn’t do squat in terms of studying subjects.  They went back through 40-year old records of subjects who had undergone formula feeding in the 1950s and 1960s to drag out records of 13 subjects (they actually drug out 16, but three were of children) who met their experimental parameters.  They weren’t looking for evidence of a metabolic advantage; they were looking to see if fat intake irrespective of calories made people gain weight.

Out of the countless studies done in those early years, they wanted to see if any could show that fat intake increased weight gain to a greater extent than the calories consumed as fat.  As they put it in the Introduction to their paper:

One group of investigators concluded that “fat intake may play a role in obesity that is independent of energy intake.”

The Leibel et al paper was published in 1992, the time in which the low-fat mantra was at its zenith.  It was a time that many people who should have known better were telling us we could eat all we wanted as long as we limited fat.  Fat makes us fat, we were told.  Cut it and you lose.  What Leibel et al were trying to show in this paper was that the weight gain or loss effects of fat were a function of the calories contained in the fat, not some other magical property that makes people gain weight above and beyond calories.

Before we get to the interesting data in this study, let’s take a look at what the guy who actually did this work had to say.  Leibel’s group went through old formula feeding studies done by Edward H. Ahrens, M.D., the head of the formula feeding lab at the time and the lead author of all the old papers referenced by Leibel.  Says Dr. Ahrens about the subjects in the inpatient studies:

Thirty-eight of forty patients were observed continuously under strict metabolic ward conditions; four of the forty [I know, the math doesn’t add up] were sufficiently motivated and intelligent to follow the regimen at home. (Ahrens EH et al 1957)

A couple of points here.  First, if four subjects out of 40 were “sufficiently motivated and intelligent” to be sent home with formula and instructions, what does that say about the other 36 (or 38)?  Which is to my point earlier about the quality of subjects recruited into metabolic ward studies.  Second, were some of the patients whose data was used for the Leibel paper those who were sent home?  If so, it blows AC’s notion of being unable to rely on any data gathered from free-living subjects.

Dr. Ahrens in another paper describing his 15 years of experience using formula diets says this about cheating in metabolic ward studies:

Such cheating is a natural (but dismaying) consequence when a patient’s dissatisfactions with any part of the ward routine are not quickly enough appreciated by the ward personnel.  Anticipation of the discontent is the clinician’s daily concern.  The closer the relationship between the patient and his medical attendants, the less likely cheating is to occur.  We have detected [my italics] cheating in only eight patients; undoubtedly others have gone undetected, but we feel the problem has been surprisingly minor. (Ahrens, EH 1970)

These are the subjects under lock and key.  The people running the study have to maintain constant vigilance to prevent cheating.  How about those who only check into the metabolic ward to sleep and spend the rest of their days at work or home?  And those are the subjects who make up most of the metabolic studies you read about.

One last interesting point about the Leibel paper.  The subjects they looked up in their retrospective analysis had undergone experiments during which they were given formula in amounts sufficient to maintain their weight.  As they lost or gained weight, their caloric intake was increased or decreased to compensate so that their weight stayed about the same.  According to the old papers about the original studies, the researchers tried to keep the subjects from fluctuations greater than one kg.  One kg equals two pounds.  If there was a metabolic advantage, it would probably show up within this two pound range and would be considered insignificant in terms of how this study was presented.

Some of the subjects, however, did lose or gain weight. Leibel et al then adjusted their caloric intake on paper to compensate for the weight differential.  In other words, if a patient lost weight on a given number of calories of a precise formula in the original study, Leibel et al would adjust the intake (40 years after the fact) to compensate for the weight loss.

One subject, a 55-year-old male with a BMI of 32, maintained his weight on a high-carb formula at 2871 calories per day.  The same subject then required 3501 calories to maintain his weight on a 70% fat, 15% carbohydrate diet.  Sounds like a metabolic advantage to me.

There were two papers in AC’s list of 17 that did show what could be considered a metabolic advantage.  In other words, subjects on the low-carb diet lost greater amounts of weight than subjects on low-fat, high-carb diets of the same number of calories.  These are two of the three studies by Rabast et al that are the 4th and 6th studies on the list of 17 shown above.

How did AC deal with this seeming refutation of his notion that no metabolic advantage exists?  By typical AC flimflammery.

In their 1981 study, Rabast et al observed significantly greater potassium excretion on the low-carbohydrate diets during weeks one and two.  A considerable amount of potassium inside our bodies is bound up with glycogen, so the greater potassium losses in Rabast’s low-carbohydrate dieters may indeed be a reflection of greater glycogen, and hence water losses.  Until recently, potassium excretion was often used a a marker or lean tissue loss; in Rabast’s study, this would indicate that the low-carbohydrate diet subjects lost more lean tissue.  As lean tissue holds a considerable amount of glycogen, this would again point to glycogen-related water loss as the explanation for the allegedly “significant” differences in weight loss. [Italics in the original] If the low-carbohydrate groups maintained greater lean tissue and/or glycogen losses at the end of the study, then this would easily explain their greater weight loss.

Regardless of whether Rabast et al’s findings were the result of water loss from glycogen depletion, pure chance, or some other unidentified factor, they should be regarded for what they are: An anomaly that has never been replicated by any other group of researchers.  For a research finding to be considered valid, it must be consistently reproducible when tested by other researchers.  As proof of the alleged weight-loss advantage of low-carbohydrate diets, the findings by Rabast and colleagues fail dismally on this key requirement.

Wow!  Where do we start?

First, AC didn’t mention Rabast’s 1979 study in which 117 patients were admitted to the hospital and studied on formula diets.  I assume these subjects were hospitalized round the clock because in the body of the paper it states:

…and as the patients were under constant supervision differences in food intake between the two groups could be excluded.

Unlike the Kinsell study (the first of AC’s 17 I described in detail above), the authors of this study were expecting a different outcome.  As discussed, Kinsell was obviously biased going in against the notion of anything other than calories count.  Rabast et al went in biased against low-carb diets:

The popularity of so-called ‘fad’ diets, low in carbohydrates and relatively high in fat, has continued to spread, especially among lay groups.  The caloric intake is only slightly limited, if al all; alcohol is allowed most of the time, and fat is consumed in the form of saturated fatty acids.  However, this kind of dieting, which must always be carried out on a long-term basis, has proved harmful.  The cholesterol intake can lead to severe health damage and clearly contributes to atherosclerosis.

After keeping the 117 subjects on low-carb vs high-carb diets of the same number of calories for 25 – 50 days, and probably hoping to find that those on the low-carb diet didn’t lose any more weight than those on the low-fat diet, the subjects on the low-carb formula diet lost considerably more weight than those on the low-fat diets.  Here are the graphs from the paper.

After going through all the data, Rabast et al conclude

Differences in fluid and electrolyte balance could not be measured but marked fluctuations can occur.  However, the change in body water and electrolytes could only be considered in short-term studies as the cause of the differences in weight loss.  Variation in the depletion of the glycogen pool is also a feasible explanation, as up to now, sufficiently long-term studies have not been reported.  However, the glycogen pool can be restored even under fasting conditions.  Therefore, an increased rate of metabolism presents itself as the most feasible explanation. [my italics]

The 1981 Rabast study that AC does comment upon refutes his commentary on the difference being due to greater fluid loss from the low-carb diet.

Potassium excretion during the low-carbohydrate diets was significantly greater for as long as 14 days, but at the end of the experimental period the observed differences no longer attained statistical significance.  At no time did the intake and loss of fluid and the balances calculated therefrom show significant differences.  From the findings obtained it appears that the alterations in the water and electrolyte balance observed during the low-carbohydrate diets are reversible phenomenon and should thus not be regarded as causal agents.

As to AC’s comment that the work of Rabast et al should be ignored because it has never been replicated by another group of researchers, I’ll leave to you to decide the validity of that.  There have been a number of such studies, including ones (as I’ll describe in a moment) in AC’s own list that confirm what Rabast found.  The 1979 Rabast paper discussed earlier lists 17 of them.

Hang in there; we’re almost through.  If I have to read all these papers and type all this stuff, the least you can do is stick with me ‘til the end.

Most of these studies don’t list the amounts of weight lost by the subjects because most of them aren’t designed to really look at weight loss.  Most are designed to look at other metabolic parameters such as protein sparing or branch chain amino acid use or nitrogen balance and the authors weren’t particularly interested in how much weight the subjects lost.  The authors mention that the two groups of subjects lost similar amounts of weight.  Other than the Rabast studies that we’ve already discussed, only four studies listed the weight lost over the course of the study by the subjects on either low-carb or high-carb diets.  In none of these cases did the weight loss difference reach statistical significance, so AC is presenting them as if there is no difference.

But in reality, there was a difference.  It just wasn’t statistically significant.

Statistical significance as it pertains to weight loss is a function of both number of subjects and amount of weight loss.  If I enroll 10 obese subjects in a weight-loss study and put five subjects on one diet and five on another, observe them for four weeks, and find that one group has lost an average of 2 pounds more than the other, that probably won’t be a statistically significant difference.  Why?  Because with only five subjects in each arm of the study, it requires a much larger weight loss to show a statistically significant difference.

If I do the same exact study, but enroll 100 subjects with 50 in each arm, and get exactly the same results – a two pound differential – then I achieve statistical significance.  The more subjects, the smaller the difference in outcomes it takes to reach significance.

In the case of these metabolic ward studies, the numbers of subjects are small.  As we’ve discussed, it is extremely expensive to keep subjects hospitalized 24 hours per day.  Consequently, most metabolic ward studies don’t enroll very many subjects.

I went through all the papers in AC’s list and found four (aside from the Rabast that we’ve already discussed) that list both starting and ending weights for the subjects.  I’ve listed them in the chart below.

As you can see, the study with the largest number of subjects had only 22 subjects in each arm.  These studies all use a caloric intake that is lower than would be expected to produce any kind of a metabolic advantage because all are at an almost starvation level.  Yet, as you can see, three out of the four show a greater weight loss in the low-carb arm than in the low-fat arm of the study.  Equal caloric intake, greater weight loss with the low-carbohydrate diet.  But, due to the small number of subjects, the difference doesn’t reach statistical significance.

If we had these same findings and same difference in weight loss between the two diets with a larger number of subjects, we would indeed have a significant difference.  If we did a meta-analysis of these studies, we might find that adding the subjects together would end up showing a significantly difference in weight loss.  Even though these differences don’t add up to statistical significance given the number of subjects involved, you can see the definite trend.

But what about the Piatti study, the one that showed the low-fat diet producing more weight loss than the low-carb?  I have it marked with an asterisk for a reason.  The paper by Piatti et al titled Hypocaloric High-Protein Diet Improves Glucose Oxidation and Spares Lean Body Mass: Comparison to Hypocaloric High-Carbohydrate Diet looked at how 25 obese women fared in terms of lean body mass and insulin sensitivity.  They were put on 800 kcal diets for 21 days.  It was found that the low-carb diet spared more muscle tissue and improved insulin sensitivity more than the low-fat diet of an equal number of calories.

Since the authors weren’t specifically studying weight loss, they didn’t really randomize the subjects by weight but did so by other parameters.  As it turned out, the group on the low-fat, high-carb diet were much heavier than those that ended up in the low-carb arm.  The average starting weight of the subjects in the low-fat arm was 213 pounds (96.8 kg) whereas the starting weight of those on the low-carb arm was 191 pounds (86.8 kg), a significant difference.  It would stand to reason that subjects starting off at 213 pounds on a 800 calorie diet would lose more over 21 days than subjects starting out at 191 pounds and following the same diet, and indeed they did.

This post has gone on way, way too long, but I think it’s pretty obvious that these studies fail to ‘prove’ that a metabolic advantage does not exist.  I would say, if anything, that they ‘prove’ just the opposite.

Just so you can go through these studies yourselves if you so desire, I’ve put them all up on Scribd.  The links are below to the full text of all.

The next post will a) be much, much shorter and will b) go into detail on a beautiful study that AC totally disses in his book.  We’ll look at his diss and what the study really says.  That should put paid to AC.

All the papers referenced by AC listed below.  All full text.

Kinsell et al

Grey Kipnes

Rabast et al 1979

Rabast et al 1981

Yang et al

Bogardus et al

Hoffer et al

Leibel et al

Vazquez 1992

Vazquez 1994

Vazquez 1995

Piatti et al

Golay et al

Myashita

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.

The video below shows Chris Gardner, Ph.D., researcher from Stanford University, giving a presentation about the data he generated when he compared the Atkins diet to the Ornish diet, the Zone diet and the LEARN diet.  You all probably remember this study, which he published in JAMA in 2007, showing the low-carb diet brought about greater weight loss and better lab value improvement than the other three diets.

Click here to view the embedded video.

As you watch this long video (and you should watch it; it’s extremely entertaining and filled with a ton of good info), there are a few things you should note.

Before we get to that though, let me fill you in on the LEARN diet.

Most of you, I’m sure, are familiar with the ultra-low-fat Ornish diet and the 30-40-30 protein-carb-fat ratio of the Zone diet, but you may not be aware of the LEARN diet.  LEARN stands for Lifestyle, Exercise, Attitudes, Relationships and Nutrition and is the brainchild of Kelly Brownell at Yale.  The LEARN diet is a low-calorie regimen that recommends 55-60 percent of calories as carbohydrate and under 10 percent of calories as saturated fat.  The LEARN program is big with academics (since it was created by one of their own) and is the diet typically used when a diet program is required as part of a study.  In fact, the LEARN manual was developed to bring some consistency to the nutritional regimens followed in research.  As a consequence of its widespread use in academia, it has also become the program that pretty much mirrors the national guidelines.  Or, to put it another way, the nutritional guidelines set by academics pretty much mirror the LEARN program.

If you look at the carb content of the LEARN program and realize that it is the basis for the national nutritional guidelines, you can LEARN why we have an obesity epidemic.  But that’s another subject.

First off, at about 17:10 in the video, Dr. Gardner talks about how Dean Ornish got mad at him for publishing this study.  (So did Barry Sears, author of the Zone, but Dr. Gardner didn’t mention him.)  Both Ornish and Sears got their noses out of joint after this study and sniffed that the study results didn’t really apply to their programs because clearly the data showed that the subjects assigned to their specific diets really weren’t following the diet as designed.  Both missed the point.

As Dr. Gardner plainly says, the study is of specific diet books and how patients lose (or don’t lose) weight following these books.  You can’t recruit a million people for a nutritional study in which you hold their hands throughout.  But you can write a book that a million or more people read and follow.  What Gardner was looking for in this study was how people would do following a diet book advocating a specific program as compared to others on different diet books promoting different diets.

As part of the structure of the study, he randomized subjects to the various diets, then had them come in weekly for eight weeks to visit with a dietitian who went over the book with them.  He relates an interesting story at about 26:10 that I’m sure is absolutely true.  Many of the people who were randomized to their particular diet were demoralized because they had already done that diet in the past and hadn’t done particularly well on it.  After going through the book with the dietitian, these same people realized they hadn’t really read the book very well – if at all – the first time through.  Once they really read and understood it, they were fired up and ready to go.  Based on may questions MD and I have received about our books, I know this only too well.

Earlier in the video, at about the 17:10 point, Dr. Gardner makes an observation that all of us using low-carb diets know well.  He is discussing how reducing carbs makes triglycerides go down and adding fat makes HDL go up.  He then says that all these people have come into the clinic he is involved with after having been on Ornish or McDougall only to find their triglycerides have skyrocketed and their HDLs have dropped off the chart.  He tells them to replace some of the carbohydrate with good quality “unsaturated fats” (sigh), and their labs revert to normal.

At about the 29:00 mark, Dr Gardner points out that as the data came in and was charted, it became apparent that it was difficult for people to stick with the Ornish or Zone diets, and when these subjects fell short of following their specific program, their macronutrient-consumption data ended up falling right smack into the middle of the LEARN data, or the national nutritional guidelines.  Those on the Atkins diet morphed a little (toward a more Protein Power sort of plan, but not quite), but not nearly as much as those on the low-fat diets did.  After a year, the data ended up showing a bunch of subjects essentially following the national nutritional guidelines and another, smaller bunch, following a semi-Atkins diet.

As Dr. Gardner points out, in virtually every parameter measured, those following the Atkins book who ended up following a semi-Atkins diet triumphed over those following the other books, all of whom ended up following the national nutritional guidelines.  Which, of course, is no surprise to most readers of this blog.

But it was a huge surprise to Dr. Gardner, a 25-year-long vegetarian.  He admitted it was a bitter pill to swallow, but the data are what the data are.  And he was man enough to admit it.  I think this study and Dr. Gardner’s engaging presentation style will start getting some notice from mainstreamers.  King Canute couldn’t hold back the tide, and I don’t think the lipophobes will be able to hold back low-carb diets forever.  This is a great video to show Doubting Thomases if they will take the time to watch it.

Aside from the finding that the low-carb diet was vastly superior, a lot of other data came to light as a consequence of this study.  Some people did great on Ornish or the Zone while others did poorly on Atkins.  Why?  You would think that since all the subjects were humans, they would all respond the same way, but they didn’t.

This intrigued Dr. Gardner, so he began slicing and dicing the data to see what he could come up with.  At about the 40:00 point on the video, he discussed a few papers showing that people who are insulin sensitive actually do better on high-carb diets than they do on low-carb diets, whereas those who are insulin resistant do just the opposite.

I pulled all the papers he discussed and plan on reading them over the next ten days while I’m spending (literally) about 24 hours in an airplane seat.  (As part of our Sous Vide Supreme tour, MD and I leave tomorrow for Dallas, then Vancouver, Seattle, San Francisco, Chicago, New York, and Las Vegas, so I’ll have plenty of time to read.) I do find this information fascinating, but I have a few reservations as well.  There are very few moderate to significantly overweight people who aren’t insulin resistant to some degree, so I’ll be curious to see how the authors of these papers define insulin resistance.

Based on my own experience with a whole lot of patients, there are a few, but not many, overweight people–usually women, but occasionally men–whose lab reports show normal insulin sensitivity. I treated them with a low-carb diet, and they did well.  But I didn’t randomize these apparently insulin-sensitive overweight patients into two groups and put one group on a low-carb diet and the other on a low-fat, high-carb diet, so I can’t really say the ones I treated did better than they would have on a low-fat diet.

What I do know, however, is that those who have been overweight and insulin resistant, and who lose their weight and restore their insulin sensitivity with a low-carb diet, will regain in a heartbeat if they go on a high-carb diet for maintenance.  So, it’s hard to reconcile this fact that I know from hands-on experience with the data Dr. Gardner presented.

It could have something to do with the genetics that prevent the development of insulin resistance in the first place.  I’ll post on my thought about this paradox after I’ve read the relevant papers and reflected on them.

I had only one real objection to this presentation.  At the end, during the Q & A, someone asked a question about ketosis, and Dr. Gardner was clearly in above his head.  He did make the distinction between the ketosis one experiences on a low-carb diet and the dangerous ketoacidosis that those with uncontrolled type I diabetes are subject to, but he seemed to be uncertain as to whether low-carb ketosis was harmful over the long run.  He did remark that everyone is in ketosis part of the day, but then he kind of tossed it off by saying that the people on the Atkins diet weren’t really following it that closely and so weren’t really in ketosis for that long.  I wish had addressed the ketosis situation head on.  There is no danger in being in ketosis for extended periods of time.  Ketones are normal fuels of respiration and don’t pose any problems over the long haul.  In fact, some research has shown that ketones are a preferred fuel of many organs including the heart. (Veech et al)

As I’ll be traveling a lot the next 10 days, and since I don’t know my exact schedule even yet, I can’t promise a lot of regular posting.  But I will check the blog often and put up the comments as they come in.  If any of you have experience with trying a low-fat diet after losing on a low-carb diet, I would love to hear about it.